chrysin and Hypertrophy--Right-Ventricular

Chrysin (CH) is the main ingredient of many medicinal plants. Our previous study showed that CH could suppress hypoxia-induced pulmonary arterial smooth muscle cells proliferation and alleviate chronic hypoxia-induced pulmonary hypertension by targeting store-operated Ca entry (SOCE)-[Ca]i pathway. In this study, we investigated the effect of CH on monocrotaline-induced pulmonary hypertension (MCTPH) and the mechanism behind it. Results show that, in MCTPH model rats, (1) CH significantly reduced the enhancement of right ventricular pressure, right ventricular hypertrophy, and pulmonary vascular remodeling; (2) CH markedly suppressed the promotion of SOCE and [Ca]i in pulmonary arterial smooth muscle cells; and (3) CH obviously inhibited the MCT-upregulated proliferating cell nuclear antigen, TRPC1, TRPC4, and TRPC6 expression in distal pulmonary arteries. These results demonstrate that CH likely alleviates MCTPH by targeting TRPC1,4,6-SOCE-[Ca]i pathway.

Topics: Animals; Antihypertensive Agents; Arterial Pressure; Calcium Signaling; Disease Models, Animal; Flavonoids; Hypertension, Pulmonary; Hypertrophy, Right Ventricular; Monocrotaline; Muscle, Smooth, Vascular; Pulmonary Artery; Rats, Sprague-Dawley; TRPC Cation Channels; Vascular Remodeling; Ventricular Function, Right; Ventricular Pressure; Ventricular Remodeling