PMID: 29089075Nov 2, 2017Paper

Pyruvate attenuates the injury of PC12 cells induced by hypoxia via inhibiting p38MAPK phosphorylation

Xi bao yu fen zi mian yi xue za zhi = Chinese journal of cellular and molecular immunology
Min WeiHuilin Liu

Abstract

Objective To observe the protective effect of pyruvate against hypoxia-induced neuron injury and its mechanism. Methods PC12 cells were treated with pyruvate, and then exposed to 10 mL/L O2 for 12, 24 and 48 hours. The proliferation of PC12 cells was detected by MTT assay. The cell apoptosis was observed via the detection of caspase-3 activity. The levels of interleukin-1β (IL-1β), IL-6 and tumor necrosis factor α (TNF-α) were detected by ELISA. The expressions of p38MAPK and phosphorylated p38MAPK (p-p38MAPK) protein were tested by Western blotting. Results The levels of IL-1β, IL-6, TNF-α and p-p38-MAPK increased in hypoxia exposure for 24 and 48 hours, which inhibited the proliferation of PC12 cells and increased the activity of caspase-3. Pyruvate treatment significantly promoted cell proliferation and inhibited cell apoptosis, decreased the levels of IL-1β, IL-6 and TNF-α, and depressed p38MAPK phosphorylation. Conclusion Pyruvate protects hypoxia-induced neuron injury by inhibiting the phosphorylation of p38MAPK and decreasing the levels of inflammatory factors in PC12 cells.

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Apoptosis

Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis

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