黄芩苷抑制低氧性肺动脉平滑肌细胞增殖的机制

目的:研究黄芩苷对低氧性大鼠肺动脉平滑肌细胞(pulmonary artery smooth muscle cells,PASMCs)增殖的影响及其作用机制.方法:体外培养大鼠PASMCs,免疫组化方法鉴定；CCK-8染色法检测常氧、低氧及黄芩苷不同浓度(5、10、20、40μmol/L)对PASMCs增殖的影响；离体细胞分为正常组、低氧组、低氧+黄芩苷组、低氧+腺苷A2A受体(A2A adenosine receptor,A2AAR)特异性激动剂(CGS21680,1μmol/L)组、低氧+ A2AAR特异性拮抗剂(SCH58261,100 nmol/L)组,RT-PCR和Western-Blot检测A2AAR的表达变化.结果:低氧使CCK-8吸光度(absorbance,A)值升高(P＜0.01),黄芩苷干预使A值下降,当浓度为40μmol/L时,A值接近正常组；RT-PCR和Western-Blot显示黄芩苷组A2AAR表达量显著增加(P＜0.01).结论:黄芩苷能抑制低氧PASMCs增殖,可能与上调A2AAR的表达有关.

Mechanisms of the inhibition of baicalin on the proliferation induced by hypoxia of pulmonary artery smooth muscle cells

Objective To evaluate the effects of baicalin on the proliferation induced by hypoxia of pulmonary artery smooth muscle cells(PASMCs) and its mechanism.Methods PASMCs were isolated from rat small pulmonary arteries,and veryficated by immunocytochemistry.The proliferation of PASMCs under normoxic,hypoxic,and different concentrations of baicalin(5,10,20,40 μmol/L) were measured by CCK-8.PASMCs were divided into 5 groups:normoxic group,hypoxia group,hypoxia + baicalin group,hypoxia + CGS21680 group,hypoxia + SCH58261 group.The expression of A2AAR was determined by RT-PCR and Western-Blot.Results The absorbance of CCK-8 was increased in hypoxia group(P < 0.01),which could be inhibited by baicalin,and reached the same as that in normoxic group with baicalin at the concentration of 40 μmol/L.RT-PCR and Western-Blot showed that the expression of A2AAR was up-regulated(P < 0.01 or P < 0.05).Conclusions Baicalin could inhibit the proliferation induced by hypoxia of PASMCs through up-regulating the expression of A2AAR.