Effect of Dima Decoction on BNIP3 Protein and mRNA Expressions inIntestinal Epithelial Cells of Ulcerative Colitis Mice / 中国实验方剂学杂志
Chinese Journal of Experimental Traditional Medical Formulae
; (24): 107-112, 2020.
Article
in Zh
| WPRIM
| ID: wpr-873354
Responsible library:
WPRO
ABSTRACT
Objective:To study the regulatory level of Dima decoction on adenovirus E1B 19 kD interacting protein 3(BNIP3) protein and to understand the mechanism in intervening mitophagy and controlling inflammation in ulcerative colitis. Method:The 60 SPF SD rats were randomly divided into normal control group, model control group, low, medium ang high dose Dima decoction(8.5,17.0,34.0 g·kg-1)group and mesalazine(3.0 g·kg-1) group,10 for each group. The model of UC rats was established by the method of environmental diet intervention +2,4,6-trinitro-Benzenesulfonicacid(TNBS)+ethanol,the administration group was administered for 14 days.Hematoxylin-eosin (HE) was used to detect pathological changes of colonic mucosal tissues in rats.Western blot and real-time fluorescence quantitative polymerase chain reaction(Real-time PCR) were used to detect the expressions of BNIP3 protein and mRNA in intestinal epithelial cells. Result:HE staining results showed that a large number of inflammatory cell infiltration and non-cheesy granulation tissue were observed in the colon of rats in the model group, while the rats in each drug group showed different degrees of fibrous repair. Compared with normal group, the expression of BNIP3 protein and mRNA in model group were significantly increased (P<0.05). Compared with model group, the expression of BNIP3 protein and mRNA in low, medium and high-dose Dima decoction group and mesalazine group were significantly increased (P<0.01). Compared with low-dose group, the expression of BNIP3 protein and mRNA in medium and high-dose groups and mesalazine group were significantly increased (P<0.05). Conclusion:Dima decoction can increase the expression of BNIP3 in the intestinal epithelium of UC active rats, which may be one of the mechanisms of promoting mitochondrial autophagy against UC inflammation.
Full text:
1
Database:
WPRIM
Language:
Zh
Journal:
Chinese Journal of Experimental Traditional Medical Formulae
Year:
2020
Document type:
Article