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Ozone alleviates ischemia/reperfusion injury by inhibiting mitochondrion‐mediated apoptosis pathway in SH‐SY5Y cells
Author(s) -
Cai HuaAn,
Tao Xi,
Zheng LiJun,
Huang Liang,
Peng Yan,
Liao RuoYi,
Zhu YiMin
Publication year - 2020
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.11294
Subject(s) - superoxide dismutase , apoptosis , cytochrome c , sh sy5y , mitochondrion , chemistry , oxidative stress , microbiology and biotechnology , biochemistry , biology , cell culture , genetics , neuroblastoma
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 (Δ Ψ 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.