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Implication of the c-Jun-NH2-terminal kinase pathway in the neuroprotective effect of puerarin against 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis in PC-12 cells.
Neurosci Lett. 2011 Jan 03; 487(1):88-93.NL

Abstract

Apoptosis is a widely accepted component of the pathogenesis of Parkinson's disease (PD), a debilitating neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra. In this study, we investigated the neuroprotective effects of puerarin and possible mechanisms by which puerarin acts against MPP(+)-induced toxicity in rat pheochromocytoma PC12 cells. PC12 cells exposed to MPP(+) (500 μM) significantly decreased the viability of PC12 cells when examined by MTT assay, DNA ELISA assay, and Annexin V assays, which was prevented by puerarin in a dose-dependent manner. PC12 cells exposed to MPP(+) (500 μM) elicited phosphorylation of MKK7, c-Jun-NH(2)-terminal kinase (JNK), and c-Jun which followed by the increase in cytochrome c levels, and which was prevented by puerarin. Moreover, puerarin inhibited the activation of caspase-9 and caspase-3 in MPP(+)-exposed PC12 cells. Whereas, the neuroprotective effect of puerarin against MPP(+) insults can be blocked by SP600125 (inhibitor of JNK). Taken together, these results suggest that puerarin protected PC12 cells against MPP(+)-induced neurotoxicity through the inhibition of the JNK signaling pathways. Therefore, puerarin has the possible beneficial effects in PD by attenuating MPP(+)-induced toxicity.

Authors+Show Affiliations

The Institute of Medicine, Qiqihar Medical University, Qiqihar, Heilongjiang, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20934486

Citation

Wang, Gang, et al. "Implication of the c-Jun-NH2-terminal Kinase Pathway in the Neuroprotective Effect of Puerarin Against 1-methyl-4-phenylpyridinium (MPP+)-induced Apoptosis in PC-12 Cells." Neuroscience Letters, vol. 487, no. 1, 2011, pp. 88-93.
Wang G, Zhou L, Zhang Y, et al. Implication of the c-Jun-NH2-terminal kinase pathway in the neuroprotective effect of puerarin against 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis in PC-12 cells. Neurosci Lett. 2011;487(1):88-93.
Wang, G., Zhou, L., Zhang, Y., Dong, M., Li, X., Liu, J., & Niu, Y. (2011). Implication of the c-Jun-NH2-terminal kinase pathway in the neuroprotective effect of puerarin against 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis in PC-12 cells. Neuroscience Letters, 487(1), 88-93. https://doi.org/10.1016/j.neulet.2010.10.002
Wang G, et al. Implication of the c-Jun-NH2-terminal Kinase Pathway in the Neuroprotective Effect of Puerarin Against 1-methyl-4-phenylpyridinium (MPP+)-induced Apoptosis in PC-12 Cells. Neurosci Lett. 2011 Jan 3;487(1):88-93. PubMed PMID: 20934486.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Implication of the c-Jun-NH2-terminal kinase pathway in the neuroprotective effect of puerarin against 1-methyl-4-phenylpyridinium (MPP+)-induced apoptosis in PC-12 cells. AU - Wang,Gang, AU - Zhou,Li, AU - Zhang,Yingbo, AU - Dong,Miaoxian, AU - Li,Xiaoming, AU - Liu,Jicheng, AU - Niu,Yingcai, Y1 - 2010/10/08/ PY - 2010/07/30/received PY - 2010/09/09/revised PY - 2010/10/01/accepted PY - 2010/10/12/entrez PY - 2010/10/12/pubmed PY - 2011/3/10/medline SP - 88 EP - 93 JF - Neuroscience letters JO - Neurosci Lett VL - 487 IS - 1 N2 - Apoptosis is a widely accepted component of the pathogenesis of Parkinson's disease (PD), a debilitating neurodegenerative disorder characterized by loss of dopaminergic neurons in the substantia nigra. In this study, we investigated the neuroprotective effects of puerarin and possible mechanisms by which puerarin acts against MPP(+)-induced toxicity in rat pheochromocytoma PC12 cells. PC12 cells exposed to MPP(+) (500 μM) significantly decreased the viability of PC12 cells when examined by MTT assay, DNA ELISA assay, and Annexin V assays, which was prevented by puerarin in a dose-dependent manner. PC12 cells exposed to MPP(+) (500 μM) elicited phosphorylation of MKK7, c-Jun-NH(2)-terminal kinase (JNK), and c-Jun which followed by the increase in cytochrome c levels, and which was prevented by puerarin. Moreover, puerarin inhibited the activation of caspase-9 and caspase-3 in MPP(+)-exposed PC12 cells. Whereas, the neuroprotective effect of puerarin against MPP(+) insults can be blocked by SP600125 (inhibitor of JNK). Taken together, these results suggest that puerarin protected PC12 cells against MPP(+)-induced neurotoxicity through the inhibition of the JNK signaling pathways. Therefore, puerarin has the possible beneficial effects in PD by attenuating MPP(+)-induced toxicity. SN - 1872-7972 UR - https://www.unboundmedicine.com/medline/citation/20934486/Implication_of_the_c_Jun_NH2_terminal_kinase_pathway_in_the_neuroprotective_effect_of_puerarin_against_1_methyl_4_phenylpyridinium__MPP+__induced_apoptosis_in_PC_12_cells_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0304-3940(10)01319-4 DB - PRIME DP - Unbound Medicine ER -