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Ginsenoside Rg1 protects against 6-OHDA-induced toxicity in MES23.5 cells via Akt and ERK signaling pathways.
J Ethnopharmacol. 2010 Jan 08; 127(1):118-23.JE

Abstract

AIM OF THE STUDY

The present study was designed to investigate the neuroprotective effects of ginsenoside Rg1 against 6-hydroxydopamine (6-OHDA)-induced toxicity in MES23.5 cells and their possible mechanisms.

MATERIALS AND METHODS

MES23.5 cells were treated with or without Rg1 for 24h before exposure to 6-OHDA. Cell viability was determined by MTS assay. The gene and protein expressions of Bcl-2 were detected by real time RT-PCR and western blotting. Phosphorylation of Akt and ERK1/2 were examined by western blotting.

RESULTS

Pretreatment with ginsenoside Rg1 had obvious neuroprotective effects on cell viability against 6-OHDA-induced toxicity. 6-OHDA decreased the gene and protein expressions of Bcl-2. These effects could be reversed by Rg1 pretreatment. Potential cell signaling candidates involved in this neuroprotective effect were examined. 6-OHDA significantly inhibited the phosphorylation of Akt and increased the phosphorylation of ERK1/2 in MES23.5 cells. Pretreatment with ginsenoside Rg1 could increase the Akt phosphorylation and inhibit the ERK1/2 phosphorylation induced by 6-OHDA. Further study revealed that LY294002, an inhibitor of phosphatidylinositol 3-kinase (PI3-K), attenuated the neuroprotective effect of Rg1 on cell viability against 6-OHDA-induced toxicity.

CONCLUSIONS

Taken together, our results strongly suggest that ginsenoside Rg1 has neuroprotective effects against 6-OHDA-induced toxicity in MES23.5 cells. Its mechanism includes the up-regulation of Bcl-2 gene expression, the activation of Akt phoshphorylation as well as the inhibition of ERK1/2 phosphorylation induced by 6-OHDA.

Authors+Show Affiliations

Department of Physiology, Medical College of Qingdao University, No. 308 Ningxia Road, Boya Building, Qingdao, Shandong 266071, PR China.No 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

19799986

Citation

Ge, Ke-Li, et al. "Ginsenoside Rg1 Protects Against 6-OHDA-induced Toxicity in MES23.5 Cells Via Akt and ERK Signaling Pathways." Journal of Ethnopharmacology, vol. 127, no. 1, 2010, pp. 118-23.
Ge KL, Chen WF, Xie JX, et al. Ginsenoside Rg1 protects against 6-OHDA-induced toxicity in MES23.5 cells via Akt and ERK signaling pathways. J Ethnopharmacol. 2010;127(1):118-23.
Ge, K. L., Chen, W. F., Xie, J. X., & Wong, M. S. (2010). Ginsenoside Rg1 protects against 6-OHDA-induced toxicity in MES23.5 cells via Akt and ERK signaling pathways. Journal of Ethnopharmacology, 127(1), 118-23. https://doi.org/10.1016/j.jep.2009.09.038
Ge KL, et al. Ginsenoside Rg1 Protects Against 6-OHDA-induced Toxicity in MES23.5 Cells Via Akt and ERK Signaling Pathways. J Ethnopharmacol. 2010 Jan 8;127(1):118-23. PubMed PMID: 19799986.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Ginsenoside Rg1 protects against 6-OHDA-induced toxicity in MES23.5 cells via Akt and ERK signaling pathways. AU - Ge,Ke-Li, AU - Chen,Wen-Fang, AU - Xie,Jun-Xia, AU - Wong,Man-Sau, Y1 - 2009/09/30/ PY - 2009/02/23/received PY - 2009/09/18/revised PY - 2009/09/21/accepted PY - 2009/10/6/entrez PY - 2009/10/6/pubmed PY - 2010/4/22/medline SP - 118 EP - 23 JF - Journal of ethnopharmacology JO - J Ethnopharmacol VL - 127 IS - 1 N2 - AIM OF THE STUDY: The present study was designed to investigate the neuroprotective effects of ginsenoside Rg1 against 6-hydroxydopamine (6-OHDA)-induced toxicity in MES23.5 cells and their possible mechanisms. MATERIALS AND METHODS: MES23.5 cells were treated with or without Rg1 for 24h before exposure to 6-OHDA. Cell viability was determined by MTS assay. The gene and protein expressions of Bcl-2 were detected by real time RT-PCR and western blotting. Phosphorylation of Akt and ERK1/2 were examined by western blotting. RESULTS: Pretreatment with ginsenoside Rg1 had obvious neuroprotective effects on cell viability against 6-OHDA-induced toxicity. 6-OHDA decreased the gene and protein expressions of Bcl-2. These effects could be reversed by Rg1 pretreatment. Potential cell signaling candidates involved in this neuroprotective effect were examined. 6-OHDA significantly inhibited the phosphorylation of Akt and increased the phosphorylation of ERK1/2 in MES23.5 cells. Pretreatment with ginsenoside Rg1 could increase the Akt phosphorylation and inhibit the ERK1/2 phosphorylation induced by 6-OHDA. Further study revealed that LY294002, an inhibitor of phosphatidylinositol 3-kinase (PI3-K), attenuated the neuroprotective effect of Rg1 on cell viability against 6-OHDA-induced toxicity. CONCLUSIONS: Taken together, our results strongly suggest that ginsenoside Rg1 has neuroprotective effects against 6-OHDA-induced toxicity in MES23.5 cells. Its mechanism includes the up-regulation of Bcl-2 gene expression, the activation of Akt phoshphorylation as well as the inhibition of ERK1/2 phosphorylation induced by 6-OHDA. SN - 1872-7573 UR - https://www.unboundmedicine.com/medline/citation/19799986/Ginsenoside_Rg1_protects_against_6_OHDA_induced_toxicity_in_MES23_5_cells_via_Akt_and_ERK_signaling_pathways_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0378-8741(09)00598-4 DB - PRIME DP - Unbound Medicine ER -