Cistanche deserticola ethanol extract attenuates left ventricular remodeling and dysfunction by reducing the inflammatory response after myocardial infarction

Objective: This study aimed to investigate whether Cistanche deserticola extract (CDE) exerted an inhibi- tory effect on the cardiac inflammatory response and prevented adverse remodeling after myocardial infarction (MI) in rats. Methods: Wistar rats were randomly divided into seven groups: normal, sham, MI (LAD coronary artery ligation), 3 CDE groups (high dosage, middle dosage, and low dosage (LAD ligation and treated with CDE)), and a captopril group (LAD ligation and treated with captopril as the positive control drug). After six weeks, the effect of CDE on left ventricular (LV) remodeling was assessed by examining cardiac function and histology. Indicators of fibrosis (Masson and matrix metalloproteinases (MMPs)) and inflammation-related factors were evaluated. Results: CDE treatment significantly reduced the heart weight to body weight ratio and LV dilation and improved ejection fraction and fractional shortening in rat hearts. It also decreased myocardial hypertrophy and interstitial fibrosis in the non-infarcted myocardium and significantly decreased inflammatory cytokines (TNF-α and IL-1β) and inhibited the expression of MMP-9. However, CDE treatment produced no effect on MMP-2 and markedly diminished TLR-4 and NF-κB p65 expression in the non-infarcted area. Conclusion: CDE has the potential to improve cardiac remodel- ing and dysfunction following MI by modulation of myocardial inflammation, which may be attributed to mitigation of the TLR-4/NF-κB signaling pathway. CDE may be considered a potential therapeutic drug for the treatment of cardiac diseases.