2017PubMedRequires access

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

Min Wei, Kun Zhang, Zhijun Li, Ping Yang, Jianxiang Zhang, Huilin Liu

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Abstract

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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What this paper is about

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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Available abstract

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.

Key concepts: Apoptosis, Phosphorylation, p38 mitogen-activated protein kinases, Hypoxia (environmental), Chemistry, Blot, Tumor necrosis factor alpha, Cell growth

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[Pyruvate attenuates the injury of PC12 cells induced by hypoxia via inhibiting p38MAPK phosphorylation]. — Research Paper | ScholarLens