方法热休克预处理诱导热休克蛋白产生，然后制作烧伤大鼠急性胃黏膜损伤模型，进行胃黏膜损伤指数评分。
Methods After heat shock proteins (HSPs) were induced by heat shock pretreatment, burn-induced gastric mucosal lesion model was established according to the protocol of Kitajima.
结论模拟失重可诱导PC 12细胞NO的合成，增加蛋白质氧化损伤程度。
Conclusions Simulated weightlessness may induce the (over) production of NO, and resulted in increased protein oxidative damage in PC12 cells.
目的探讨内毒素（LPS）诱导的急性肺损伤（ALI）大鼠肺组织甲状腺转录因子-1（TTF-1）、肺表面活性物质相关蛋白-A（SP-A）表达的变化。
Objective To investigate the change of the expression of TTF-1 and SP-A in lung tissue of ALI rats induced by LPS.
ROS通过氧化线粒体心磷脂、线粒体dna和线粒体重要的蛋白质对线粒体造成氧化损伤，进而诱导细胞凋亡。
Through oxidizing the mitochondrial cardiolipin, mitochondrial DNA and important proteins in mitochondria, ROS leads to the oxidative stress towards mitochondria, further induces the cell apoptosis.
结论抗凋亡蛋白肽高剂量预处理对脂多糖诱导的大鼠肺损伤有保护作用。
Condusion High-dose anti - apoptotic peptide have a protective effect on LPS-induced acute lung injury in rats.
目的探讨在紫外线诱导的人晶状体上皮细胞DNA损伤修复过程中端粒酶活性和氧化损伤蛋白的变化和作用。
Objective To investigate the changes and the role of telomerase activity and other stress-related proteins in the process of UV-induced DNA damage and repair in human lens epithelial cells.
结论增龄能够促进脂多糖诱导的急性肺损伤大鼠肺组织纤维蛋白沉积，增强纤维蛋白的内皮细胞损伤作用。
Conclusions Aging could accelerate fibrin deposition in pulmonary tissue of LPS-induced rat model of acute lung injury, and promote the injury of endothelial cell function caused by fibrin deposition.
讨论急性肺损伤治疗的启示并综述早期关于抗胸腺细胞球蛋白诱导急性肺损伤的文献。
Implications for treatment of acute lung injury are discussed and earlier literature is reviewed concerning antithymocyte globulin-induced acute lung injury.
白色念珠菌入侵上皮细胞会导致显着的上皮细胞的损伤，这可能是由溶解酶，如蛋白酶和分泌的磷脂酶的有机体诱导。
C. albicans invasion of epithelial cells results in significant epithelial cell damage, which is probably induced by lytic enzymes, such as proteases and phospholipase secreted by the organism.
白色念珠菌入侵上皮细胞会导致显着的上皮细胞的损伤，这可能是由溶解酶，如蛋白酶和分泌的磷脂酶的有机体诱导。
C. albicans invasion of epithelial cells results in significant epithelial cell damage, which is probably induced by lytic enzymes, such as proteases and phospholipase secreted by the organism.
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