Tags

Type your tag names separated by a space and hit enter

Protective effect of glycyrrhizin on 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death in differentiated PC12 cells.
J Pharmacol Exp Ther. 2007 May; 321(2):816-22.JP

Abstract

Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The aim of the present study was to assess the preventive effect of licorice compounds glycyrrhizin and 18beta-glycyrrhetinic acid against the toxicity of parkinsonian neurotoxin 1-methyl-4-phenylpyridinium (MPP+) in relation to the mitochondria-mediated cell death process and role of oxidative stress. MPP+ induced the nuclear damage, the changes in the mitochondrial membrane permeability, leading to the cytochrome c release and caspase-3 activation, the formation of reactive oxygen species, and the depletion of glutathione (GSH) in differentiated PC12 cells. Glycyrrhizin up to 100 microM significantly attenuated cell death and depletion of GSH due to MPP+ concentration-dependently. Meanwhile, 18beta-glycyrrhetinic acid showed a maximal inhibitory effect at 10 microM; beyond this concentration, the inhibitory effect declined. The protective effect of licorice compounds was also detected in the rotenone-treated PC12 cells. Glycyrrhizin and 18beta-glycyrrhetinic acid prevented the MPP+-induced formation of the mitochondrial permeability transition. The results show that both glycyrrhizin and a metabolite, 18beta-glycyrrhetinic acid, exhibit a depressant effect against the MPP+ toxicity. Glycyrrhizin and 18beta-glycyrrhetinic acid may prevent the cytotoxicity of MPP+ by suppressing the mitochondrial permeability transition formation. The preventive effect seems to be ascribed to the inhibitory effect on the formation of reactive oxygen species and depletion of GSH.

Authors+Show Affiliations

Department of Neurology, Gangneung Asan Hospital, College of Medicine, University of Ulsan, Gangwon-do, South Korea.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

17314199

Citation

Yim, Soo Bin, et al. "Protective Effect of Glycyrrhizin On 1-methyl-4-phenylpyridinium-induced Mitochondrial Damage and Cell Death in Differentiated PC12 Cells." The Journal of Pharmacology and Experimental Therapeutics, vol. 321, no. 2, 2007, pp. 816-22.
Yim SB, Park SE, Lee CS. Protective effect of glycyrrhizin on 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death in differentiated PC12 cells. J Pharmacol Exp Ther. 2007;321(2):816-22.
Yim, S. B., Park, S. E., & Lee, C. S. (2007). Protective effect of glycyrrhizin on 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death in differentiated PC12 cells. The Journal of Pharmacology and Experimental Therapeutics, 321(2), 816-22.
Yim SB, Park SE, Lee CS. Protective Effect of Glycyrrhizin On 1-methyl-4-phenylpyridinium-induced Mitochondrial Damage and Cell Death in Differentiated PC12 Cells. J Pharmacol Exp Ther. 2007;321(2):816-22. PubMed PMID: 17314199.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Protective effect of glycyrrhizin on 1-methyl-4-phenylpyridinium-induced mitochondrial damage and cell death in differentiated PC12 cells. AU - Yim,Soo Bin, AU - Park,Sang Eun, AU - Lee,Chung Soo, Y1 - 2007/02/21/ PY - 2007/2/23/pubmed PY - 2007/6/7/medline PY - 2007/2/23/entrez SP - 816 EP - 22 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 321 IS - 2 N2 - Defects in mitochondrial function have been shown to participate in the induction of neuronal cell injury. The aim of the present study was to assess the preventive effect of licorice compounds glycyrrhizin and 18beta-glycyrrhetinic acid against the toxicity of parkinsonian neurotoxin 1-methyl-4-phenylpyridinium (MPP+) in relation to the mitochondria-mediated cell death process and role of oxidative stress. MPP+ induced the nuclear damage, the changes in the mitochondrial membrane permeability, leading to the cytochrome c release and caspase-3 activation, the formation of reactive oxygen species, and the depletion of glutathione (GSH) in differentiated PC12 cells. Glycyrrhizin up to 100 microM significantly attenuated cell death and depletion of GSH due to MPP+ concentration-dependently. Meanwhile, 18beta-glycyrrhetinic acid showed a maximal inhibitory effect at 10 microM; beyond this concentration, the inhibitory effect declined. The protective effect of licorice compounds was also detected in the rotenone-treated PC12 cells. Glycyrrhizin and 18beta-glycyrrhetinic acid prevented the MPP+-induced formation of the mitochondrial permeability transition. The results show that both glycyrrhizin and a metabolite, 18beta-glycyrrhetinic acid, exhibit a depressant effect against the MPP+ toxicity. Glycyrrhizin and 18beta-glycyrrhetinic acid may prevent the cytotoxicity of MPP+ by suppressing the mitochondrial permeability transition formation. The preventive effect seems to be ascribed to the inhibitory effect on the formation of reactive oxygen species and depletion of GSH. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/17314199/Protective_effect_of_glycyrrhizin_on_1_methyl_4_phenylpyridinium_induced_mitochondrial_damage_and_cell_death_in_differentiated_PC12_cells_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=17314199 DB - PRIME DP - Unbound Medicine ER -