Wang Ya-Feng, Wang Ai-Xia, Wang Sheng-Biao, Duo De-Long, Li Qian, Yan Ying-Jun
PIVAS of QingHai Provincial People's Hospital, Xining 810007, China.
Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2019 Nov;35(6):533-536. doi: 10.12047/j.cjap.5854.2019.117.
To investigate the interventive effects of Salvia przewalskii Maxim.(SPM)on high-altitude pulmonary hypertension(HAPH)in rats and possible mechanism.
The male SD rats were randomly divided into the control group, the hypoxia group and SPM(0.5 g/kg,1 g/kg and 2 g/kg) group. There were 14 rats in each group. The rats in control group were feed in Xining(with an altitude about 2 260 m), and the other group rats were all feed in Maduo county people's hospital(with an altitude about 4 260 m). The rats in SPM groups were treated with SPM at the doses of 0.5 g/kg,1 g/kg and 2 g/kg by gavage respectively (100 g/ml). The rats in control and the hypoxia groups were received equal volume of distilled water, once a day. After 4 weeks, the mean pulmonary artery pressure (mPAP) of rats was measured and the same part of lung tissue of each rat was collected and stored in liquid nitrogen. Then the relative mRNA expression levels of the proliferation cell nuclear antigen(PCNA), the cell cycle dependent kinase 4(CDK4), CyclinD1, RhoA, ROCK1, ROCK2 in lung tissues of each group rats were all tested by RT-PCR.
Compared with the control group, the mPAP and the relative mRNA expression levels of PCNA, CDK4, CyclinD1, RhoA, ROCK1 and ROCK2 were increased significantly in the hypoxia group(P＜0.01). Compared with the hypoxia group, the mPAP and the relative mRNA expression levels of PCNA, CDK4, CyclinD1, RhoA, ROCK1 and ROCK2 in the lung tissues of the SPM group rats were all decreased significantly(P＜ 0.05 or P＜0.01).
SPM can prevent the HAPH in rats, and the mechanisms may be related to the inhibition of the excessive proliferation of smooth muscle cells in pulmonary artery and the excessive activation of the RhoA/Rho kinase(ROCK) signaling pathway.
探讨 przewalskii 鼠尾草（SPM）对大鼠高原性肺动脉高压（HAPH）的干预作用及可能机制。
将雄性 SD 大鼠随机分为对照组、缺氧组和 SPM（0.5 g/kg、1 g/kg 和 2 g/kg）组。每组 14 只大鼠。对照组大鼠在西宁（海拔约 2260 米）饲养，其他组大鼠均在玛多县人民医院（海拔约 4260 米）饲养。SPM 组大鼠分别以 0.5 g/kg、1 g/kg 和 2 g/kg 的剂量通过灌胃给予 SPM（100 g/ml）。对照组和缺氧组大鼠给予等体积蒸馏水，每日 1 次。4 周后，测量大鼠平均肺动脉压（mPAP），并收集每只大鼠相同部位的肺组织，保存于液氮中。然后通过 RT-PCR 检测每组大鼠肺组织中增殖细胞核抗原（PCNA）、细胞周期蛋白依赖性激酶 4（CDK4）、细胞周期蛋白 D1、RhoA、ROCK1、ROCK2 的相对 mRNA 表达水平。
与对照组相比，缺氧组 mPAP 及 PCNA、CDK4、细胞周期蛋白 D1、RhoA、ROCK1 和 ROCK2 的相对 mRNA 表达水平显著升高（P＜0.01）。与缺氧组相比，SPM 组大鼠肺组织中 mPAP 及 PCNA、CDK4、细胞周期蛋白 D1、RhoA、ROCK1 和 ROCK2 的相对 mRNA 表达水平均显著降低（P＜0.05 或 P＜0.01）。
SPM 可预防大鼠 HAPH，其机制可能与抑制肺动脉平滑肌细胞过度增殖及 RhoA/ Rho 激酶（ROCK）信号通路过度激活有关。
