Renshen Baidusan Regulates Autophagy to Repair Mucosa in Ulcerative Colitis
10.13422/j.cnki.syfjx.20231039
- VernacularTitle:人参败毒散调控自噬修复溃疡性结肠炎黏膜的机制
- Author:
Peiyu XIONG
1
;
Xu CHEN
1
;
Wei ZHANG
1
;
Junyu LIU
1
;
Xinglong LIU
1
;
Yitong WANG
1
;
Bo JIA
1
Author Information
1. School of Basic Medical Sciences， Chengdu University of Traditional Chinese Medicine， Chengdu 610075， China
- Publication Type:Journal Article
- Keywords:
Renshen Baidusan;
ulcerative colitis;
autophagy;
oxidative stress;
intestinal stem cells
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2023;29(19):34-41
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo explore the mechanism of Renshen Baidusan in repairing intestinal mucosa in ulcerative colitis （UC） by regulating autophagy to scavenge peroxides. MethodThe mouse model of UC was induced by free drinking of 3.0% dextran sulphate sodium （DSS） solution. Sixty male C57BL/6J mice were randomized into normal， model， mesalazine （0.3 g·kg-1）， and high-， medium-， and low-dose （12.35， 8.22， 4.11 g·kg-1， respectively） Renshen Baidusan groups （n=10）. The mice were administrated with corresponding drugs by gavage for 7 consecutive days. The colon tissue was stained with hematoxylin-eosin （HE） to reveal the pathological changes， and Alcian blue-Periodic acid Scheff （PAS/AB） staining was employed to observe the goblet cell changes. The fluorescence expression of reactive oxygen species （ROS） in the colon tissue was detected by the immunofluorescence assay. The activity of superoxide dismutase （SOD） and the content of malondialdehyde （MDA） were measured by the biochemical methods. Western blot was employed to determine the expression levels of proliferating cell nuclear antigen （PCNA）， microtubule-associated protein 1 light chain 3 （LC3）， leucine-rich repeat-containing G protein-coupled receptor 5 （LGR5）， and p62. ResultDestroyed mucosal epithelial structure， intestinal gland destruction， loss of goblet cells， and massive infiltration of inflammatory cells appeared in the model group. Compared with the normal group， the model group showed increased tissue damage injury （TDI） score of the colon tissue， decreased SOD activity and LC3Ⅱ/Ⅰ， PCNA value， and elevated levels of p62， MDA， ROS， and LGR5 （P<0.05）. Compared with the model group， different doses of Renshen Baidusan decreased the TDI score， promoted the generation of new goblet cells， elevated the levels of PCNA， LGR5， SOD， and LC3Ⅱ/Ⅰ， and lowered the levels of p62， MDA， and ROS （P<0.05）. Moreover， the low dose group showed the best performance （P<0.05）. ConclusionRenshen Baidusan can promote intestinal epithelial repair by activating intestinal autophagy， alleviating oxidative stress， and promoting intestinal stem cell proliferation and differentiation.
