Exploration of Therapeutic Effect of Wujiwan on Inflammatory Bowel Disease in Rats Based on PPARγ Signaling Pathway and T-cell Immunoregulation
10.13422/j.cnki.syfjx.20241644
- VernacularTitle:基于PPARγ信号通路和T细胞免疫调节探讨戊己丸对炎症性肠病大鼠的治疗作用
- Author:
Shiyun GUO
1
;
Yuxuan GUO
1
;
Yi SUN
1
;
Xiaoxin ZHU
1
;
Yujie LI
1
;
Ying CHEN
1
;
Qing YANG
1
;
Yajie WANG
1
;
Qi LI
1
;
Xiaogang WENG
1
;
Zhihao DENG
2
Author Information
1. Institute of Chinese Materia Medica， China Academy of Chinese Medical Sciences， Beijing 100700， China
2. Tongzhou Campus， Dongzhimen Hospital， Beijing University of Chinese Medicine， Beijing 101100， China
- Publication Type:Journal Article
- Keywords:
Wujiwan;
inflammatory bowel disease （IBD）;
peroxisome proliferator-activated receptor γ （PPARγ）;
T-cell
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2024;30(23):237-245
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveThis study explores the efficacy and pharmacological mechanism of Wujiwan in rats with inflammatory bowel disease （IBD） from the perspectives of the peroxisome proliferator-activated receptor γ （PPARγ） signaling pathway and T-cell immunity， providing reference for the treatment of IBD with traditional Chinese medicine. MethodThe study involved administering 2，4，6-trinitrobenzenesulfonic acid （TNBS） enemas to 35 rats to induce acute IBD. After 24 hours， the animals were divided into the following groups： normal group， model group， Wujiwan treatment group， and positive drug control group. Each group received gastric gavage for 8 consecutive days before the rats were dissected to compare the disease activity index （DAI） of the rat colon tissue， the colon mucosal damage index （CMDI）， and the spleen index. Enzyme-linked immunosorbent assay （ELISA） was used to measure the levels of interleukin-1β （IL-1β）， interleukin-10 （IL-10）， and tumor necrosis factor-α （TNF-α） in the serum. Quantitative real-time polymerase chain reaction （Real-time PCR） was used to determine the mRNA expression levels of T-bet （T-box expressed in T cells） and Gata3 （Gata-binding protein-3） in the colon tissue. Western blot analysis was conducted to detect the protein expression levels of PPARγ， T-bet， and nuclear factor-κB p65 （NF-κB p65） in the rat colon. ResultThe rat model of IBD was successfully established. Compared with the model group， the Wujiwan treatment group showed reduced DAI， CMDI， and spleen index， decreased content of TNF-α in the serum（P<0.01）， significantly increased content of IL-10（P<0.01）， and elevated mRNA content of T-bet and Gata3（P<0.05） in the colon tissue. The expression of PPARγ protein was augmented（P<0.05）， and the expression of T-bet and NF-κB p65 protein was decreased（P<0.05，P<0.01）. ConclusionWujiwan activates or upregulates PPARγ expression in IBD rats to inhibit the generation of pro-inflammatory factors， participates in the inflammatory immune process， and alleviates inflammatory reactions. Its mechanism may involve regulating the NF-κB pathway through PPARγ， enhancing Th2 cell transcription expression， and reducing Th1 cell transcription.
