Mechanism of aquaporin 4 (AQP 4) up-regulation in rat cerebral edema under hypobaric hypoxia and the preventative effect of puerarin

机制(生物学) 水通道蛋白1 医学 水通道蛋白4 脑水肿 缺氧(环境) 水肿 内科学 化学 脑水肿 麻醉 神经科学 药理学 葛根素 病理 生物 水道 氧气 替代医学 有机化学 机械工程 哲学 认识论 工程类 入口
作者
Chi Chiu Wang,Muyang Yan,Hui Jiang,Qi Wang,Shang He,Jingwen Chen,Chengbin Wang
出处
期刊:Life Sciences [Elsevier BV]
卷期号:193: 270-281 被引量:56
标识
DOI:10.1016/j.lfs.2017.10.021
摘要

Abstract Aim We aim to investigate the mechanism of aquaporin 4 (AQP 4) up-regulation during high-altitude cerebral edema (HACE) in rats under hypobaric hypoxia and preventative effect of puerarin. Methods Rats were exposed to a hypobaric chamber with or without the preventative treatment of puerarin or dexamethasone. Morriz water maze was used to evaluate the spatial memory injury. HE staining and W/D ratio were used to evaluate edema injury. Rat astrocytes and microglia were co-cultured under the condition of hypoxia with the administration of p38 inhibitor, NF-κB inhibitor or puerarin. Interleukin 6 (IL-6) and tumor necrosis factor α (TNF α) of cortex and culture supernatant were measured with ELISA. AQP4, phosphorylation of MAPKs, NF-κB pathway of cortex and astrocytes were measured by Western blot. Key findings Weakened spatial memory and cerebral edema were observed after hypobaric hypoxia exposure. AQP4, phosphorylation of NF-κB and MAPK signal pathway of cortex increased after hypoxia exposure and decreased with preventative treatment of puerarin. Hypoxia increased TNF-α and IL-6 levels in cortex and microglia and puerarin could prevent the increase of them. AQP4 of astrocytes increased after co-cultured with microglia when both were exposed to hypoxia. AQP4 showed a decrease after administered with p38 inhibitor, NF-κB inhibitor or puerarin. Significance Hypoxia triggers inflammatory response, during which AQP4 of astrocytes can be up regulated through the release of TNF-α and IL-6 from microglia. Puerarin can exert a preventative effect on the increase of AQP4 through inhibiting the release of TNF-α and phosphorylation of NF-κB, MAPK pathway.
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