Research progress on the mechanism of tanshinone ⅡA in alleviating sepsis-induced multiple organ dysfunction
- VernacularTitle:丹参酮ⅡA改善脓毒症所致多器官功能障碍的作用机制研究进展
- Author:
Jingyu DU
1
;
Ruifen ZHANG
2
;
Yang LI
1
;
He SU
3
;
Tingting JIA
3
;
Hairong ZHANG
3
;
Xinsheng HUANG
3
Author Information
1. School of Clinical Chinese Medicine，Inner Mongolia Medical University，Hohhot 010059，China
2. School of Clinical Chinese Medicine，Inner Mongolia Medical University，Hohhot 010059，China;Dept. of Critical Care Medicine，Inner Mongolia Hospital of Traditional Chinese Medicine，Hohhot 010020，China
3. Dept. of Critical Care Medicine，Inner Mongolia Hospital of Traditional Chinese Medicine，Hohhot 010020，China
- Publication Type:Journal Article
- Keywords:
tanshinone ⅡA;
sepsis;
multiple organ dysfunction;
mechanism;
clinical translation
- From:
China Pharmacy
2026;37(15):2063-2067
- CountryChina
- Language:Chinese
-
Abstract:
Sepsis is a systemic inflammatory response syndrome triggered by infection. It progresses rapidly and tends to develop into multiple organ dysfunction. Tanshinone ⅡA， one of the core active ingredients of Salvia miltiorrhiza， exerts remarkable targeted protective effects against sepsis-induced multiple organ dysfunction. This paper reviews the mechanisms by which tanshinone ⅡA alleviates sepsis-induced multiple organ dysfunction. Tanshinone ⅡA can relieve sepsis-induced lung injury by inhibiting the activity of Toll-like receptor 4/myeloid differentiation primary response protein 88/nuclear factor- κB， phosphatidylinositol 3-kinase/protein kinase B signaling pathways and maintaining mitochondrial homeostasis. It ameliorates sepsis- induced myocardial injury via suppressing the activation of NOD-like receptor family pyrin domain-containing 3/caspase-1 signaling pathway， downregulating the expression of inflammatory factors and regulating autophagy. It mitigates sepsis-induced renal injury by regulating oxidative stress imbalance and reducing the expression of apoptosis-related proteins. It alleviates sepsis-caused liver injury through inhibiting the release of inflammatory factors and hepatocyte apoptosis. It improves sepsis-induced intestinal barrier dysfunction by upregulating the expression of tight junction proteins and restraining inflammatory responses. Furthermore， it relieves sepsis-associated encephalopathy by activating peroxisome proliferator-activated receptor gamma coactivator-1α/nuclear respiratory factor 1/mitochondrial transcription factor A signaling pathway. Tanshinone ⅡA is expected to be a vital candidate drug for comprehensive prevention and treatment of sepsis. However， interdisciplinary research is required to break through current bottlenecks and realize the transformation from basic experiments to clinical application.
