miR-29c is implicated in the cardioprotective activity of Panax notoginseng saponins against isoproterenol-induced myocardial fibrogenesis.

ETHNOPHARMACOLOGICAL RELEVANCE

Panax notoginseng (Burkill) F.H. Chen (Araliaceae) has a long history of clinical application in China for the treatment of cardiovascular diseases. Panax notoginseng saponins (PNS) have been proven to be the major cardioprotective substances of Panax notoginseng (Burkill) F.H. Chen (Araliaceae).

AIM OF THE STUDY

The current study further investigated the molecular mechanisms associated with the cardioprotective effect of PNS.

MATERIALS AND METHODS

C57BL/6J mice were subject to isoproterenol (ISO)-induced myocardial injury in the absence or presence of PNS treatment. Histological, immunohistochemical and molecular biological approaches were taken to assess the effects of PNS treatment on ISO-induced myocardial injury and ensuing fibrogenesis.

RESULTS

PNS treatment significantly attenuated ISO-induced myocardial injury and fibrosis. The expression of an anti-fibrotic microRNA, miR-29c, was significantly decreased in ISO-challenged mouse hearts. In contrast, PNS treatment resulted in increased cardiac expression of miR-29c. The expression of miR-29c target genes including Collagen (Col) 1a1, Col1a2, Col3a1 and Col5a1, fibrillin 1 (Fbn1) as well as TGFβ1 was significantly increased by ISO, which exhibited decreased expression by PNS intervention.

CONCLUSIONS

Our results demonstrate for the first time that the cardioprotective effects of PNS could in part implicate increased expression of miR-29c in the heart, which may help increase the understanding of the pharmacological activities of PNS in treating cardiovascular disorders.