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Ginsenoside Rg3 treats acute radiation proctitis through the TLR4/MyD88/NF-κB pathway and regulation of intestinal flora  ( SCI-EXPANDED收录)   被引量:7

文献类型:期刊文献

英文题名:Ginsenoside Rg3 treats acute radiation proctitis through the TLR4/MyD88/NF-κB pathway and regulation of intestinal flora

作者:Duan, Xiaoyu[1];Cai, Hongyi[2];Hu, Tingting[2];Lin, Lili[1];Zeng, Lu[1];Wang, Huixia[1];Cao, Lei[1];Li, Xuxia[1]

第一作者:Duan, Xiaoyu

通信作者:Cai, HY[1]

机构:[1]Gansu Univ Chinese Med, Gansu Prov Hosp, Clin Med Coll 1, Lanzhou, Peoples R China;[2]Gansu Prov Hosp, Dept Radiotherapy, Lanzhou, Peoples R China

第一机构:甘肃中医药大学

通信机构:[1]corresponding author), Gansu Prov Hosp, Dept Radiotherapy, Lanzhou, Peoples R China.

年份:2023

卷号:12

外文期刊名:FRONTIERS IN CELLULAR AND INFECTION MICROBIOLOGY

收录:;Scopus(收录号:2-s2.0-85146531377);WOS:【SCI-EXPANDED(收录号:WOS:000918184000001)】;

基金:This work was supported by the Natural Science Foundation of Gansu Province [No.21JR11RA200]; Major project of Gansu Provincial Department of education "reform and practical exploration of talent training mode of "joint construction of colleges and universities": Postgraduate "Innovation Fund" project [No.LCCX2021009]; Internal Medicine Research Fund Project of Gansu Provincial People's Hospital [No.18GSSY2-2].

语种:英文

外文关键词:TLR4; ginsenoside Rg3; acute radiation proctitis; intestinal microflora; mechanism

摘要:Objectives This study aimed to investigate the protective effect of ginsenoside Rg3 (GRg3) against acute radiation proctitis (ARP) in rats.Methods Wistar rats were randomly divided into control, model, dexamethasone-positive, GRg3 low-dose, GRg3 medium-dose, and GRg3 high-dose groups. The ARP rat model was established by a single 22-Gy irradiation of 6 MV) X-rays. The distribution and function of intestinal flora were detected using 16S rRNA high-throughput sequencing, rectal tissue was observed by hematoxylin and eosin (H & E) staining, the expression of interleukin 1 beta (IL-1 beta) and IL-10 inflammatory factors was detected by ELISA, and mRNA and protein expression of toll-like receptor 4 (TLR4), myeloid differentiation primary response 88 (MyD88), and nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappa B) were detected by RT-qPCR and Western blotting, respectively.Results GRg3 improved the symptoms of ARP in rats in a dose-dependent manner. The species distribution of intestinal flora in GRg3 rats was significantly different from that in ARP rats. These differences were more significant in the high-dose group, where the numbers of Ruminococcus, Lactobacillus, and other beneficial bacteria were significantly increased, whereas those of Escherichia, Alloprevotella, and other harmful bacteria were decreased. In addition, GRg3 was closely related to amino acid metabolism. After GRg3 treatment, the mRNA and protein expression of TLR4, MyD88, and NF-kappa B in rectal tissue was significantly down-regulated, and the level of downstream inflammatory factor IL-1 beta decreased, whereas that of IL-10 increased.Conclusion Our study indicated GRg3 as a new compound for the treatment of ARP by inhibiting the TLR4/MyD88/NF-kappa B pathway, down-regulating the expression of proinflammatory factors, thus effectively regulating intestinal flora and reducing inflammatory reactions.

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