Wang Lei, Chen Hui, Liu Xiu-Heng, Chen Zhi-Yuan, Weng Xiao-Dong, Qiu Tao, Liu Lin
Department of Urology, Renmin Hospital of Wuhan University , Wuhan, Hubei Province , P.R. China.
Ren Fail. 2014 Oct;36(9):1449-54. doi: 10.3109/0886022X.2014.950934.
Abstract Ozone (O3) has been viewed as a novel treatment for different diseases in these years and oxidative stress and apoptosis play a key role in the pathogenesis of kidney diseases including renal ischemia and reperfusion (I/R). In the present study, we investigated the role of ozone oxidative preconditioning (OzoneOP) in attenuating oxidative stress and apoptosis in a hypoxia/reoxygenation (H/R) injury model using rat kidney cells. We induced H/R injury in kidney cells treated with or without OzoneOP. Oxidative stress parameters such as superoxide dismutase (SOD), malondialdehyde (MDA) and lactate dehydrogenase (LDH) were determined, as well as some apoptotic proteins. We observed that oxidative stress and apoptosis were increased in H/R group compared to OzoneOP group; however, these changes were significantly decreased by the treatment with OzoneOP. We concluded that OzoneOP can protect the kidney cells against H/R injury and its mechanism may be through the reduction of oxidative stress and apoptosis.
近年来，臭氧（O3）已被视为一种针对不同疾病的新型治疗方法，氧化应激和细胞凋亡在包括肾缺血再灌注（I/R）在内的肾脏疾病发病机制中起关键作用。在本研究中，我们使用大鼠肾细胞，在缺氧/复氧（H/R）损伤模型中研究了臭氧氧化预处理（OzoneOP）在减轻氧化应激和细胞凋亡方面的作用。我们在经或未经OzoneOP处理的肾细胞中诱导H/R损伤。测定了超氧化物歧化酶（SOD）、丙二醛（MDA）和乳酸脱氢酶（LDH）等氧化应激参数以及一些凋亡蛋白。我们观察到，与OzoneOP组相比，H/R组的氧化应激和细胞凋亡增加；然而，OzoneOP处理可显著降低这些变化。我们得出结论，OzoneOP可保护肾细胞免受H/R损伤，其机制可能是通过减少氧化应激和细胞凋亡。
