Mechanism of Dahuang Zhechongwan Against Multiple Organ Fibrosis： A Review
10.13422/j.cnki.syfjx.20211693
- VernacularTitle:大黄䗪虫丸抗多器官纤维化作用机制的研究进展
- Author:
Jing-tao LIANG
1
;
Zhi-ying HUO
2
;
Min WANG
2
;
Xiao-yan HE
2
;
Li-juan WU
2
Author Information
1. Affiliated Hospital of Chengdu University of Traditional Chinese Medicine（TCM）， Chengdu 610075，China
2. Chengdu University of TCM，Chengdu 611137，China
- Publication Type:Research Article
- Keywords:
Dahuang Zhechongwan;
multiple organ fibrosis;
experimental research;
review
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2021;27(16):237-244
- CountryChina
- Language:Chinese
-
Abstract:
Dahuang Zhechongwan （DHZCW） is a classic prescription from the Jingui Yaolue（《金匮要略》） by ZHANG Zhong-jing，with the effects of tonifying deficiency， relaxing the middle， promoting regeneration， and resolving stasis. It has been widely used in the clinical treatment of various diseases with definite efficacy achieved. The research on multiple organ fibrosis has shown that DHZCW can slow down the development of organ fibrosis in the heart， liver， kidney， lung， etc.， and good results in both clinical practice and experimental research have been obtained. The present study reviewed the previous investigations on the experimental mechanism of DHZCW in the treatment of multiple organ fibrosis and revealed that the pathogenesis was closely related despite different disease sites. From the perspective of traditional Chinese medicine （TCM），these diseases shared a common pathogenesis，which was manifested by deficiency. Long-term diseases led to the formation of "dried blood". From the perspective of modern medicine， the diseases all showed pathological changes in the deposition of extracellular matrix （ECM）， and their occurrence and development were all based on certain effector cells ［such as hepatic stellate cell （HSC） and pancreatic stellate cell （PSC）］， with same cytokines ［such as tumor necrosis factor-α （TNF-α），interleukin-6 （IL-6），IL-1β，and α-smooth muscle actin （α-SMA）］ and some key pathways ［transforming growth factor-β1 （TGF-β1）/Smad， phosphatidylinositol-3-kinase （PI3K）/protein kinase B （Akt）， and lipopolysaccharide （LPS） paracrine and autocrine mechanisms］ involved. As a classic prescription for "deficiency-induced dry blood"， DHZCW was effective in treating fibrosis， which was presumedly related to the inhibition of ECM deposition by intervening in the above-mentioned mechanisms， thereby delaying the disease progression. This study is expected to provide literature support to clarify the scientific connotation of DHZCW in the treatment of multiple organ fibrosis and lay a foundation for further experimental and clinical research.
