Cerebral ischemia/reperfusion (I/R) injuries are common and often cause severe complications. Ozone has been applied for protecting I/R injury in animal models of several organs including cerebra, but the detailed mechanism remains unclear. 3‐(4,5‐Dimethylthiazol‐2‐yl)‐2,5‐diphenyltetrazolium bromide (MTT) assay and lactate dehydrogenase measurement were used to determine the influence of ozone on cell activity and damage of SH‐SY5Y cells. Some redox items such as catalase (CAT), malondialdehyde (MDA), glutathione peroxidase (GSH‐Px), and superoxide dismutase (SOD) were measured by enzyme‐linked immunosorbent assay. The mitochondrial membrane potential (ΔΨ_m) was determined by JC‐1 assay. Cytochrome‐c (cyt‐c) level in the cytoplasm and mitochondrion was measured by western blotting. Apoptosis was determined by flow cytometry, and some apoptosis‐related molecules were detected by quantitative real‐time polymerase chain reaction and western blotting. Ozone alleviated oxidative damage by increasing GSH‐Px, SOD, CAT, and decreasing MDA. Ozone decreased mitochondrial damage caused by I/R injury and inhibited the release of cyt‐c from mitochondrion to cytoplasm in SH‐SY5Y cells. The cell apoptosis caused by I/R was inhibited by ozone, and ozone could decrease apoptosis by increasing the ratio of Bcl‐2/Bax and inhibiting caspase signaling pathway in SH‐SY5Y cells. Ozone has the ability of maintaining redox homeostasis, decreasing mitochondrion damage, and inhibiting neurocytes apoptosis induced by I/R. Therefore, ozone may be a promising protective strategy against cerebral I/R injury.

中文翻译：

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臭氧通过抑制线粒体介导的SH‐SY5Y细胞凋亡途径来减轻缺血/再灌注损伤

脑缺血/再灌注（I / R）损伤很常见，通常会导致严重的并发症。在包括大脑在内的多个器官的动物模型中，臭氧已被用于保护I / R损伤，但具体机理尚不清楚。使用3-（4,5-二甲基噻唑-2-基）-2-，5-二苯基四唑溴化物（MTT）测定法和乳酸脱氢酶测定法确定臭氧对SH-SY5Y细胞活性和损伤的影响。通过酶联免疫吸附测定法测量了一些氧化还原物质，例如过氧化氢酶（CAT），丙二醛（MDA），谷胱甘肽过氧化物酶（GSH-Px）和超氧化物歧化酶（SOD）。线粒体膜电位（Δ Ψ_米）是通过JC-1分析确定的。通过蛋白质印迹法检测细胞质和线粒体中的细胞色素c（cyt-c）水平。通过流式细胞术确定细胞凋亡，并通过定量实时聚合酶链反应和蛋白质印迹检测到一些凋亡相关分子。臭氧通过增加GSH-Px，SOD，CAT和降低MDA减轻了氧化损伤。臭氧减少了I / R损伤引起的线粒体损伤，并抑制了cyt-c从线粒体到SH-SY5Y细胞的细胞质释放。I / R引起的细胞凋亡受到臭氧的抑制，臭氧可以通过增加Bcl-2 / Bax的比例和抑制SH-SY5Y细胞中的caspase信号传导途径来降低细胞凋亡。臭氧具有维持氧化还原稳态，减少线粒体损伤和抑制I / R诱导的神经细胞凋亡的能力。