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目的:探究红景天苷对高糖诱导下内皮细胞表面损伤的保护作用及机制。方法:对人脐静脉内皮细胞(HUVECs)以高糖诱导其损伤,并用10-6、10-5、10-4mol/L的红景天苷处理,检测并比较HUVECs细胞活力、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)、丙二醛(MDA)、细胞凋亡、细胞表面血管细胞粘附分子-1(VCAM-1)、细胞间粘附分子-1(ICAM-1)、ATP、Bcl-2、Bax、肿瘤坏死因子(TNF-α)、白介素-1β(IL-1β)、白介素-6(IL-6)、单核细胞趋化蛋白-1(MCP-1)和活性氧(ROS)等指标。结果:与正常对照组比较,模型组细胞活力、SOD、ATP和Bcl-2显著降低(P<0.05),LDH、MDA、细胞凋亡率、VCAM-1、ICAM-1、ATP、Bcl-2、Bax、TNF-α、IL-1α、IL-6、MCP-1和ROS显著升高(P<0.05)。与模型组比较,红景天苷中、高浓度组细胞活力、SOD、ATP、Bcl-2显著升高,LDH、MDA、细胞凋亡率、VCAM-1、ICAM-1、Bax、TNF-β、IL-1α、IL-6、MCP-1、ROS显著降低(P<0.05)。结论:红景天苷对高糖诱导下的HUVECs损伤具有保护作用,其作用呈浓度依赖性,其机理可能与抗氧化、抗凋亡及抑制炎症反应有关。
Objective: To investigate the protective effect of salidroside on endothelial cell injury induced by high glucose and its mechanism. Methods: Human umbilical vein endothelial cells (HUVECs) were induced by high glucose and treated with salidroside (10-6, 10-5, 10-4 mol / L). The cell viability, lactate dehydrogenase LDH, SOD, MDA, apoptosis, VCAM-1, ICAM-1 ), ATP, Bcl-2, Bax, TNF-α, IL-1β, IL-6 and MCP- And reactive oxygen species (ROS) and other indicators. Results: Compared with the normal control group, the activities of SOD, ATP and Bcl-2 in the model group were significantly decreased (P <0.05), the activities of LDH, MDA, apoptosis, VCAM-1, ICAM-1, ATP and Bcl- , Bax, TNF-α, IL-1α, IL-6, MCP-1 and ROS were significantly increased (P <0.05). Compared with model group, the activities of SOD, ATP, Bcl-2, LDH, MDA, apoptosis rate, VCAM-1, ICAM-1, Bax, , IL-1α, IL-6, MCP-1 and ROS were significantly decreased (P <0.05). CONCLUSION: Salidroside has a protective effect on HUVECs induced by high glucose, and its mechanism is in a concentration-dependent manner. Its mechanism may be related to its anti-oxidation, anti-apoptosis and anti-inflammation.