Context: Xin Bao San, a traditional Chinese herbal formula, is widely used in clinical treatment for cardiovascular diseases; however, the therapeutic effect of Xin Bao San on myocardial ischaemia-reperfusion injury (MI/RI) is unclear.
Objective: This study evaluates the cardioprotective effect and molecular mechanism of Xin Bao San against myocardial ischaemia-reperfusion injury.
Materials and methods: A phytochemistry-based network pharmacology analysis was used to uncover the mechanism of Xin Bao San against myocardial ischaemia-reperfusion injury. Ultra performance liquid chromatography coupled with quadrupole time-of-flight mass spectrometry method was used to identify chemicals. Myocardial ischaemia-reperfusion injury-related targets of Xin Bao San were predicted using TargetNet database, OMIC database, etc. Sprague-Dawley rats under anterior descending artery ligation model were divided into Sham, myocardial ischaemia-reperfusion injury and Xin Bao San (180 mg/kg, intragastric administration).
After 30 min ischaemia and 24 h reperfusion, heart tissues were collected for measurement of myocardial infarct size. After oxygen glucose deprivation for 6 h, H9c2 cells were treated with Xin Bao San (60, 240 and 720 μg/mL) and diazoxide (100 μM) for 18 h of reperfusion.
Results: Thirty-seven chemicals were identified in Xin Bao San; 50 MI/RI-related targets of Xin Bao San were predicted using indicated databases. Xin Bao San significantly reduced infarct size and creatine kinase MB (CK-MB) level after myocardial ischaemia-reperfusion injury; Xin Bao San protected H9c2 cells against OGD/R injury. Gene ontology (GO) and KEGG pathway enrichment analyses by String database showed that the cardioprotective effect of Xin Bao San was associated with autophagy and apoptosis signalling pathways. Experimental investigation also verified that Xin Bao San suppressed apoptosis, autophagy and endoplasmic reticulum stress.
Conclusions: Xin Bao San showed therapeutic effects against myocardial ischaemia-reperfusion injury mainly via attenuating apoptosis though suppressing excessive autophagy and endoplasmic reticulum stress.