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首页> 美国卫生研究院文献>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：白藜芦醇通过通过Akt / p38 MAPK信号传导减弱细胞凋亡从而保护神经元细胞免受异氟烷诱导的炎症和与氧化应激相关的死亡。

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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% O2 + 5% CO2 for 6 h and pre-treated with resveratrol (0–1,000 µM) for 0, 24 or 48 h prior to isoflurane treatment. An MTT assay, flow cytometry and ELISA of tumor necrosis factor-α, 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：本研究的目的是确定白藜芦醇是否通过通过Akt / p38丝裂原活化蛋白激酶（MAPK）信号传导减弱细胞凋亡来保护神经元细胞免受炎症和异氟烷诱导的氧化应激相关死亡。将PC12大鼠嗜铬细胞瘤细胞系用2％异氟烷+ 21％O2 + 5％CO2处理6 h，并在异氟烷处理之前用白藜芦醇（0–1,000 µM）预处理0、24或48 h。肿瘤坏死因子-α，白细胞介素-6，丙二醛和超氧化物歧化酶的MTT分析，流式细胞仪和ELISA结果表明，白藜芦醇可降低PC12细胞中异氟烷诱导的生长抑制，抑制细胞凋亡并抑制炎症和氧化应激。白藜芦醇预处理可有效降低异氟烷诱导的PC12细胞中的caspase-3活性和诱导型一氧化氮合酶蛋白的表达。此外，蛋白质印迹分析表明，白藜芦醇处理可显着减弱异氟烷诱导的PC12细胞中活化的磷酸化（p）-Akt / Akt比值的降低和p-p38 / p38 MAPK蛋白比值的增加。这些发现表明，白藜芦醇能够通过通过Akt / p38 MAPK信号传导减弱细胞凋亡，从而保护神经元细胞免受异氟烷诱导的炎症和与氧化应激相关的死亡。

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