In vitro investigation of protective mechanisms of triptolide against coronary heart disease by regulating miR-24-3p-BCL2L11 axis and PPARs-PGC1α pathway.

Coronary heart disease (CHD) is a fatal disease associated with coronary atherosclerosis. Although triptolide (TTL) has been reported to protect against CHD, the mechanism has not yet been determined. This study intended to explore its molecular regulation mechanism in CHD. It is shown in this study that TTL contributed to the proliferation and migration of cell models of CHD (endothelial cells) and the inhibition of apoptosis, and had an improvement effect on apoptosis factors and endoplasmic reticulum stress (ERS). From its mechanisms, TTL evidently downregulates miR-24-3p which is elevated in CHD, and evidently upregulates BCL2-like 11 (BCL2L11) which is suppressed in CHD, as well as affects the activation of peroxisome proliferator-activated receptors (PPARs)-Peroxisome proliferator activated receptor-γ co-activator-1α (PGC-1α) pathway of nuclear receptor transcription factors. In addition, miR-24-3p-BCL2L11-PPARs-PGC1α axis regulates protective effects of TTL against CHD.