天麻素联合地塞米松保护缺糖缺氧诱导的H9C2细胞损伤

目的：探讨天麻素（gastrodin, GAS）联合地塞米松（dexamethasone, DEX）在缺糖缺氧诱导心肌细胞损伤中的作用及可能机制。方法：建立缺糖缺氧细胞（oxygen-glucose deprivation, OGD）模型，细胞分为5组，即正常对照组（normal group），缺糖缺氧组（OGD group），DEX组，GAS组，DEX+GAS组。利用CCK-8实验检测各组心肌细胞活性，利用比色法检测乳酸脱氢酶（LDH）的活性；利用TUNEL法检测各组心肌细胞的凋亡情况；利用ELISA实验检测各组心肌细胞培养液中炎性因子；利用Western blot检测各组心肌细胞中Notch1、Bax、Bcl-2及Beclin1的表达情况。结果：结果显示GAS与DEX联合使用可显著提高损伤心肌细胞的活性，减少心肌细胞的凋亡；降低促炎因子TNF-α、IL-6和IL-1β的产生及促进抑炎因子IL-10的产生，降低LDH的释放；Western blot结果显示GAS与DEX联合使用可促进Notch信号通路中Notch1的表达，显著降低受损心肌细胞中促凋亡蛋白Bax的表达，促进抑凋亡蛋白Bcl-2的表达，促进自噬相关基因Beclin1的表达。 结论：GAS与DEX联合使用，可能通过促进Notch信号通路的激活，促进其自噬，提高细胞的活性，抑制心肌细胞的凋亡，减轻炎症反应，从而减轻OGD诱导的心肌细胞损伤。

Gastrodin combined with dexamethasone protects H9C2 cell from injury induced by oxygen-glucose deprivation

AIM: To investigate the role and possible mechanism of gastrodin combined with dexamethasone in myocardial cell injury induced by oxygen-glucose deprivation. METHODS: Oxygen-glucose deprivation (OGD) model was established. The cells were divided into 5 groups: normal control group, OGD group, DEX group, GAS group and DEX+GAS group. The activity of myocardial cells was detected by CCK-8 test in each group. The activity of LDH was detected by colorimetry in each group. The apoptosis of myocardial cells was detected by TUNEL method in each group. The ELISA assay was used to detect the inflammatory factors in culture medium of myocardial cells in each group. Western blot was used to detect the expression of Notch1, Bax, Bcl-2 and Beclin1 in myocardial cells in each group.RESULTS: The results showed that GAS combined with DEX could significantly increase the activity of myocardial cells and decrease the apoptosis, reduce production of TNF-α, IL-6, IL-1β and promote production of IL-10, decrease the release of LDH significantly of myocardial cells induced by OGD. The results of Western blot showed that GAS combined with DEX increased the expression of Notch1, Bcl-2 and autophagy-related gene Beclin1, but decreased the expression of Bax of myocardial cells induced by OGD. CONCLUSION: The combination of GAS and DEX may promote autophagy and increase cell activity, inhibit apoptosis and inflammatory reaction by activating Notch signaling pathway, thereby reducing OGD-induced myocardial cells damage.