P70-S6激酶1
核糖体蛋白s6
医学
免疫印迹
基底神经节
脑出血
水肿
药理学
麻醉
内科学
磷酸化
生物化学
生物
中枢神经系统
基因
蛛网膜下腔出血
蛋白激酶B
作者
Zhiyong Qin,Ya Hua,W. Liu,Robert Silbergleit,Yonggen He,Richard F. Keep,Julian T. Hoff,Guohua Xi
标识
DOI:10.1007/978-3-211-85578-2_60
摘要
Background New protein synthesis is key to ischemic tolerance induced by preconditioning and ribosomal protein S6 kinases (p70 S6 K) are important enzymes in protein synthesis. Hyperbaric oxygen preconditioning (HBOP) reduces ischemic brain damage. This study investigated if HBOP can activate p70 S6 K and increase new protein synthesis and if HBOP induces brain tolerance against brain swelling after intracerebral hemorrhage (ICH). Methods There were two parts of the studies. 1) Rats received five consecutive sessions of HBOP. Twenty-four hours after HBOP, the rats had an ICH and were sacrificed one or three days later for brain edema measurement. 2) Rats received five sessions of HBOP or control pretreatment and were sacrificed for Western blot analysis and immunohistochemistry of activated p70 S6 K and heme oxygenase-1 (HO-1). Findings Five sessions of HBOP significantly reduced brain edema in the ipsilateral basal ganglia after ICH. Western blot analysis showed that HBOP activated p70 S6 K and increased HO-1 levels in the basal ganglia. Strong activated p70 S6 K immunoreactivity was also found in the basal ganglia. Conclusions Our results suggest activation of p70 S6 K may have a role in heat shock protein synthesis after HBOP and may contribute to HBOP-induced brain protection.
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