Wendantang Regulates Energy Metabolism in Treatment of Myocardial Ischemia via SIRT3/PGC-1α Pathway
10.13422/j.cnki.syfjx.20241706
- VernacularTitle:基于调控SIRT3/PGC-1α通路干预能量代谢探讨温胆汤防治心肌缺血机制
- Author:
Xinjun ZHANG
1
;
Zhiqiang XIAO
1
;
Jia LU
2
;
Wenliang DUN
2
;
Ning GU
2
Author Information
1. Nanjing University of Chinese Medicine，Nanjing 210046，China
2. Nanjing Hospital of Chinese Medicine Affiliated to Nanjing University of Chinese Medicine，Nanjing 210022，China
- Publication Type:Journal Article
- Keywords:
Wendantang;
myocardial ischemia;
hyperlipidemia;
oxidative stress;
energy metabolism;
silent information regulator 3 （SIRT3）/peroxisome proliferator-activated receptor-gamma coactivator-1α （PGC-1α） signaling pathway
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2025;31(2):1-8
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the mechanism by which Wendantang regulates the silent information regulator 3 （SIRT3）/peroxisome proliferator-activated receptor-gamma coactivator-1α （PGC-1α） pathway to influence energy metabolism and thereby prevent and treat myocardial ischemia （MI） in a rat model of hyperlipidemia （HL）. MethodsThirty SD rats were randomly assigned into five groups： control， model， low-dose （3.702 g·kg-1·d-1） Wendantang， high-dose （7.404 g·kg-1·d-1） Wendantang， and positive control （trimetazidine， 0.006 g·kg-1·d-1）， with six rats in each group. The control group was fed normally， while the other groups were fed with a high-fat diet for six weeks for the modeling of HL. Subsequently， the drug intervention groups were administrated with corresponding drugs by gavage， and the control and model groups received an equivalent volume of normal saline for 14 days. One hour after the last gavage， the other groups except the control group were injected intraperitoneally with posterior pituitary hormone （30 U·kg-1） to induce MI. Electrocardiography （ECG） was employed to detect changes in the electrocardiogram. Hematoxylin-eosin staining was performed to observe cardiac pathological changes. Enzyme-linked immunosorbent assay was employed to measure the serum levels of cardiac troponin I（cTnI）， myoglobin （MYO）， and creatine kinase-MB （CK-MB）. Colorimetry was used to determine the levels of total cholesterol （TC） and triglycerides （TG） in the serum and ATP， malondialdehyde （MDA）， and superoxide dismutase （SOD） in the myocardial tissue. Western blot was employed to determine the protein levels of SIRT3， PGC-1α， adenosine monophosphate-activated protein kinase （AMPK）， and phosphorylated AMPK （p-AMPK） in the myocardial tissue. Real-time PCR was employed to measure the mRNA levels of SIRT3， PGC-1α， and AMPKα in the myocardial tissue. ResultsCompared with the control group， the model group showed significant J-point deviation and elevation in the ECG image， increased heart rate， disarrangement of myocardial fibers with unclear boundaries， elevated levels of CK-MB， cTnI， MYO， TC， and TG （P<0.05， P<0.01）， declined levels of SOD and ATP （P<0.01）， down-regulated mRNA levels of SIRT3， PGC-1α， and AMPK （P<0.05）， and down-regulated protein levels of SIRT3， PGC-1α， and p-AMPK （P<0.05）. Compared with the model group， the low-dose and high-dose Wendantang groups and the trimetazidine group showed inhibited J-point deviation and elevation in the ECG image， slowed heart rate， reduced inflammatory cell infiltration， alleviated disarrangement of myocardial fibers， declined levels of CK-MB， cTnI， MYO， TC， and TG （P<0.05， P<0.01）， elevated level of SOD （P<0.01）， up-regulated mRNA levels of SIRT3， PGC-1α， and AMPK （P<0.05， P<0.01） and up-regulated protein levels of SIRT3， PGC-1α， and p-AMPK （P<0.05， P<0.01）. ConclusionWendantang can effectively intervene in HL-associated MI in rats by reducing oxidative stress in myocardial cells， alleviating lipid metabolism disorders， and improving myocardial energy metabolism via the SIRT3/PGC-1α signaling pathway.
