Mitochondrial injury of pulmonary artery smooth muscle cells (PASMCs) is an important stage in the development of
pulmonary arterial hypertension (PAH). Recent studies revealed that
Paeonol exerts anti-proliferative effects on vascular smooth muscle cells. However, whether
Paeonol is directly involved in mitochondrial injury related to PAH remains unknown. Here, we found that
hypoxia-induced mitochondrial injury in vivo was alleviated in the presence of
Paeonol.
Hypoxia mediated the mitochondrial
injuries in PASMCs in vitro, including decreased
ATP generation, morphological alterations, mitochondrial polarization and increased
reactive oxygen species production, which were suppressed by
Paeonol. Our results also indicated that the expression of
peroxisome proliferator-activated receptor-gamma coactivator 1α (PGC-1α) was regulated by
Paeonol.
Paeonol caused significant alterations in mitochondrion-dependent apoptosis through PGC-1α in PASMCs. Taken together, these results provide the first evidence confirming the protective effect of
Paeonol in mediating mitochondrial injury under
hypoxia and elucidating the necessary role of PGC-1α in the effects of
Paeonol in inducing PASMC apoptosis.