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Nan Xu,Pengcheng Kan,Xiuhua Yao,Ping Yang,Jiwei Wang,Lei Xiang,Yu Zhu 한국미생물학회 2018 The journal of microbiology Vol.56 No.11
Acute ischaemic stroke (AIS) seriously affects patient quality of life. We explored the role of the intestinal microbiota on oxidative stress and autophagy in stroke, and Astragaloside IV (AS-IV) reversed the changes induced by intestinal microbiota. We determined the characteristics of the intestinal microbiota of AIS and transient ischaemic attack (TIA) patients by 16S sequencing and found that the structure and diversity of the intestinal microbiota in patients with AIS and TIA were significantly different from those in healthy subjects. Specifically, the abundance of genus Bifidobacterium, Megamonas, Blautia, Holdemanella, and Clostridium, content of homocysteine and triglyceride was increased significantly, thus it may be as a potential mechanism of AIS and TIA. Furthermore, germ-free mice were infused intracolonically with fecal supernatants of TIA and AIS with/without feed AS-IV for 12 weeks, and we found that the feces of AIS up-regulated the autophagy markers Beclin-1, light chain 3 (LC3)-II and autophagy-related gene (Atg)12, and the expression of reactive oxygen species (ROS) and NADPH oxidase 2/4 (NOX2/4), malondialdehyde (MDA), however, the expression of total antioxidant capacity (T-AOC) and activity of superoxide dismutase (SOD) and glutathione (GSH) was down-regulated in brain tissue, the content of homocysteine and free fatty acids (FFA) in serum of the mice. Meanwhile, AS-IV could reverse the above phenomenon, however, it does not affect the motor function of mice. AS-IV reversed these changes and it may be a potential drug for AIS therapeutics.
Yan Cui,Qing Ye,Heya Wang,Yingchao Li,Xiuhua Xia,Weirong Yao,He Qian 대한약학회 2014 Archives of Pharmacal Research Vol.37 No.12
The present study was designed to investigatethe protective effect of aloin against alcoholic liver disease ina chronic alcohol feeding mouse model. Mice were givenalcohol twice a day by intragastric administration for11 weeks (4.0, 4.7, 5.5 g/kg bw/day for the first 3 weeksrespectively, 6.3 g/kg bw/day for the following 8 weeks). Aloin (10, 30 mg/kg bw) or vehicle was given by gavage tomice after each alcohol administration. Alcohol elevated theserum transaminases alanine aminotransferase, aspartateaminotransferase, total cholesterol and triglyceride levelswhich were significantly attenuated by the co-administrationof aloin (p\0.05). Histopathological observations wereconsistent with these indices. Co-administration of aloinsignificantly suppressed the alcohol-dependent induction ofsterol regulatory element-binding protein-1c expression(p\0.01) and remarkably up-regulated themRNA levels ofAMP-activated protein kinase-a2 (p\0.001). Furthermore,aloin supplementation significantly inhibited the alcoholdependentelevation of malondialdehyde and cytochromeP4502E1 expression (p\0.05), and significantly elevatedsuperoxide dismutase activity (p\0.01). The up-regulationof serum lipopolysaccharide (LPS), hepatic nitric oxide,tumor necrosis factor a, toll-like receptor-4, and myeloiddifferentiation primary response gene 88 were also markedlysuppressed by the co-administration of aloin (p\0.05) inalcohol-treated mice. These results suggest that aloin mayrepresent a novel, protective strategy against chronic alcoholicliver injury by attenuating lipid accumulation, oxidativestress and LPS-induced inflammatory response.