2014Shiyong yixue zazhiRequires access

Resveratrol protects H9c2 cells from death induced by lipopolysaccharide via down-regulating the phosphoration of P38MAPK

Li L

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Abstract

Objective To investigate whether treating H9c2 cells with Resveratrol attenuates the cell death and apoptosis induced by lipopolysaccharide via regulating the activation of p38 MAPK. Methods H9c2 cells were divided into four groups : control, LPS(10 μg/mL lipopolysaccharide), Res(5 μmol/L Resveratrol), and RL(5 μmol/L Resveratrol+ 10 μg/mL LPS). H9c2 cells from group Res and RL were pretreated with Resveratrol, and then,only cells from group LPS and RL, were incubated with LPS for 30 min and 12 hours. MTT and Flow cytometry were used to detect cell proliferation and death. The protein level of phosphorylation of p38MAPK was measured by Western blot. Result Compared with control, LPS significantly reduced cell proliferation(P 0.05), increased(P 0.01)cell death, and up-regulated the level of phosphorylation of p38MAPK(P 0.01). Pretreatment of Resveratrol attenuated the inhibition of LPS on cell viability and down-regulated the level of phosphorylation of p38MAPK. Conclusion Resveratrol may exert its cytoprotection effects on LPS-induced H9c2 cells via downregulating the activation of P38MAPK.

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Objective To investigate whether treating H9c2 cells with Resveratrol attenuates the cell death and apoptosis induced by lipopolysaccharide via regulating the activation of p38 MAPK. Methods H9c2 cells were divided into four groups : control, LPS(10 μg/mL lipopolysaccharide), Res(5 μmol/L Resveratrol), and RL(5 μmol/L Resveratrol+ 10 μg/mL LPS). H9c2 cells from group Res and RL were pretreated with Resveratrol, and then,only cells from group LPS and RL, were incubated with LPS for 30 min and 12 hours. MTT and Flow cytometry were used to detect cell proliferation and death. The protein level of phosphorylation of p38MAPK was measured by Western blot. Result Compared with control, LPS significantly reduced cell proliferation(P 0.05), increased(P 0.01)cell death, and up-regulated the level of phosphorylation of p38MAPK(P 0.01). Pretreatment of Resveratrol attenuated the inhibition of LPS on cell viability and down-regulated the level of phosphorylation of p38MAPK. Conclusion Resveratrol may exert its cytoprotection effects on LPS-induced H9c2 cells via downregulating the activation of P38MAPK.

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Available abstract

Objective To investigate whether treating H9c2 cells with Resveratrol attenuates the cell death and apoptosis induced by lipopolysaccharide via regulating the activation of p38 MAPK. Methods H9c2 cells were divided into four groups : control, LPS(10 μg/mL lipopolysaccharide), Res(5 μmol/L Resveratrol), and RL(5 μmol/L Resveratrol+ 10 μg/mL LPS). H9c2 cells from group Res and RL were pretreated with Resveratrol, and then,only cells from group LPS and RL, were incubated with LPS for 30 min and 12 hours. MTT and Flow cytometry were used to detect cell proliferation and death. The protein level of phosphorylation of p38MAPK was measured by Western blot. Result Compared with control, LPS significantly reduced cell proliferation(P 0.05), increased(P 0.01)cell death, and up-regulated the level of phosphorylation of p38MAPK(P 0.01). Pretreatment of Resveratrol attenuated the inhibition of LPS on cell viability and down-regulated the level of phosphorylation of p38MAPK. Conclusion Resveratrol may exert its cytoprotection effects on LPS-induced H9c2 cells via downregulating the activation of P38MAPK.

Key concepts: Resveratrol, Lipopolysaccharide, Flow cytometry, Viability assay, Apoptosis, Cytoprotection, Western blot, Phosphorylation

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