The Journal of pharmacy and pharmacology · 2011
Similar potency of catechin and its enantiomers in alleviating 1-methyl-4-phenylpyridinium ion cytotoxicity in SH-SY5Y cells.
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Ruan Hao-lan, Yang Yi, Zhu Xiao-nan, Wang Xue-lan, Chen Ru-zhu
Аннотация
OBJECTIVES: Previously, the flavonoid (±)-catechin was shown to exert potent neuroprotective action in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-induced Parkinson's disease model. The purpose of this study was to investigate whether the different enantiomers of catechin ((+)-catechin, (-)-catechin and (±)-catechin, a 50:50 mixture of (+)-catechin and (-)-catechin) could protect SH-SY5Y cells against 1-methyl-4-phenylpyridinium ion (MPP(+) ) toxicity by decreasing the generation of oxygen free radicals. The inhibitive effect of (±)-catechin on JNK/c-Jun activation was investigated.
METHODS: The effects of (+)-catechin, (-)-catechin or (±)-catechin in protecting against MPP(+) toxicity were evaluated and compared in SH-SY5Y cells by testing the release of lactate dehydrogenase. The generation of reactive oxygen species (ROS) was measured by immunochemistry and the phosphorylation level of JNK/c-Jun was determined by Western blotting.
KEY FINDINGS: In SH-SY5Y cells, (+)-catechin, (-)-catechin or (±)-catechin reduced apoptosis induced by MPP(+) and decreased ROS generation caused by MPP(+) . Different enantiomers of catechin showed protective effects at similar potency. Moreover (±)-catechin decreased JNK/c-Jun phosphorylation which was increased by MPP(+).
CONCLUSIONS: Catechin and its two enantiomers could protect SH-SY5Y cells against MPP(+) cytotoxicity at a similar potency. Antioxidative stress and inhibition of the JNK/c-Jun signalling pathway might have been involved in the neuroprotective mechanisms of catechin against MPP(+) cytotoxicity in SH-SY5Y cells.
METHODS: The effects of (+)-catechin, (-)-catechin or (±)-catechin in protecting against MPP(+) toxicity were evaluated and compared in SH-SY5Y cells by testing the release of lactate dehydrogenase. The generation of reactive oxygen species (ROS) was measured by immunochemistry and the phosphorylation level of JNK/c-Jun was determined by Western blotting.
KEY FINDINGS: In SH-SY5Y cells, (+)-catechin, (-)-catechin or (±)-catechin reduced apoptosis induced by MPP(+) and decreased ROS generation caused by MPP(+) . Different enantiomers of catechin showed protective effects at similar potency. Moreover (±)-catechin decreased JNK/c-Jun phosphorylation which was increased by MPP(+).
CONCLUSIONS: Catechin and its two enantiomers could protect SH-SY5Y cells against MPP(+) cytotoxicity at a similar potency. Antioxidative stress and inhibition of the JNK/c-Jun signalling pathway might have been involved in the neuroprotective mechanisms of catechin against MPP(+) cytotoxicity in SH-SY5Y cells.