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- 저자 : Zhu Yunzhen (검색결과 2 건)
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Yunzhen Zhu,Juan Luo,Zhaoqing Yang,Yinglei Miao 한국유전학회 2020 Genes & Genomics Vol.42 No.10
Background Previous investigations reported that the imbalance of intestinal microfora may be the initiation and promotion factor in the pathogenesis of infammatory bowel disease such as ulcerative colitis (UC). Glucocorticoid is a very important class of regulatory molecules in the body. The response of diferent individuals to glucocorticoids can be divided into glucocorticoid sensitive, glucocorticoid resistance and glucocorticoid dependence. Objective We aimed to investigate the diferences in intestinal microfora composition and related metabolic pathways in UC patients with these three diferent glucocorticoid response types. Methods The whole genomic DNA was extracted from fecal specimens. High-throughput sequencing technology was used to analyze the fecal 16S rRNA genome of UC patients with diferent glucocorticoid response types, and functional prediction was performed by PICRUSTs software. Results The results showed that the intestinal microfora of the three groups were mainly composed of Firmicutes, Proteobacteria and Bacteroidetes. Although the species abundance and diversity of intestinal microfora in UC patients difered little among the three groups, the composition of intestinal microfora showed signifcant heterogeneity, which directly led to diferences in the function of intestinal microbiota of UC patients with diferent glucocorticoid responses. Furthermore, of the 240 pathways, “PANTO-PWY: phosphopantothenate biosynthesis I”, “COA-PWY-1: coenzyme A biosynthesis II (mammalian)” and “PWY-4242: pantothenate and coenzyme A biosynthesis III” were signifcantly diferent in the three groups. Conclusions These results indicate that UC patients with diferent glucocorticoids response types have diferent bacterial compositions and functions, which lays a foundation for further study of glucocorticoid resistance in UC patients.
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Luo Juan,Bai Luyan,Tao Jun,Wen Yu,Li Mingke,Zhu Yunzhen,Luo Sufeng,Pu Guangyu,Ma Lanqing 한국유전학회 2021 Genes & Genomics Vol.43 No.10
Background Vacuolating cytotoxin (VacA) is an important virulence factor of Helicobacter pylori (H. pylori). It was previously believed that VacA can trigger the cascade of apoptosis on mitochondria to lead to cell apoptosis. Recently, it was found that VacA can induce autophagy. However, the molecular mechanism by which VacA induces autophagy is largely unknown. Objective We aimed to explore the molecular mechanism of autophagy induced by H. pylori in gastric cancer cells and the efect of autophagy on the survival of gastric cancer cells. Methods The autophagy of human gastric cancer cell line SGC7901 was detected by Western blot and RT-PCR in the treatment of VacA protein of H. pylori. The relationship between autophagy and reactive oxygen species (ROS) in the proliferation of gastric cancer cells were studied by gene expression silences (siRNA) and CM-H2DCFDA (DCF) staining. Results The results showed that VacA protein secreted by H. pylori in the supernatant stimulated autophagy in SGC7901 cells. After VacA protein treatment, the mRNA expressions of BECN1, ATG7 and PIK3C3, were up-regulated. ATG7 silencing by siRNA inhibited VacA-induced autophagy. Furthermore, our data demonstrated that VacA protein increased ROS levels. Addition of the antioxidant N-acetyl-l-cysteine (NAC) suppressed the levels of ROS, leading to inhibition of autophagy. Conclusions H. pylori VacA is a key toxin that induces autophagy by increased ROS levels. And our fndings demonstrated that VacA signifcantly inhibited proliferation in SGC7901 cells.
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