2013Zhongguo shouyi xuebaoRequires access

The role of the MAPK signaling pathways in the apoptosis of rat hepatocytes induced by cadmium

Liu Zong-ping

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Abstract

To investigate the effect of mitogen-activated protein kinase(MAPK) on the apoptosis of rat hepatocytes induced by cadmium.Rat hepatocytes were isolated by a two-step perfusion technique.After 24 h planting,hepatocytes were treated with cadmium in the presence or absence of MAPK signaling inhibitors(p38 MAPK inhibitor SB202190,JNK inhibitor SP600125,ERK inhibitor U0126).Cell viability was evaluated with a colorimetric using MTT level.Cell morphology and apoptosis were photographed under inverted and fluorescence microscope.Immunohistochemistry analysis was performed to recognize the activated phosphorylated forms of p38 MAPK kinases in Cd-treated hepatocytes in the presence or absence SB202190 and NAC.The results showed that the phosphorylation of p38 MAPK increased after Cd treatment and the activations were inhibited by the treatment with its inhibitor SB202190.SB202190 reversed significantly Cd-induced cell death.SB202190 effectively inhibited Cd-induced alterations in the morphology and apoptosis of hepatocytes.While SP600125 and U0126 increased Cd-induced cell death significantly.The findings suggested that Cd induced rat hepatocytes apoptosis through p38 MAPK pathway.

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What this paper is about

To investigate the effect of mitogen-activated protein kinase(MAPK) on the apoptosis of rat hepatocytes induced by cadmium.Rat hepatocytes were isolated by a two-step perfusion technique.After 24 h planting,hepatocytes were treated with cadmium in the presence or absence of MAPK signaling inhibitors(p38 MAPK inhibitor SB202190,JNK inhibitor SP600125,ERK inhibitor U0126).Cell viability was evaluated with a colorimetric using MTT level.Cell morphology and apoptosis were photographed under inverted and fluorescence microscope.Immunohistochemistry analysis was performed to recognize the activated phosphorylated forms of p38 MAPK kinases in Cd-treated hepatocytes in the presence or absence SB202190 and NAC.The results showed that the phosphorylation of p38 MAPK increased after Cd treatment and the activations were inhibited by the treatment with its inhibitor SB202190.SB202190 reversed significantly Cd-induced cell death.SB202190 effectively inhibited Cd-induced alterations in the morphology and apoptosis of hepatocytes.While SP600125 and U0126 increased Cd-induced cell death significantly.The findings suggested that Cd induced rat hepatocytes apoptosis through p38 MAPK pathway.

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Available abstract

To investigate the effect of mitogen-activated protein kinase(MAPK) on the apoptosis of rat hepatocytes induced by cadmium.Rat hepatocytes were isolated by a two-step perfusion technique.After 24 h planting,hepatocytes were treated with cadmium in the presence or absence of MAPK signaling inhibitors(p38 MAPK inhibitor SB202190,JNK inhibitor SP600125,ERK inhibitor U0126).Cell viability was evaluated with a colorimetric using MTT level.Cell morphology and apoptosis were photographed under inverted and fluorescence microscope.Immunohistochemistry analysis was performed to recognize the activated phosphorylated forms of p38 MAPK kinases in Cd-treated hepatocytes in the presence or absence SB202190 and NAC.The results showed that the phosphorylation of p38 MAPK increased after Cd treatment and the activations were inhibited by the treatment with its inhibitor SB202190.SB202190 reversed significantly Cd-induced cell death.SB202190 effectively inhibited Cd-induced alterations in the morphology and apoptosis of hepatocytes.While SP600125 and U0126 increased Cd-induced cell death significantly.The findings suggested that Cd induced rat hepatocytes apoptosis through p38 MAPK pathway.

Key concepts: MAPK/ERK pathway, Apoptosis, p38 mitogen-activated protein kinases, Cell biology, Kinase, Biology, Viability assay, Programmed cell death

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