To discuss the effect of
puerarin (Pue) on the proliferation of
hypoxia-induced pulmonary artery smooth muscle cells (PASMCs) and discuss whether its mechanism is achieved by regulating reactive
oxygen. PASMCs of primarily cultured rats (2-5 generations) were selected in the experiment. MTT, Western blot, FCM and
DCFH-DA were used to observe Pue's effect the proliferation of PASMCs. The Western blot was adopted to detect whether ROS participated in Pue's effect in inhibiting PASMC proliferation. The PASMCs were divided into five groups: the normoxia group, the
hypoxia group, the
hypoxia + Pue group, the
hypoxia + Pue +
Rotenone group and the
hypoxia +
Rotenone group, with
Rotenone as the ROS blocker. According to the results, under the conditions of normoxia, Pue had no effect on the PASMC proliferation; But, under the conditions of
hypoxia, it could inhibit the PASMC proliferation; Under the conditions of normoxia and
hypoxia, Pue had no effect on the expression of the
tumor necrosis factor-α (TNF-α) among PASMCs, could down-regulate the expression of
hypoxia-induced cell cycle
protein Cyclin A and proliferative
nuclear antigen (
PCNA).
DCFH-DA proved Pue could reverse ROS rise caused by
hypoxia. Both
Rotenone and Pue could inhibit the up-regulated expressions of HIF-1α,
Cyclin A,
PCNA caused by
anoxia, with a synergistic effect. The results suggested that Pue could inhibit the
hypoxia-induced PASMC proliferation. Its mechanism may be achieved by regulating ROS.