硫化氢通过调控瘦素保护心肌细胞对抗高糖引起的损伤  

Hydrogen sulfide protects cardiomyocytes against high glucose-induced injury by modulating leptin espression

作　　者：张莉莉[1] 陈景福[2] 华潇潇[3] 靳思思[4] 庄晓东[5] 廖新学[5] 陈培熹[6] 冯鉴强[6] 

机构地区：[1]广东省人民医院广东省医学科学院广东省老年医学研究所,广东广州510080 [2]广东医学院附属医院心内科,广东湛江524001 [3]中山大学附属第一医院黄埔院区麻醉科,广东广州510700 [4]广东省人民医院东病区内分泌科,广东广州510080 [5]中山大学附属第一医院高血压血管病科,广东广州510080 [6]中山大学中山医学院生理学教研室,广东广州510080

出　　处：《解剖学研究》2013年第4期291-295,共5页Anatomy Research

基　　金：广东省科技计划项目(2012B031800358);国家自然科学基金(81270296)

摘　　要：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 high glucose （HG）-induced cardiomyocyte injury and whether hy- drogen sulfide （H2S） protects cardiomyocytes against HG-indueed injury by modulating leptin expression. Methods Cell viability was measured by cell counter kit （CCK-8） ; The changes in morphology and amount of apoptotic cells were detected by Hoechst nu- clear staining; The level of intracellular reactive oxygen species （ROS） was tested by DCFH-DA Staining and photofluorography. Mi- tochondrial membrane potential （MMP） was observed by rhodamine 123 （Rh123） staining followed by photofluorography. The expres- sion of leptin protein was evaluated by Western blot assay. Results Exposure of H9c2 cardiac cells to 35 mmol/L glucose （high glu- cose, HG） for 9 h markedly enhanced the expression of leptin and induced significant injuries, as evidenced by a decrease in cell via- bility, the increases in apoptotie cells and ROS generation as well as a loss of MMP. Pretreatment with NariS （a donor of H2S） inhib- ited HG-induced upregulation of leptin expression in H9c2 cardiac cells. Pretreatment with either NariS or leptin antagonist protected H9c2 cardiac cells against the HG-induced injuries mentioned above. Conclusion Leptin is involved in HG-induced eardiomyocyte injury. Exogenous H2S may protect cardioyocytes against HG-indueed injuries by modulating leptin expression.

关 键 词：硫化氢 瘦素 高糖 活性氧 心肌细胞 

分 类 号：R587.2[医药卫生—内分泌]