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Evidence that hydroxysafflor yellow A protects the heart against ischaemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening.
Clin Exp Pharmacol Physiol. 2008 Feb; 35(2):211-6.CE

Abstract

1. The present study was conducted to investigate whether hydroxysafflor yellow A (HSYA) has a protective effect against heart injury after ischaemia-reperfusion and to determine the possible mechanism involved. 2. Hearts isolated from male Sprague-Dawley rats were perfused on a Langendorff apparatus and subjected to 30 min global ischaemia, followed by 120 min reperfusion. Infarct size and the level of lactate dehydrogenase (LDH) in the coronary effluent were determined. In mitochondria from isolated perfused hearts, Ca(2+)-induced swelling was observed. In isolated ventricular myocytes, depolarization of the mitochondrial membrane was determined by tetramethyl-rhodamine ethyl ester (TMRE) fluorescence. Furthermore, levels of phosphorylated endothelial nitric oxide synthase (eNOS) protein were measured by western blot. 3. Pretreatment with HSYA for 5 min before ischaemia reduced infarct size and the release of LDH. Administration of 20 micromol/L atractyloside, an opener of the mitochondrial permeability transition pore, and 10 micromol/L N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS, attenuated the protective effects of HSYA. In mitochondria isolated from hearts pretreated with 0.1 mmol/L HSYA for 5 min, a significant inhibition of Ca(2+)-induced swelling was observed and this inhibition was attenuated by l-NAME. In isolated ventricular myocytes, pretreatment with HSYA prevented ischaemia-induced cell death and depolarization of the mitochondrial membrane, whereas atractyloside or l-NAME attenuated the effects of HSYA. Levels of phosphorylated eNOS protein were significantly enhanced in the HSYA-treated group. 4. The findings of the present study indicate that HSYA protects the myocardium against ischaemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening. The effect of HSYA on mitochondrial permeability transition pore opening may be mediated through enhanced nitric oxide production by eNOS activation.

Authors+Show Affiliations

Department of Cardiology, Second Affiliated Hospital, School of Medicine, Zhejiang University, Hangzhou, China.No affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

17941891

Citation

Liu, Yi-Na, et al. "Evidence That Hydroxysafflor Yellow a Protects the Heart Against Ischaemia-reperfusion Injury By Inhibiting Mitochondrial Permeability Transition Pore Opening." Clinical and Experimental Pharmacology & Physiology, vol. 35, no. 2, 2008, pp. 211-6.
Liu YN, Zhou ZM, Chen P. Evidence that hydroxysafflor yellow A protects the heart against ischaemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening. Clin Exp Pharmacol Physiol. 2008;35(2):211-6.
Liu, Y. N., Zhou, Z. M., & Chen, P. (2008). Evidence that hydroxysafflor yellow A protects the heart against ischaemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening. Clinical and Experimental Pharmacology & Physiology, 35(2), 211-6.
Liu YN, Zhou ZM, Chen P. Evidence That Hydroxysafflor Yellow a Protects the Heart Against Ischaemia-reperfusion Injury By Inhibiting Mitochondrial Permeability Transition Pore Opening. Clin Exp Pharmacol Physiol. 2008;35(2):211-6. PubMed PMID: 17941891.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Evidence that hydroxysafflor yellow A protects the heart against ischaemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening. AU - Liu,Yi-Na, AU - Zhou,Zhong-Min, AU - Chen,Peng, Y1 - 2007/10/17/ PY - 2007/10/19/pubmed PY - 2008/2/1/medline PY - 2007/10/19/entrez SP - 211 EP - 6 JF - Clinical and experimental pharmacology & physiology JO - Clin. Exp. Pharmacol. Physiol. VL - 35 IS - 2 N2 - 1. The present study was conducted to investigate whether hydroxysafflor yellow A (HSYA) has a protective effect against heart injury after ischaemia-reperfusion and to determine the possible mechanism involved. 2. Hearts isolated from male Sprague-Dawley rats were perfused on a Langendorff apparatus and subjected to 30 min global ischaemia, followed by 120 min reperfusion. Infarct size and the level of lactate dehydrogenase (LDH) in the coronary effluent were determined. In mitochondria from isolated perfused hearts, Ca(2+)-induced swelling was observed. In isolated ventricular myocytes, depolarization of the mitochondrial membrane was determined by tetramethyl-rhodamine ethyl ester (TMRE) fluorescence. Furthermore, levels of phosphorylated endothelial nitric oxide synthase (eNOS) protein were measured by western blot. 3. Pretreatment with HSYA for 5 min before ischaemia reduced infarct size and the release of LDH. Administration of 20 micromol/L atractyloside, an opener of the mitochondrial permeability transition pore, and 10 micromol/L N(G)-nitro-L-arginine methyl ester (L-NAME), an inhibitor of NOS, attenuated the protective effects of HSYA. In mitochondria isolated from hearts pretreated with 0.1 mmol/L HSYA for 5 min, a significant inhibition of Ca(2+)-induced swelling was observed and this inhibition was attenuated by l-NAME. In isolated ventricular myocytes, pretreatment with HSYA prevented ischaemia-induced cell death and depolarization of the mitochondrial membrane, whereas atractyloside or l-NAME attenuated the effects of HSYA. Levels of phosphorylated eNOS protein were significantly enhanced in the HSYA-treated group. 4. The findings of the present study indicate that HSYA protects the myocardium against ischaemia-reperfusion injury by inhibiting mitochondrial permeability transition pore opening. The effect of HSYA on mitochondrial permeability transition pore opening may be mediated through enhanced nitric oxide production by eNOS activation. SN - 1440-1681 UR - https://www.unboundmedicine.com/medline/citation/17941891/Evidence_that_hydroxysafflor_yellow_A_protects_the_heart_against_ischaemia_reperfusion_injury_by_inhibiting_mitochondrial_permeability_transition_pore_opening_ L2 - https://doi.org/10.1111/j.1440-1681.2007.04814.x DB - PRIME DP - Unbound Medicine ER -