Study on the efficacy and mechanism of Tongbianling capsule in the treatment of constipation
10.12206/j.issn.2097-2024.202404008
- VernacularTitle:通便灵胶囊治疗便秘的药效与机制研究
- Author:
Ying CHEN
1
;
Zihua XU
1
;
Bei HU
1
;
Yaling CUI
1
;
Huan GAO
1
;
Qiong WU
1
Author Information
1. The Laboratory of Pharmacy Department , General Hospital of Northern Theater Command of the PLA, Shenyang 110000, China.
- Publication Type:ColumnfromGeneralHospitalofNorthernTheaterCommand
- Keywords:
Tongbianling capsule;
constipation;
mechanism
- From:
Journal of Pharmaceutical Practice and Service
2025;43(1):10-16
- CountryChina
- Language:Chinese
-
Abstract:
Object To study the efficacy and potential mechanism of Tongbianling capsule in constipation. Methods The effects of Tongbianling capsule on intestinal motility in normal mice and carbon powder propulsion rate in small intestine of constipation model mice after were observed administration. The potential targets and key pathways of Tongbianling capsule in treating constipation were identified through network pharmacology. To verify the mechanism, the expression of p-PI3K/PI3K, p-AKT/AKT and CASP3 proteins in mouse colon tissue was detected by the western blot. Results The time for mice to excrete the first black stool was shortened and the number of fecal particles was increased in Tongbianling capsule administration group, and the carbon powder propulsion rate of mice in each Tongbianling capsule administration group was increased. The results of network pharmacology showed that treatment of constipation by Tongbianling capsule may be related to signaling pathways such as PI3K-Akt signaling pathway and 5-HT. The protein expression of p-PI3K/PI3K, p-AKT/AKT, and CASP3 in mouse colon tissue could be significantly downregulated in administration group. Conclusion Tongbianling capsule could effectively promote intestinal peristalsis in mice, increase the frequency of defecation, and effectively treat constipation. The mechanism of its action may be related to the direct or indirect regulation of intestinal motility by the PI3K-Akt signaling pathway.
