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Updated: Feb 8, 2026

Isolation of Primary Rat Hepatocytes with Multiparameter Perfusion Control
Published on: April 5, 2021
[Effects of MAPKs inhibitors on GSH metabolic enzymes in rat hepatocytes]
Wei-Na Gao1, Ling-Ling Pu1, Jing-Yu Wei1
1Department of Nutrition, Institute of Health and Environmental Medicine, Academy of Military Medical Sciences, Tianjin 300050, China.
Objective:
To investigate the effects of mitogen-activated protein kinases (MAPKs) inhibitors on glutathione (GSH) metabolism, and to explore the pathway related to GSH metabolism.
Methods:
BRL rat hepatocytes were treated by c-Jun NH2-terminal kinase (JNK),p38, and extracellular signal-regulated kinase 1/2 (ERK1/2) inhibitors:SP600125, SB203580 and PD98659, respectively, for 24 h. MTT method was used to measure hepatocytes viability. The content of GSH was determined by high performance liquid chromatography. The protein expressions of JNK and phosphorylated JNK (p-JNK) was tested by Luminex method. Activities of GSH metabolic enzymes were detected by commercial kits.
Results:
Hepatocytes vitality was inhibited when the concentrations of SP600125, SB203580 and PD98659 were higher than 10 μmol/L, 20 μmol/L, and 40 μmol/L, respectively; SP600125 decreased the content of GSH in hepatocytes, while SB203580 and PD98659 had no effect. SP600125 reduced p-JNK protein expression, and enhanced GSH-Px activity significantly.
Conclusions:
JNK MAPK pathway takes part in the GSH metabolism in hepatocytes.
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