Ischemic Postconditioning Relieves Cerebral Ischemia and Reperfusion Injury Through Activating T-LAK Cell–Originated Protein Kinase/Protein Kinase B Pathway in Rats | Zendy

Haiping Zhao | Zendy; Rongliang Wang | Zendy; Zhen Tao | Zendy; Li Gao | Zendy; Feng Yan | Zendy; Zhi Gao | Zendy; Xiangrong Liu | Zendy; Xunming Ji | Zendy; Yumin Luo | Zendy

Open Access

Ischemic Postconditioning Relieves Cerebral Ischemia and Reperfusion Injury Through Activating T-LAK Cell–Originated Protein Kinase/Protein Kinase B Pathway in Rats

Author(s) -

Haiping Zhao,

Rongliang Wang,

Zhen Tao,

Li Gao,

Feng Yan,

Zhi Gao,

Xiangrong Liu,

Xunming Ji,

Yumin Luo

Publication year - 2014

Publication title -

stroke

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 3.397

H-Index - 319

eISSN - 1524-4628

pISSN - 0039-2499

DOI - 10.1161/strokeaha.114.006135

Subject(s) - medicine , pharmacology , protein kinase b , neuroprotection , reperfusion injury , malondialdehyde , reactive oxygen species , superoxide dismutase , ischemia , oxidative stress , biochemistry , apoptosis , chemistry

Ischemic postconditioning (IPostC) protects against ischemic brain injury. To date, no study has examined the role of T-LAK-cell-originated protein kinase (TOPK) in IPostC-afforded neuroprotection. We explored the molecular mechanism related with TOPK in antioxidant effect of IPostC against ischemia/reperfusion.

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