中国病理生理杂志
中國病理生理雜誌
중국병리생리잡지
CHINESE JOURNAL OF PATHOPHYSIOLOGY
2015年
6期
967-972
,共6页
闫蕊%单虎%林琳%刁佳宇%张明%朱延河%谭武红%魏瑾
閆蕊%單虎%林琳%刁佳宇%張明%硃延河%譚武紅%魏瑾
염예%단호%림림%조가우%장명%주연하%담무홍%위근
高糖%钙网蛋白%线粒体损伤%细胞凋亡
高糖%鈣網蛋白%線粒體損傷%細胞凋亡
고당%개망단백%선립체손상%세포조망
KEY WORDS] High glucose%Calreticulin%Mitochondrial injury%Apoptosis
目的:观察高糖培养对心肌细胞钙网蛋白( calreticulin,CRT)表达的变化、线粒体功能和细胞凋亡的影响。方法:将培养的AC-16人心肌细胞随机分为正常糖浓度组、高糖组、高糖+CRT siRNA ( small interfering RNA)组及等渗组,分别测定各组心肌细胞凋亡率、细胞内活性氧水平、线粒体功能和CRT表达水平的变化。结果:与正常糖浓度培养的心肌细胞相比,高糖组心肌细胞凋亡率增加,活性氧生成增多,线粒体膜电位及呼吸链酶活性降低,同时CRT表达升高;CRT siRNA可以减轻高糖组心肌细胞线粒体损伤,但细胞内活性氧的生成与高糖组相比未见显著差异。结论:CRT介导的线粒体损伤可能参与高糖时心肌细胞凋亡的增加。
目的:觀察高糖培養對心肌細胞鈣網蛋白( calreticulin,CRT)錶達的變化、線粒體功能和細胞凋亡的影響。方法:將培養的AC-16人心肌細胞隨機分為正常糖濃度組、高糖組、高糖+CRT siRNA ( small interfering RNA)組及等滲組,分彆測定各組心肌細胞凋亡率、細胞內活性氧水平、線粒體功能和CRT錶達水平的變化。結果:與正常糖濃度培養的心肌細胞相比,高糖組心肌細胞凋亡率增加,活性氧生成增多,線粒體膜電位及呼吸鏈酶活性降低,同時CRT錶達升高;CRT siRNA可以減輕高糖組心肌細胞線粒體損傷,但細胞內活性氧的生成與高糖組相比未見顯著差異。結論:CRT介導的線粒體損傷可能參與高糖時心肌細胞凋亡的增加。
목적:관찰고당배양대심기세포개망단백( calreticulin,CRT)표체적변화、선립체공능화세포조망적영향。방법:장배양적AC-16인심기세포수궤분위정상당농도조、고당조、고당+CRT siRNA ( small interfering RNA)조급등삼조,분별측정각조심기세포조망솔、세포내활성양수평、선립체공능화CRT표체수평적변화。결과:여정상당농도배양적심기세포상비,고당조심기세포조망솔증가,활성양생성증다,선립체막전위급호흡련매활성강저,동시CRT표체승고;CRT siRNA가이감경고당조심기세포선립체손상,단세포내활성양적생성여고당조상비미견현저차이。결론:CRT개도적선립체손상가능삼여고당시심기세포조망적증가。
[ ABSTRACT] AIM:To observe the effect of high glucose on the protein expression of calreticulin ( CRT) and its association with cell apoptosis and mitochondrial dysfunction in the cardiomyocytes.METHODS: AC-16 cardiomyocytes were randomly divided into normal glucose group, high glucose group, high glucose+CRT siRNA group and isotonic con-trol group.The cell apoptotic rate, reactive oxygen species (ROS), mitochondrial membrane potential level, respiratory enzyme activity, and protein expression of CRT were observed.RESULTS: Compared with the cardiomyocytes in normal glucose group, the apoptotic rate and ROS production of cardiomyocytes increased in high glucose group, accompanying with the decreases in the mitochondrial membrane potential level and enzyme activitiy of the respiratory chain.The protein expression of CRT was significantly increased in high glucose group.However, compared with high glucose group, high glucose+CRT siRNA decreased the expression of CRT and attenuated the damage of mitochondria, but CRT siRNA did not reduce the ROS level in cardiomyocytes.CONCLUSION:High glucose brings about CRT over-expression to induce mito-chondrial injury, thus increasing myocardial apoptosis.