Experimental and Therapeutic Medicine · 2017 · 34 citations · 22 references
Life SciencesCell BiologyPharmacologyApoptosisCell SignalingInflammationAntioxidant DefenseApoptosis ModulationApoptosis RegulationApoptotic SignalingCell DeathNeuroprotectionGrowth Inhibition AssaysMapk SignalingMitogen-activated Protein Kinase SignalingNeuroprotective Apoptosis ModulationOxidative Stress InjuryP38 Mitogen-activated Protein Kinase SignalingPi3k-akt Signaling PathwayProtein Expression Levels
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.
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Oxidative Stress Status During Exposure to Propofol, Sevoflurane and Desflurane
Bernard Allaouchiche, Richard Debon, J. Goudable et al. · Anesthesia & Analgesia · 2001 · 155 citations