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Chinese Journal of Clinical Pharmacology and Therapeutics ›› 2013, Vol. 18 ›› Issue (1): 1-5.

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Effect of pretreatment with pentamethylquercetin on mitochondrial function in rat cardiomyocyte

WAN Qing1, PENG Yi-an2, LIU Dan2, HUANG Huang1, LIU Ji-chun1, HE Ming1,2   

  1. 1Jiangxi Provincial Institute of Hypertension, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China;
    2Department of Pharmacology & Molecular Therapeutics, Nanchang University School of Pharmaceutical Science, Nanchang 330006, Jiangxi, China
  • Received:2012-07-23 Revised:2012-07-23 Published:2013-02-05

Abstract: AIM: To explore the protective effect of pretreatment with pentamethylquercetin(PMQ) on anoxia/reoxygenation (A/R) injury and mitochondrial function in rat cardiomyocytes. METHODS: Primary neonatal SD rat cardiomyocytes were cultured and pretreated with PMQ in final dose of 10, 30, 100 μmol/L for 24 h, and then underwent A/R injury. After treatment, the activity of LDH was determined by auto-biochemistry analysator, cells viability was analyzed by MTT, cell apoptosis and mitochondrial membrane potential were detected by flow cytometry, opening of mitochondrial permeability transition pore (mPTP) was determined by Ca2+-induced swelling of isolated cardiac mitochondria.RESULTS: Pretreated with different dose of PMQ (10, 30,100 μmo/L) for 24 h could reduce LDH activity, increase cell viability, decrease cell apoptosis(P<0.05 or P<0.01)in dose-dependent manner; Moreover, pretreated with 30, 100 μmol/L PMQ for 24 h, mitochondrial membrane potential could be more stable(P<0.05 or P<0.01), and the opening of mPTP could be more lessened(P<0.05 or P<0.01). CONCLUSION: Pretreated with PMQ for 24 h could have Pharmacology delay protection, the mechanism involved in stabilizing mitochondrial membrane potential, inhibiting mPTP opening, and reducing cell apoptosis.

Key words: Pentamethylquercetin, Cardiomyocyte, Injury, Mitochondrial

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