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首页> 外文期刊>Experimental and therapeutic medicine >Resveratrol protects neuronal cells from isoflurane-induced inflammation and oxidative stress-associated death by attenuating apoptosis via Akt/p38 MAPK signaling
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Resveratrol protects neuronal cells from isoflurane-induced inflammation and oxidative stress-associated death by attenuating apoptosis via Akt/p38 MAPK signaling

机译:白藜芦醇通过AKT / P38 MAPK信号传导来保护来自异氟醚诱导的异氟烷诱导的炎症和氧化应激相关的死亡的神经元细胞

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摘要

The aim of the present study was to determine whether resveratrol protects neuronal cells from inflammation and isoflurane-induced oxidative stress-associated death via attenuating apoptosis via Akt/p38 mitogen-activated protein kinase (MAPK) signaling. The PC12 rat pheochromocytoma cell line was treated with 2% isoflurane + 21% O-2 + 5% CO2 for 6 h and pre-treated with resveratrol (0-1,000 mu M) for 0, 24 or 48 h prior to isoflurane treatment. An MTT assay, flow cytometry and ELISA of tumor necrosis factor-, interleukin-6, malondialdehyde and superoxide dismutase revealed that resveratrol reduced growth inhibition, restrained apoptosis and suppressed inflammation and oxidative stress induced by isoflurane in PC12 cells. Pretreatment with resveratrol effectively reduced caspase-3 activity and inducible nitric oxide synthase protein expression in isoflurane-induced PC12 cells. In addition, western blot analysis demonstrated that resveratrol treatment significantly attenuated isoflurane-induced decreases in the activated phosphorylated (p)-Akt/Akt ratio and increases in the p-p38/p38 MAPK protein ratio in PC12 cells. These findings indicated that resveratrol was able to protect neuronal cells from isoflurane-induced inflammation and oxidative stress-associated death by attenuating apoptosis via Akt/p38 MAPK signaling.
机译:本研究的目的是通过通过AKT / P38丝裂原激活的蛋白激酶(MAPK)信号传导来确定白藜芦醇是否保护神经元细胞免受炎症和异氟醚诱导的氧化应激相关死亡。用2%异氟醚+ 21%O-2 + 5%CO 2处理PC12大鼠噬细胞瘤细胞系6小时,并在异氟烷处理之前用白藜芦醇(0-1,000μm)预处理0,24或48小时。肿瘤坏死因子,白细胞介素-6,丙二醛和超氧化物歧化酶的MTT测定,流式细胞术和ELISA显示,白藜芦醇降低了PC12细胞中异氟烷诱导的凋亡,抑制凋亡和抑制炎症和氧化应激。与白藜芦醇的预处理有效地降低了异氟烷诱导的PC12细胞中的Caspase-3活性和诱导的一氧化氮合酶蛋白表达。此外,Western印迹分析证明,白藜芦醇处理显着减弱的异氟醚诱导的异氟醚诱导的活化磷酸化(P)-aKT / AKT比率降低,P-P38 / P38 MAPK蛋白质比在PC12细胞中增加。这些发现表明,白藜芦醇能够通过AKT / P38 MAPK信号传导来保护来自异氟醚诱导的异氟醚诱导的炎症和氧化应激相关的死亡。

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