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FOOD AND CHEMICAL TOXICOLOGY · 2012 · IF 2.999

Dietary quercetin ameliorates nonalcoholic steatohepatitis induced by a high-fat diet in gerbils

Hua-Zhong Ying,Yue-Huan Liu,Bing Yu,Zhi-Yuan Wang,Jia-Na Zang,Chen-Huan Yu

Dietary quercetin is highly abundant in edible plants, which possesses a wide range of pharmacological properties. This study was to investigate hepatoprotective effects of quercetin in the nonalcoholic steatohepatitis (NASH) gerbils induced by a high-fat diet (HFD), and to evaluate its regulatory mechanism on hepatic inflammatory response. The gerbils were fed with HFD for 28   days to induce NASH. From 15th day to 28th day, the treated drugs were given daily to each animal, respectively. The lipid profiles and biochemical markers were determined at the end of the experiment. The expressions of Sirt1, NF-κB p65 and iNOS were detected by immunohistochemistry and Western blot analysis. The results showed that oral administration of quercetin at doses of 30–60   mg/kg to hyperlipidemia rats for 14   days were highly effective in decreasing the levels of serum total cholesterol (TC), triglycerides (TG), low-density lipoprotein cholesterol (LDL-C), alanine aminotransferase (ALT) and aspartate aminotransferase (AST). It could decrease lipid accumulation in the hepatocytes, and reduce serum levels of pro-inflammatory cytokines TNF-α and IL-6 via regulating the expressions of Sirt1, NF-κB p65 and iNOS. Thus, dietary quercetin had significant therapeutic benefits and could be explored as a potential promising candidate for the prevention of NASH.

CAS / MDL: 117-39-5
研究领域: 药理学 · 肝病学 · 营养学
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INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES · 2025 ·Vol. 26 ·期 18 ·9016 · IF 4.9

Biphasic Adaptations of Gastric Epithelial Cells in Chronic H. pylori Infection from Stress to Tolerance

Xiulin Zhang,Yang He,Xiaolu Zhang,Ziyi Liang,Wendong Wang,Zhenyu Da,Jianyi Lv,Meng Guo,Xueyun Huo,Xin Liu,Jing Lu,Lixue Cao,Xiaoyan Du,Zhongming Ge,Zhenwen Chen,Xuancheng Lu,Jianzhong Zhang,Changlong Li

Helicobacter pylori(H. pylori) is a well-known pathogen associated with chronic gastric infection, progressing from gastritis to gastric adenocarcinoma, but the dynamic phenotypic and molecular characteristics of gastric epithelial cells during sustained infection remain unclear. We established a chronic infection model using the human gastric epithelial cell line GES-1, exposed toH. pylorior its lysate across 30 generations, dynamically assessing cell proliferation, migration, invasion, apoptosis, autophagy, and epithelial–mesenchymal transition (EMT) markers, with RNA sequencing for transcriptomic changes and a Mongolian gerbil model to validate chronic pathological progression. AcuteH. pyloriexposure induced pronounced morphological changes; suppressed proliferation, migration, and invasion; triggered apoptosis; and blocked autophagic flux, while long-term stimulation reversed these effects. EMT markers showed progressive loss of epithelial characteristics with chronic infection. RNA sequencing revealed a dynamic shift from inflammation-driven apoptosis to adaptive survival mechanisms. In vivo, prolonged infection induced dynamic TLR expression alongside progressive gastric pathology, including atrophy and dysplasia. Our study provides new molecular evidence for dynamic cellular and immunological adaptations of gastric epithelial cells under chronicH. pyloriinfection, highlighting critical intervention windows for preventing gastric carcinogenesis.

CAS / MDL: 548-62-9
研究领域: 微生物学 · 胃肠病学 · 分子生物学 · 传染病学 · 癌症研究 · 细胞生物学
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