内科

目的探讨是否可通过使用钙敏感受体（CaSR）激动剂增强胱硫醚-?-裂解酶（CSE）的表达促使内源性硫化氢（H2S）的含量增加，从而抑制肺动脉平滑肌细胞（PASMC）的增殖、迁移。方法以人肺动脉平滑肌细胞（HPASMC）为研究对象，将样本设置为空白对照组（使用PBS液干预）、GdCl3组（使用CaSR激动剂GdCl3干预）、NPS2390组（使用CaSR抑制剂NPS2390干预），在样本中加药孵育后，检测比较各组细胞增殖、迁移情况和细胞中CaSR、CSE、H2S的水平。结果三组细胞增殖、迁移情况和细胞中CaSR、CSE、H2S的水平比较差异有统计学意义（P＜0.05）。GdCl3组细胞CaSR、CSE的表达和H2S的含量高于对照组，MTT实验吸光度（OD值）低于对照组，细胞迁移数少于对照组，差异有统计学意义（P＜0.05）；NPS2390组细胞CaSR的表达和H2S的水平均低于对照组，MTT实验吸光度（OD值）高于对照组，细胞迁移数多于对照组，差异有统计学意义（P＜0.05）。结论CaSR激动剂可通过增强CSE的表达增加H2S的含量，进而抑制PASMC的增殖及迁移。

ObjectiveTo investigate whether calcium-sensiing receptor (CaSR) agonist can increase the level of endogenous hydrogen sulfide (H2S) by increasing the expression of cystathionine-?-lyase (CSE), and then inhibit the proliferation and migration of pulmonary artery smooth muscle cells. MethodsHuman pulmonary artery smooth muscle cells were divided into three groups: blank control group (PBS solution intervention), GdCl3 group (CaSR agonist GdCl3 intervention), NPS2390 group (CaSR inhibitor NPS2390 intervention). After incubated with drugs, the cell proliferation, cell migration and the expression of CaSR, CSE, H2S were detected, and the above indexes were compared among the three groups. ResultsThere was significant difference in the cell proliferation, cell migration and the expression of CaSR, CSE, H2S among three groups (P＜0.05), the expression of CaSR, CSE and the level of H2S in GdCl3 group were significantly higher than those in control group (P＜0.05), the OD value in GdCl3 group was significantly lower than that in control group (P＜0.05), the cell migration in GdCl3 group was significantly less than that in control group (P＜0.05); the expression of CaSR and the level of H2S in NPS2390 group were significantly lower than those in control group (P＜0.05), the OD value in NPS2390 group was significantly higher than that in control group (P＜0.05), the cell migration in NPS2390 group was significantly more than that in control group (P＜0.05). ConclusionsCaSR agonist can increase the level of H2S by enhancing the expression of CSE, and inhibit the proliferation and migration of pulmonary artery smooth muscle cells.