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目的探讨瘦素(leptin)在高糖损伤心肌细胞中的作用及硫化氢(H2S)是否通过调控瘦素保护心肌细胞对抗高糖引起的损伤。方法应用细胞计数盒(CCK-8)检测细胞存活率;Hoechst 33258核染色检测凋亡细胞形态及数量的改变,双氯荧光素(DCFH-DA)染色荧光显微镜照相测定胞内活性氧(ROS)水平;罗丹明123(Rh123)染色及荧光显微镜照相测定线粒体膜电位(MMP);Western blot法检测瘦素蛋白的表达。结果 35 mmol/L葡萄糖(高糖)作用H9c2心肌细胞9h可明显地促进瘦素表达,并引起心肌细胞损伤,表现为细胞存活率降低、凋亡细胞数量和ROS生成增多及线粒体膜电位(MMP)丢失。硫化氢钠(NaHS,为H2S的供体)预处理能抑制高糖对心肌细胞瘦素表达的上调作用。NaHS预处理或瘦素拮抗剂均能保护H9c2心肌细胞对抗高糖引起的上述损伤。结论瘦素参与高糖引起的心肌细胞损伤。外源性H2S可通过抑制瘦素表达保护心肌细胞对抗高糖引起的损伤。
Objective To investigate the role of leptin in myocardial injury induced by high glucose and whether hydrogen sulfide (H2S) protects cardiomyocytes against high glucose by regulating leptin. Methods Cell viability was detected by cell counting kit (CCK-8). The morphology and number of apoptotic cells were detected by Hoechst 33258 nuclear staining. Fluorescence microscopy was used to determine intracellular reactive oxygen species (ROS) (Rh123) staining and fluorescence microscopy were used to measure the mitochondrial membrane potential (MMP). Western blot was used to detect the expression of leptin. Results The H9c2 cardiomyocytes treated with 35 mmol / L glucose (high glucose) for 9 h significantly enhanced the expression of leptin and induced cardiomyocyte injury. The results showed that the cell viability decreased, the number of apoptotic cells and ROS production increased, and mitochondrial membrane potential (MMP Lost. Pretreatment with sodium hydrogen sulphide (a donor of H2S) can inhibit the upregulation of leptin expression in cardiomyocytes induced by high glucose. NaHS pretreatment or leptin antagonist can protect H9c2 cardiomyocytes against the high glucose-induced injury. Conclusion Leptin is involved in cardiomyocyte injury induced by high glucose. Exogenous H2S protects cardiomyocytes against high glucose-induced damage by inhibiting leptin expression.