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This model was found at
6390 locations
The model is used in
68 countries
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About the Tecan Infinite M200

The model Tecan Infinite M200 was found in 6390 unique locations in 68 countries where it was mentioned from 2008 until recentlyIt is used by scientists in various research fields such as General Medicine, Molecular Biology, Biochemistry, Molecular Medicine, and Organic Chemistry. The model is also used in Cell Biology, Cancer Research, Oncology, Pharmaceutical Science, Microbiology, Genetics, Physical and Theoretical Chemistry, General Biochemistry, Genetics and Molecular Biology, Drug Discovery, General Chemistry, Biotechnology, Immunology, Pharmacology, Microbiology (medical), Computer Science Applications, Catalysis, Spectroscopy, Inorganic Chemistry, Analytical Chemistry, Biomedical Engineering, Bioengineering, General Materials Science, General Physics and Astronomy, Physiology, and Biomaterials.
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Research that uses the Tecan Infinite M200

Witold Rant, Aurelia Radzik-Rant, Marcin Świątek, Roman Niżnikowski, Żaneta Szymańska, Magdalena Bednarczyk, Emil Orłowski, Anna Morales-Villavicencio, Magdalena Ślęzak, Archives Animal Breeding, 62, 383-391 (2), 2019
Abstract. The research carried out on meat from 45 ram lambs of the Polish merino breed allowed to determine the effect of meat aging and muscle type on physicochemical characteristics and oxidative stability of lipids. Analysis of physicochemical traits (pH, meat color, expressed juice, cooking loss, shear force, moisture, protein, fat and total collagen content) was performed on fresh and meat aged for 14 d in the longissimus lumborum (LL) and gluteus medius (GM) muscles. The meat aging determined all physicochemical characteristics except protein and fat content. More changes in pH and meat color parameters were defined in the GM muscle compared to the LL muscle. The increase in the tenderness of meat expressed as a reduction (P < 0.05) of shear force values was observed in both muscles aged for 14 d. A lower value (P < 0.05) of the shear force, despite the higher content of collagen, was determined in the GM muscle compared to LL. The investigated muscles differed in the degree of lipid peroxidation expressed as thiobarbituric acid-reactive substances (TBARS) in both fresh and aged meat. The TBARS value was lower (P < 0.05) in the LL muscle than in GM. In the longissimus lumborum muscle, the significantly lower content of polyunsaturated fatty acids (PUFAs) and PUFA n-6 has been recorded. The oxidation stability was not influenced by the meat aging.
Isa Santos, Henrique G. Colaço, Ana Neves-Costa, Elsa Seixas, Tiago R. Velho, Dora Pedroso, André Barros, Rui Martins, Nuno Carvalho, Didier Payen, Sebastian Weis, Hyon-Seung Yi, Minho Shong, Luís F. Moita, Proceedings of the National Academy of Sciences, 117, 12281-12287 (22), 2020
Significance Sepsis remains a leading cause of death. New insights into its pathophysiology are likely to be key to the development of effective therapeutic strategies against sepsis. Given the role of GDF15 in metabolism regulation and in cachexia during late stages of cancer, features that also occur in sepsis, elucidation of the possible mechanistic role of GDF15 in sepsis is of great importance. We find that septic patients have very high levels of GDF15 in the peripheral blood, which correlate with clinical outcomes. Using Gdf15 -deficient mice, we show that GDF15 plays a causal role in sepsis by delaying the local control of infection. These findings suggest GDF15 as a potential therapeutic target in sepsis secondary to a bacterial infection.
Yang Yu, Dong Guo, Tingting Qu, Shuchao Zhao, Chang Xu, Longlong Wang, Zhongjun Wang, Haiyang Fu, Xiangyan Zhang, Na Zhou, BioMed Research International, 2020, 1-6, 2020
The aim of this study was to explore the epidemiology of Toxoplasma gondii infection in patients with colorectal cancer (CRC) in eastern China. Therefore, 287 primary CRC patients and 287 age-matched healthy control subjects were recruited to estimate the seroprevalence of T. gondii and identify the risk factors of infection. Enzyme-linked immunoassays were used to test for anti-T. gondii immunoglobulin G (IgG) and IgM antibodies. Forty-six (16%) samples were positive for anti-T. gondii IgG antibodies in patients with CRC, compared with 26 (9.1%) in the healthy controls, a significant difference ( P = 0.007 ). By contrast, eight (2.8%) patients tested positive for T. gondii IgM antibodies, compared with three (1.1%) in the controls, a difference that was not significant ( P = 0.13 ). Multivariable backward stepwise logistic regression analysis revealed that a rural residence (OR 2.83; 95% CI 1.15–7.01; P = 0.024 ) and treatment with chemotherapy (OR 2.16; 95% CI 1.02–4.57; P = 0.045 ) were risk factors for T. gondii infection in patients with CRC. Thus, T. gondii infection is serious in patients with CRC, and a rural residence and treatment with chemotherapy are independent risk factors for infection by this parasite. Therefore, medical professionals should be aware of this pathogen in patients with CRC, and the causes of T. gondii infection in these patients need to be explored further.
Aleksandra Janas, Ewa Kruczek, Piotr Londzin, Sławomir Borymski, Zenon P. Czuba, Joanna Folwarczna, Mediators of Inflammation, 2020, 1-21, 2020
Although postmenopausal osteoporosis often occurs concurrently with diabetes, little is known about interactions between estrogen deficiency and hyperglycemia in the skeletal system. In the present study, the effects of estrogen deficiency on the development of biochemical, microstructural, and mechanical changes induced by streptozotocin-induced diabetes mellitus (DM) in the rat skeletal system were investigated. The experiments were carried out on nonovariectomized (NOVX) and ovariectomized (OVX) control and diabetic mature female Wistar rats. Serum levels of bone turnover markers (CTX-I and osteocalcin) and 23 cytokines, bone mass and mineralization, histomorphometric parameters, and mechanical properties of cancellous and compact bone were determined. The results were subjected to two-way ANOVA and principal component analysis (PCA). Estrogen deficiency induced osteoporotic changes, with increased bone resorption and formation, and worsening of microstructure (femoral metaphyseal BV/TV decreased by 13.0%) and mechanical properties of cancellous bone (the maximum load in the proximal tibial metaphysis decreased by 34.2%). DM in both the NOVX and OVX rats decreased bone mass, increased bone resorption and decreased bone formation, and worsened cancellous bone microarchitecture (for example, the femoral metaphyseal BV/TV decreased by 17.3% and 18.1%, respectively, in relation to the NOVX controls) and strength (the maximum load in the proximal tibial metaphysis decreased by 35.4% and 48.1%, respectively, in relation to the NOVX controls). Only in the diabetic rats, profound increases in some cytokine levels were noted. In conclusion, the changes induced by DM in female rats were only slightly intensified by estrogen deficiency. Despite similar effects on bone microstructure and strength, the influence of DM on the skeletal system was based on more profound systemic homeostasis changes than those induced by estrogen deficiency.
Zepeng Zhang, Lu Zhai, Jing Lu, Sanmiao Sun, Dandan Wang, Daqing Zhao, Liwei Sun, Weimin Zhao, Xiangyan Li, Ying Chen, Oxidative Medicine and Cellular Longevity, 2020, 1-19, 2020
Atherosclerosis (AS) is the killer of human health and longevity, which is majorly caused by oxidized lipoproteins that attack macrophages in the endarterium. The Shen-Hong-Tong-Luo (SHTL) formula has shown great clinical efficacy and vascular protective effect for over 30 years in China, to attenuate AS progression. However, its pharmacological mechanism needs more investigation. In this study, we first investigated the chemical composition of SHTL by fingerprint analysis using high-performance liquid chromatography. In primary mouse peritoneal macrophages induced by lipopolysaccharide (LPS), we found that SHTL pretreatment suppressed reactive oxygen species accumulation and reversed the increases of the inflammatory factors, TNF-α and IL-6. Moreover, lipid accumulation induced by oxidized low-density lipoprotein (Ox-LDL) in macrophages was inhibited by SHTL. Additionally, network pharmacology was used to predict the potential targets of SHTL as the PPAR-γ/LXR-α/ABCA1 signaling pathway, which was validated in macrophages and ApoE-/- mice by histopathological staining, qPCR, and Western blot analysis. Importantly, the protective effect of SHTL in the LPS- and Ox-LDL-induced macrophages against inflammation and lipid accumulation was attenuated by GW9662, a PPAR-γ antagonist, which confirmed the prediction results of network pharmacology. In summary, these results indicated that SHTL pretreatment reduced inflammation and lipid accumulation of macrophages by activating the PPAR-γ/LXR-α/ABCA1 pathway, which may provide a new insight into the mechanism of SHTL in the suppression of AS progression.
Rumiana Bakalova, Severina Semkova, Donika Ivanova, Zhivko Zhelev, Thomas Miller, Tsuguhide Takeshima, Sayaka Shibata, Dessislava Lazarova, Ichio Aoki, Tatsuya Higashi, Oxidative Medicine and Cellular Longevity, 2020, 1-30, 2020
Redox-active substances and their combinations, such as of quinone/ascorbate and in particular menadione/ascorbate (M/A; also named Apatone®), attract attention with their unusual ability to kill cancer cells without affecting the viability of normal cells as well as with the synergistic anticancer effect of both molecules. So far, the primary mechanism of M/A-mediated anticancer effects has not been linked to the mitochondria. The aim of our study was to clarify whether this “combination drug” affects mitochondrial functionality specifically in cancer cells. Studies were conducted on cancer cells (Jurkat, Colon26, and MCF7) and normal cells (normal lymphocytes, FHC, and MCF10A), treated with different concentrations of menadione, ascorbate, and/or their combination (2/200, 3/300, 5/500, 10/1000, and 20/2000 μM/μM of M/A). M/A exhibited highly specific and synergistic suppression on cancer cell growth but without adversely affecting the viability of normal cells at pharmacologically attainable concentrations. In M/A-treated cancer cells, the cytostatic/cytotoxic effect is accompanied by (i) extremely high production of mitochondrial superoxide (up to 15-fold over the control level), (ii) a significant decrease of mitochondrial membrane potential, (iii) a decrease of the steady-state levels of ATP, succinate, NADH, and NAD+, and (iv) a decreased expression of programed cell death ligand 1 (PD-L1)—one of the major immune checkpoints. These effects were dose dependent. The inhibition of NQO1 by dicoumarol increased mitochondrial superoxide and sensitized cancer cells to M/A. In normal cells, M/A induced relatively low and dose-independent increase of mitochondrial superoxide and mild oxidative stress, which seems to be well tolerated. These data suggest that all anticancer effects of M/A result from a specific mechanism, tightly connected to the mitochondria of cancer cells. At low/tolerable doses of M/A (1/100-3/300 μM/μM) attainable in cancer by oral and parenteral administration, M/A sensitized cancer cells to conventional anticancer drugs, exhibiting synergistic or additive cytotoxicity accompanied by impressive induction of apoptosis. Combinations of M/A with 13 anticancer drugs were investigated (ABT-737, barasertib, bleomycin, BEZ-235, bortezomib, cisplatin, everolimus, lomustine, lonafarnib, MG-132, MLN-2238, palbociclib, and PI-103). Low/tolerable doses of M/A did not induce irreversible cytotoxicity in cancer cells but did cause irreversible metabolic changes, including: (i) a decrease of succinate and NADH, (ii) depolarization of the mitochondrial membrane, and (iii) overproduction of superoxide in the mitochondria of cancer cells only. In addition, M/A suppressed tumor growth in vivo after oral administration in mice with melanoma and the drug downregulated PD-L1 in melanoma cells. Experimental data suggest a great potential for beneficial anticancer effects of M/A through increasing the sensitivity of cancer cells to conventional anticancer therapy, as well as to the immune system, while sparing normal cells. We hypothesize that M/A-mediated anticancer effects are triggered by redox cycling of both substances, specifically within dysfunctional mitochondria. M/A may also have a beneficial effect on the immune system, making cancer cells “visible” and more vulnerable to the native immune response.
Mateusz Maciejczyk, Piotr Gerreth, Anna Zalewska, Katarzyna Hojan, Karolina Gerreth, Oxidative Medicine and Cellular Longevity, 2020, 1-14, 2020
Stroke is one of the leading causes of disability and death worldwide. Despite intensive medical care, many of the complaints directly threatening the patient’s life marginalize their dental needs after the stroke. Recent studies indicate reduced saliva secretion in stroke patients in addition to the increased incidence of caries and periodontal disease. Since oxidative stress plays a vital role in the pathogenesis of salivary gland hypofunction and neurodegenerative disorders (including stroke), this is the first to evaluate the relationship between salivary gland activity and protein glycoxidation and nitrosative damage. The content of glycation and protein oxidation products and nitrosative stress was assessed in nonstimulated (NWS) and stimulated (SWS) whole saliva of stroke patients with normal salivary secretion and hyposalivation (reduced saliva production). The study included 30 patients in the stroke’s subacute phase and 30 healthy controls matched by age and sex. We have shown that stroke patients with hyposalivation show increased contents of protein glycation (↑Amadori products and ↑advanced glycation end products), glycoxidation (↑dityrosine), and nitration (↑nitrotyrosine) products compared to stroke cases with normal salivary secretion and control group. Interestingly, higher oxidative/nitrosative stress was found in NWS, which strongly correlates with salivary flow rate, total protein content, and salivary amylase activity. Such relationships were not observed in the control group. Summarizing, oxidative and nitrosative stress may be one of the mechanisms responsible for the impairment of saliva secretion in stroke patients. However, extraglandular sources of salivary oxidative stress in stroke patients cannot be excluded. Further studies to assess salivary gland hypofunction in stroke cases are necessary.
Karen L. Latorre, Paula A. Baldion, International Journal of Dentistry, 2020, 1-14, 2020
Dentinal hypersensitivity is a frequent reason for dental consultation, and its pathophysiology has not been fully clarified. Previous findings have made it possible to establish a relationship between the cellular sensory capacity and the activation of the polymodal transient receptor potential vanilloid 1 (TRPV1), which is responsible for the nociceptive response and whose desensitization could cause analgesia. Thus, the objective of this study was to determine the expression, localization, and functional activity of TRPV1 in human odontoblasts-like-cells (hOLCs) and the effect of eugenol (EUG) on its activation and desensitization. Human dental pulp stem cells (hDPSCs) were obtained from third molars and were characterized using flow cytometry, and their differentiation potential toward the osteoblastic, chondrogenic, and adipogenic lineages was investigated. Subsequently, the hDPSCs underwent odontogenic differentiation for 7, 14, and 21 days, and their phenotype (odontogenic markers dentin matrix protein-1 (DMP-1) and dentin sialoprotein (DSP)) was evaluated using immunofluorescence. The TRPV1 gene expression in hOLCs was estimated using RT-qPCR, and its localization was analyzed using immunofluorescence. Half-maximal effective concentration (EC50) from both eugenol (EUG) and capsaicin (CAP) was determined; in addition, receptor activation was evaluated against chemical, thermal, and pH stimuli. For the statistical analysis, a one-way ANOVA with a Tukey post hoc test ( p < 0.05 ) was used. After establishing the in vitro model of hOLCs and the membrane location of TRPV1, its chemical activation with EUG and CAP was demonstrated, as well as its thermal activation at ≥ 43°C and with an acidic (<6) or basic pH (between 9 and 12). Receptor desensitization was achieved after 20 min of exposure to two concentrations of EUG (603.5 and 1000 µM). These findings represent a stepping-stone for the construction of a pulp pain study model oriented toward a therapeutic alternative for the treatment of dentinal hypersensitivity.
Jong Min Kim, Uk Lee, Jin Yong Kang, Seon Kyeong Park, Jong Cheol Kim, Ho Jin Heo, Oxidative Medicine and Cellular Longevity, 2020, 1-19, 2020
This study was conducted to assess the protective effect of extract of match (EM) on high-fat diet- (HFD-) induced cognitive deficits in male C57BL/6 mice. It was found that EM improved glucose tolerance status by measuring OGTT and IPGTT with HFD-induced mice. EM protected behavioral and memory dysfunction in Y-maze, passive avoidance, and Morris water maze tests. Consumption of EM reduced fat mass, dyslipidemia, and inflammation in adipose tissue. Also, EM ameliorated hepatic and cerebral antioxidant systems. EM improved the cerebral cholinergic system by regulating ACh contents and expression of AChE and ChAT. Also, EM restored mitochondrial function in liver and brain tissue. EM attenuated hepatic inflammatory effect, lipid synthesis, and cholesterol metabolism by regulating the protein expression of TNF-α, TNFR1, p-IRS-1, p-JNK, IL-1β, iNOS, COX-2, HMGCR, PPARγ, and FAS. Finally, EM regulated cognitive function and neuroinflammation in the whole brain, hippocampus, and cerebral cortex by regulating the protein expression of p-JNK, p-Akt, p-tau, Aβ, BDNF, IDE, COX-2, and IL-1β. These findings suggest that EM might be a potential source of functional food to improve metabolic disorder-associated cognitive dysfunction.
Nishchitha Hemmige Natesh, Mercy O. Ijenyo, Samuel Kwaku Asiedu, H. P. Vasantha Rupasinghe, Lord Abbey, International Journal of Agronomy, 2021, 1-11, 2021
Nitrogen (N) fertilization at critical planting time is important to optimize productivity and reduce nitrate accumulation in edible portions of green leafy vegetable plants. A field experiment was performed to determine the effects of variations in N rate and planting time on plant growth, yield, and nutritional quality attributes of Basella alba under Atlantic maritime climatic conditions. The N rates were 0 (control), 40 (low), 80 (medium), and 120 kg ha−1 (high) at planting times 15 June–3 August (early season), 6 July–20 August (mid-season), and 4 August–8 September (late season). Plant height, number of branches, and stem girth were increased after 45 days after sowing in early and mid-season plantings, but leaf length decreased during the same time by 32.8% in the late planting. The average yield obtained in early, mid-, and late plantings were 171, 464, and 328 g plant−1, respectively. Low N gave the highest yield in early planting while medium N gave higher yields in mid- and late plantings. However, the medium N increased nitrate accumulation in B. alba by 7% compared to the high N rate. In general, there was no significant effect of N on B. alba total phenolic and total carotenoid contents. Overall, the highest yield was obtained during the warmest summer months of mid- and late plantings. Therefore, there is a potential to grow B. alba as a summer vegetable under Canadian Atlantic maritime conditions. However, it is recommended to reduce the rate of N fertilizer application during high-temperature conditions. Future studies are required to investigate phosphorus and potassium fertilization and nitrate accumulation in B. alba and potential health risks.
Menghuan Guo, Zhiyuan Liu, Jing Si, Jinhua Zhang, Jin Zhao, Zhong Guo, Yi Xie, Hong Zhang, Lu Gan, BioMed Research International, 2021, 1-11, 2021
Lung cancer remains the leading cause of cancer death worldwide. Late diagnosis, chemoresistance, and metastasis are the main reasons for the high mortality rate of lung cancer. Therefore, the development of other treatments is urgent. Cediranib (CED), a vascular endothelial growth factor receptor (VEGFR) kinase inhibitor, shows promising antitumour activities in various cancers including lung cancer. Here, we explored the effects and the underlying molecular mechanism of CED on non-small-cell lung cancer (NSCLC) cell line A549 cells in vitro. Our results show that CED could inhibit A549 cell proliferation and cloning formation. Meanwhile, G1 phase cell cycle arrest was also found, as featured by the increased proportion of G1 phase cells as well as the reduction of G1 phase relative proteins CDK4/cyclin D1 and CDK2/cyclin E. Moreover, the ratio of LC3-II/LC3-I was elevated significantly in CED-treated groups compared with the controls. Furthermore, the expression of p-Akt, p-P38, p-Erk1/2, and p-mTOR proteins was decreased obviously in the treatment groups. These results suggest that CED could induce apoptosis and G1 phase cell cycle arrest in A549 cells. Meanwhile, CED may induce autophagy through MAPK/Erk1/2 and Akt/mTOR signal pathway in A549 cells.
Kai Wang, Xiangfeng Kong, Md. Abul Kalam Azad, Qian Zhu, Liang Xiong, Yuzhong Zheng, Zhangli Hu, Yulong Yin, Qinghua He, Oxidative Medicine and Cellular Longevity, 2021, 1-14, 2021
The present study was conducted to investigate the effects of maternal probiotic or synbiotic supplementation during gestation and lactation on antioxidant capacity, mitochondrial function, and intestinal microbiota abundance in offspring weaned piglets. A total of 64 pregnant Bama mini-sows were randomly allocated into the control group (basal diet), antibiotic group ( basal diet + 50 g/t virginiamycin), probiotic group ( basal diet + 200  mL/d probiotics per pig), or synbiotic group ( basal diet + 200  mL/d probiotics per pig + 500  g/t xylo-oligosaccharides). On day 30 of post-weaning, eight piglets per group with average body weight were selected for sample collection. The results showed that maternal probiotic supplementation increased the catalase (CAT) activity in plasma and glutathione peroxidase (GSH-Px) and superoxide dismutase (SOD) activities in plasma, jejunum, and colon of piglets while decreased the malondialdehyde (MDA) and H2O2 concentrations in plasma compared with the control group ( P < 0.05 ). Moreover, maternal synbiotic supplementation increased the plasma CAT activity, jejunal glutathione and GSH-Px activities, jejunal and colonic total antioxidant capacity activity, and plasma and colonic SOD activity while decreased the colonic MDA concentration of offspring piglets compared with the control group ( P < 0.05 ). The mRNA levels of antioxidant enzyme-related genes (copper- and zinc-containing superoxide dismutase, nuclear factor erythroid 2-related factor 1, and nuclear factor erythroid 2-related factor 2) and mitochondrial-related genes (adenosine triphosphate synthase alpha subunit, adenosine triphosphate synthase β, and mitochondrial transcription factor A) in the jejunal mucosa were significantly upregulated, while the level of colonic peroxisome proliferator-activated receptor γ coactivator-1α was downregulated by maternal synbiotic supplementation ( P < 0.05 ). Maternal probiotic supplementation increased ( P < 0.05 ) the Bacteroidetes abundance in the jejunum and Bifidobacterium abundance in the jejunum and colon, and synbiotic supplementation increased ( P < 0.05 ) the abundances of Firmicutes, Bacteroidetes, Bifidobacterium, and Lactobacillus in the jejunum of piglets. Furthermore, correlation analysis revealed that intestinal microbiota abundances were significantly correlated with antioxidant enzyme activities and mitochondrial-related indexes. These findings indicated that maternal probiotic or synbiotic supplementation might be a promising strategy to improve the antioxidant capacity and mitochondrial function of offspring weaned piglets by altering the intestinal microbiota.
Wai-Rong Zhao, Wen-Ting Shi, Jing Zhang, Kai-Yu Zhang, Ye Qing, Jing-Yi Tang, Xin-Lin Chen, Zhong-Yan Zhou, Evidence-Based Complementary and Alternative Medicine, 2021, 1-11, 2021
Inflammation response is a regulated cellular process and excessive inflammation has been recognized in numerous diseases, such as cardiovascular disease, neurodegenerative disease, inflammatory bowel disease, and cancer. Tribulus terrestris L. (TT), also known as Bai Jili in Chinese, has been applied in traditional Chinese medicine for thousands of years while its anti-inflammatory activity and underlying mechanism are not fully elucidated. Here, we hypothesize Tribulus terrestris L. extract (BJL) which presents anti-inflammatory effect, and the action mechanism was also investigated. We employed the transgenic zebrafish line Tg(MPO:GFP), which expresses green fluorescence protein (GFP) in neutrophils, and mice macrophage RAW 264.7 cells as the in vivo and in vitro model to evaluate the anti-inflammatory effect of BJL, respectively. The production of nitric oxide (NO) was measured by Griess reagent. The mRNA expression levels of inflammatory cytokines and inducible nitric oxide synthase (iNOS) were measured by real-time PCR, and the intracellular total or phosphorylated protein levels of NF-κB, Akt, and MAPKs including MEK, ERK, p38, and JNK were detected by western blot. We found that BJL significantly inhibited fin transection or lipopolysaccharide- (LPS-) induced neutrophil migration and aggregation in zebrafish in vivo. In mice macrophage RAW 264.7 cells, BJL ameliorated LPS-triggered excessive release of NO and transcription of inflammatory cytokine genes including tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and interleukin-1 beta (IL-1β). BJL also reduced the LPS-induced elevations of intracellular iNOS and nuclear factor kappa B (NF-κB) which mediate the cellular NO and inflammatory cytokine productions, respectively. Moreover, LPS dramatically increased the phosphorylation of Akt and MAPKs including MEK, ERK, p38, and JNK in RAW 264.7 cells, while cotreatment BJL with LPS suppressed their phosphorylation. Taken together, our data suggested that BJL presented potent anti-inflammatory effect and the underlying mechanism was closely related to the inhibition of Akt/MAPKs and NF-κB/iNOS-NO signaling pathways.
Mi-Rae Shin, Min Ju Kim, Hae-Jin Park, Jegeun Han, Seong-Soo Roh, Evidence-Based Complementary and Alternative Medicine, 2021, 1-12, 2021
Objective. Liver kinase B (LKB) 1 and AMP-activated protein kinase (AMPK) are master regulators and sensors for energy homeostasis. AMPK is mainly activated via phosphorylation of LKB1 under energy stress. Here, we highlighted the antiobesity effect and underlying mechanism of Taraxacum coreanum Nakai (TCN) in connection with LKB1-AMPK signaling pathway. Methods. Male C57BL/6 mice were fed on a high-fat diet (60% kcal fat; HFD) to induce obesity. Simultaneously, they received 100 or 200 mg/kg TCN orally for 5 weeks. We measured the body weight gain and liver weight along with liver histology. Moreover, the changes of factors related to lipid metabolism and β-oxidation were analyzed in the liver, together with blood parameters. Results. The body weights were decreased in mice of the TCN200 group more than those of the HFD control group. Moreover, TCN supplementation lowered serum triglyceride (TG) and total cholesterol (TC) levels, whereas TCN increased HDL-cholesterol level. Liver pathological damage induced by HFD was alleviated with TCN treatment and accompanied with significant reduction in serum AST and ALT activities. In addition, TCN significantly increased the expression of p-AMPK compared with the HFD control group via the activation of LKB1/AMPK signaling pathway. Lipid synthesis gene like ACC was downregulated and factors related to β-oxidation such as carnitine palmitoyl transferase-1 (CPT-1) and uncoupling protein 2 (UCP-2) were upregulated through peroxisome proliferator-activated receptor (PPAR) α activation. Conclusion. Taken together, these data suggest that TCN treatment regulates lipid metabolism via LKB1-AMPK signaling pathway and promotes β-oxidation by PPARα; hence, TCN may have potential remedy in the prevention and treatment of obesity.
Yu Jiao, Sang Chan Kim, Yuhua Wang, Tong Wu, Haifeng Jin, Chul Won Lee, Sook Jahr Park, Bong Hyo Lee, Hee Young Kim, Chae Ha Yang, Zhenglin Zhao, Rongjie Zhao, Evidence-Based Complementary and Alternative Medicine, 2021, 1-14, 2021
Both the positive (manifested by locomotor sensitization) and negative (withdrawal symptoms) reinforcing effects of ethanol (EtOH) involve central nitric oxide (NO) signaling. Sauchinone (a bioactive lignan in Saururus chinensis) has been shown to improve methamphetamine-induced behavioral and neurochemical changes via the NO signaling pathway. Thus, this study evaluated the effects of sauchinone on locomotor sensitization and anxiety during EtOH withdrawal (EtOHW). Male adult Sprague-Dawley rats were treated with 1.5 g/kg/day of EtOH (20%, vol/vol) via intraperitoneal injection for 28 days, followed by a 3-day withdrawal. During withdrawal, the rats were given intragastric sauchinone (2.5, 7.5, or 25 mg/kg/day) once a day. EtOH locomotor sensitization was determined by challenging EtOHW rats with 0.75 g/kg EtOH, while EtOHW-induced anxiety was assessed using the elevated plus maze (EPM). None of the three doses of sauchinone affected EtOH locomotor sensitization. However, in the EPM, treatment of EtOHW rats with sauchinone at 7.5 or 25 mg/kg/day increased both the number of entries into and the time spent in the open arms. Moreover, the two doses of sauchinone inhibited the oversecretion of plasma corticosterone during EtOHW. In the bed nucleus of the stria terminalis (BNST), EtOHW increased NO production, enhanced gene and protein expression of both inducible nitric oxide synthase (iNOS) and neuronal NOS (nNOS), and also elevated protein levels of corticotropin-releasing factor, which were all inhibited by 25 mg/kg/day sauchinone. In an in vitro experiment, sauchinone (3, 10, and 30 μM) inhibited H2O2-stimulated nNOS protein expression in neuronal PC12 cells. Finally, intra-BNST infusion of sodium nitroprusside, a NO donor, after sauchinone (25 mg/kg/day) administration, abolished its expected anxiolytic effect. Taken together, these results indicate that sauchinone attenuates anxiety-like behavior in rats during EtOHW but spares EtOH locomotor sensitization, and the anxiolytic effect is mediated via the NO signaling pathway in the BNST.
Di Zhang, Qi Shen, Xiaolei Wu, Da Xing, Oxidative Medicine and Cellular Longevity, 2021, 1-20, 2021
Accumulating evidence indicates that dysfunction of the glutamatergic neurotransmission has been widely involved in the pathophysiology and treatment of depression. Photobiomodulation therapy (PBMT) has been demonstrated to regulate neuronal function both in vitro and in vivo. Herein, we aim to investigate whether the antidepressant phenotype of PBMT is associated with the improvement of glutamatergic dysfunction and to explore the mechanisms involved. Results showed that PBMT decreased extracellular glutamate levels via upregulation of glutamate transporter-1 (GLT-1) and rescued astrocyte loss in the cerebral cortex and hippocampus, which also alleviated dendritic atrophy and upregulated the expression of AMPA receptors on the postsynaptic membrane, ultimately exhibiting behaviorally significant antidepressant effects in mice exposed to chronic unpredictable mild stress (CUMS). Notably, PBMT also obtained similar antidepressant effects in a depressive mouse model subcutaneously injected with corticosterone (CORT). Evidence from in vitro mechanistic experiments demonstrated that PBMT treatment significantly increased both the GLT-1 mRNA and protein levels via the Akt/NF-κB signaling pathway. NF-κB-regulated transcription was in an Akt-dependent manner, while inhibition of Akt attenuated the DNA-binding efficiency of NF-κB to the GLT-1 promoter. Importantly, in vitro, we further found that PKA activation was responsible for phosphorylation and surface levels of AMPA receptors induced by PBMT, which is likely to rescue excitatory synaptic transmission. Taken together, our research suggests that PBMT as a feasible therapeutic approach has great potential value to control the progression of depression.
Brice E. N. Wamba, Paramita Ghosh, Armelle T. Mbaveng, Sayantan Bhattacharya, Mitra Debarpan, Saha Depanwita, Mustafi Mitra Saunak, Victor Kuete, Nabendu Murmu, Evidence-Based Complementary and Alternative Medicine, 2021, 1-15, 2021
Piper capense belongs to Piperaceae family and has long been used as a traditional medicine to treat various diseases in several parts of Africa. The present study aims to investigate the effect of Piper capense fruit extract (PCFE) alone and in combination with dacarbazine on metastatic melanoma cell line B16-F10 and in vivo in C57BL/6J mice. Cytotoxic effects of PCFE alone and in association with dacarbazine on B16-F10 cells were studied by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyl tetrazolium bromide (MTT) assay and colony formation assay. Wound healing assay, immunofluorescence staining, and western blot analysis were performed to evaluate the individual and combined effect of PCFE and dacarbazine on epithelial-mesenchymal transition (EMT). For in vivo studies, C57BL/6J mice were subcutaneously injected with B16-F10 cells (5 × 105 cells/mL), and the effect of PCFE and dacarbazine was studied on tumor development. The alteration of EMT was evaluated by targeting E-cadherin, vimentin, and CD133 in PCFE alone and in combination with dacarbazine-treated tumor tissues by western blot analysis. Phytochemical screening of PCFE reveals the presence of certain secondary metabolites. Our results showed that PCFE alone and in association with dacarbazine has a good activity in preventing B16-F10 melanoma cell progression and clonogenicity. This extract also regulated EMT. In vivo results showed that PCFE (100 mg/kg body weight) reduced tumor size in C57BL/6J mice along with the decrease in the expression of vasculogenic mimicry (VM) tubes as well as an improvement in the qualitative and quantitative expression of markers involved in EMT. Our study suggests that PCFE may be useful for managing the growth and metastasis of melanoma.
Jin A. Lee, Mi-Rae Shin, Min Ju Kim, Ji Hye Lee, Hae-Jin Park, Seong-Soo Roh, BioMed Research International, 2021, 1-16, 2021
Gastroesophageal reflux disease (GERD) is induced by the reflux of stomach contents or gastric acid, pepsin into the esophagus for prolonged periods of time due to defection of the lower esophageal sphincter. Reflux esophagitis is a disease found in less than 50% of GERD patients. This study is aimed at evaluating the protective effect of Curcumae longae Rhizoma 30% EtOH extract (CLR) in acute reflux esophagitis (ARE) rats. CLR measured antioxidant activity through in vitro experiments. Based on the results, we performed experiments in vivo. Before 90 min ARE induction, CLR was administered orally by concentration. ARE was derived by linking the metastatic junction between pylorus and forestomach and corpus in Sprague-Dawley rats. And rats were sacrificed 5 h after surgery. We analyzed the expression of antioxidant and inflammatory-related markers by western blot and observed the production of alanine aminotransferase (ALT), aspartate aminotransferase (AST), reactive oxygen species (ROS), peroxynitrite (ONOO-), and thiobarbituric acid reactive substance (TBARS). The administration of CLR reduced esophagus tissue damage in rats with acute reflux esophagitis and decreased the elevated ALT, AST, ROS, ONOO-, and TBARS. In addition, CLR effectively increased antioxidant-related factors and reduced inflammatory protein. Overall, these results suggest that CLR would be used as a therapeutic material in protection and treatment for ARE. Overall, CLR treatment informed that markedly ameliorated inactivation of NF-κB led to the inhibition of the expressions of proinflammatory proteins. These results suggest that CLR would be used as a therapeutic material in protection and treatment for ARE.
Krzysztof Drygalski, Katarzyna Siewko, Andrzej Chomentowski, Cezary Odrzygóźdź, Anna Zalewska, Adam Krętowski, Mateusz Maciejczyk, Oxidative Medicine and Cellular Longevity, 2021, 1-18, 2021
Nonalcoholic fatty liver disease (NAFLD) is one of the most commonly occurring diseases within western dietary patterns. Usually untreated, it may lead to type 2 diabetes mellitus (T2DM), steatohepatitis (NASH), and hepatocellular carcinoma (HCC). Besides its severe aftermath, up to now, there is no known therapeutic approach to this disease in everyday clinical practice. Most NAFLD patients are encouraged to do physical activities or diet change and remain without pharmacological treatment. In this study, we present phloroglucinol (PHG) as a novel and promising compound in NAFLD treatment. PHG significantly increased the level of enzymatic and nonenzymatic antioxidants both in palmitate and hydrogen peroxide-induced oxidative stress models. Strengthened antioxidative defense reduced the oxidative/nitrosative damage to cell proteins, lipids, and carbohydrates. Furthermore, PHG treatment reduced hepatic steatosis; lowered inflammatory markers, such as NF-κB or HIF-1α; and inhibited cell apoptosis. Moreover, PHG had a more comprehensive effect than other commonly used antioxidants: N-acetylcysteine (NAC) and α-lipoic acid (ALA), suggesting its clinical usability. Therefore, our paper supports the benefits of natural compounds as a therapeutical approach to NAFLD.
Debra A. Brock, Suegene Noh, Alicia N.M. Hubert, Tamara S. Haselkorn, Susanne DiSalvo, Melanie K. Suess, Alexander S. Bradley, Mahboubeh Tavakoli-Nezhad, Katherine S. Geist, David C. Queller, Joan E. Strassmann, PeerJ, 8, e9151, 2020
Here we give names to three new species of Paraburkholderia that can remain in symbiosis indefinitely in the spores of a soil dwelling eukaryote, Dictyostelium discoideum. The new species P. agricolaris sp. nov., P. hayleyella sp. nov., and P. bonniea sp. nov. are widespread across the eastern USA and were isolated as internal symbionts of wild-collected D. discoideum. We describe these sp. nov. using several approaches. Evidence that they are each a distinct new species comes from their phylogenetic position, average nucleotide identity, genome-genome distance, carbon usage, reduced length, cooler optimal growth temperature, metabolic tests, and their previously described ability to invade D. discoideum amoebae and form a symbiotic relationship. All three of these new species facilitate the prolonged carriage of food bacteria by D. discoideum, though they themselves are not food. Further studies of the interactions of these three new species with D. discoideum should be fruitful for understanding the ecology and evolution of symbioses.
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