Sini decoction alleviates inflammation injury after myocardial infarction through regulating arachidonic acid metabolism.
10.1016/j.chmed.2023.12.004
- Author:
Cuiping LONG
1
;
Qian ZHOU
2
;
Min XU
3
;
Xin DING
3
;
Xingxing ZHANG
1
;
Ya ZHANG
3
;
Yuping TANG
1
;
Guangguo TAN
3
Author Information
1. School of Pharmacy, Shaanxi University of Chinese Medicine, Xianyang 712046, China.
2. Department of Traditional Chinese Medicine, Xijing Hospital, Air Force Medical University, Xi'an 710032, China.
3. Department of Pharmacy, Air Force Medical University, Xi'an 710032, China.
- Publication Type:Journal Article
- Keywords:
Sini Decoction;
anti-inflammation;
arachidonic acid metabolism pathway;
conditioned medium;
myocardial infarction
- From:
Chinese Herbal Medicines
2025;17(1):148-155
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:Myocardial inflammation during myocardial infarction (MI) could be inhibited by regulating arachidonic acid (AA) metabolism. Recent studies demonstrated that Sini Decoction (SND) was identified to be an effective prescription for treating heart failure (HF) caused by MI. But the anti-inflammatory mechanism of SND remained unclear. The work was designed to investigate the anti-inflammatory mechanism of SND through the AA metabolism pathway in vitro and in vivo experiments.
METHODS:An inflammatory injury model of H9c2 cells was established by lipopolysaccharide (LPS)-stimulated macrophage-conditioned medium (CM). The MI model was built by the ligation of left anterior descending (LAD) branch of coronary artery in rat. Meanwhile, the rats were divided into five groups: sham group, MI group, MI + Celecoxib group, MI + low-dose SND group (SND-L) and MI + high-dose SND group (SND-H). Cardiac function, histopathological changes and serum cytokines were examined four weeks later. Western blot analysis was conducted to verify the key enzymes levels in the AA metabolic pathway, including phospholipase A2 (PLA2), cyclooxygenases (COXs) and lipoxygenases (LOXs).
RESULTS:These in vivo results demonstrated that SND could improve the cardiac function and pathological changes of rats with MI, and regulate the key inflammatory molecules in the AA metabolism pathway, including sPLA2, COX-1, COX-2, 5-LOX and 15-LOX. In vitro, SND could decrease the release of pro-inflammatory cytokines including TNF-α and IL-6 and inhibit cell apoptosis in CM-induced H9c2 cells. Moreover, SND could protect H9c2 cells from the damage of CM by regulating nuclear factor kappa-B (NF-κB) signal pathway and the expression of COX-2.
CONCLUSION:SND may be a drug candidate for anti-inflammatory treatment during MI by regulating the multiple targets in the AA metabolism pathway.
