【摘 要】
：
目的 观察HK-2细胞中的L-FABP在脂肪酸和蛋白干预下,对内质网应激相关蛋白和凋亡相关蛋白表达的影响,探讨L-FABP与ERS的关系,进一步阐明游离脂肪酸引起肾小管细胞凋亡的
【出 处】
：
中国毒理学会毒性病理学专业委员会第一届会员代表大会
论文部分内容阅读
目的 观察HK-2细胞中的L-FABP在脂肪酸和蛋白干预下,对内质网应激相关蛋白和凋亡相关蛋白表达的影响,探讨L-FABP与ERS的关系,进一步阐明游离脂肪酸引起肾小管细胞凋亡的机制.方法 首先给予HK-2细胞PA、OA和Alb干预,Western blot测定L-FABP,内质网应激相关蛋白GRP78、PERK和p-PERK,内质网凋亡相关蛋白CHOP、Caspase-3、Cleave Caspase-3的表达变化；然后沉默HK-2细胞的L-FABP,观察沉默前后上述蛋白的表达变化,结果 (1)PA和OA干预使HK-2细胞中L-FABP蛋白表达有意义上调；(2)PA和OA干预HK-2细胞中GRP78、CHOP、Caspase-3、 Cleave Caspase-3蛋白水平均有意义上调,(3)沉默了HK-2细胞的L-FABP,PA和OA干预上调的GRP78以及ER相关凋亡蛋白CHOP、Caspase3和Cleave Caspase3蛋白有意义降低,；Alb组L-FABP、 GRP78、 Caspase3、Cleave Caspase3、CHOP蛋白水平无明显增高(p＞0.05),沉默L-FABP后GRP78、Caspase3、CHOP蛋白水平也无明显变化(p＞O.05).结论 L-FABP介导脂肪酸通过内质网应激凋亡途径引起人近端小管上皮细胞凋亡；证实导致肾小管上皮细胞损伤和凋亡的主要成份是脂肪酸而不是白蛋白.
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