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Cardioprotective effect of vanadyl sulfate on ischemia/reperfusion-induced injury in rat heart in vivo is mediated by activation of protein kinase B and induction of FLICE-inhibitory protein.
Cardiovasc Ther. 2008 Spring; 26(1):10-23.CT

Abstract

Here we explored the mechanism of cardioprotective action of a tyrosine phosphatase inhibitor vanadyl sulfate on myocardial infarction and cardiac functional recovery in rats subjected to myocardial ischemia/reperfusion (MI/R) in vivo. Male Sprague-Dawley rats underwent 30 min heart ischemia by left coronary artery occlusion followed by 24-h reperfusion. Rats were randomized to receive either vehicle or vanadyl sulfate (1 and 5 mg/kg) intraperitoneally 0 min and 30 min after the start of reperfusion. Posttreatment with vanadyl sulfate significantly reduced the infarct size and significantly decreased the elevated left ventricular end diastolic pressure, improved left ventricular developed pressure, and left ventricular contractility (+/- dP/dt) after 72-h reperfusion in a dose-dependent manner. Moreover, treatment with vanadyl sulfate also significantly inhibited the apoptosis-related Caspase-3 and Caspase-9 processing, thereby elicited the antiapoptotic effect. The cardioprotective effect of vanadyl sulfate was closely associated with restoration of reduced protein kinase B (Akt) activity following MI/R injury. The recovered Akt activity correlated with increased phosphorylation of forkhead transcription factors, FKHR and FKHRL-1, thereby inhibiting apoptotic signaling. Furthermore, treatment with vanadyl sulfate significantly increased FLICE-inhibitory protein (FLIP) expression, and decreased expression of Fas ligand and Bim in cardiomyocytes. Taken together, rescue of cardiomyocytes by posttreatment with vanadyl sulfate from MI/R injury was mediated by increased FLIP expression and decreased Fas ligand and Bim expression via activation of Akt. These results demonstrate that treatment with vanadyl sulfate exerts significant cardioprotective effects along with cardiac functional recovery.

Authors+Show Affiliations

Department of Pharmacology, Graduate School of Pharmaceutical Sciences, Tohoku University, Sendai, Japan.No 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

18466417

Citation

Bhuiyan, Md Shenuarin, et al. "Cardioprotective Effect of Vanadyl Sulfate On Ischemia/reperfusion-induced Injury in Rat Heart in Vivo Is Mediated By Activation of Protein Kinase B and Induction of FLICE-inhibitory Protein." Cardiovascular Therapeutics, vol. 26, no. 1, 2008, pp. 10-23.
Bhuiyan MS, Takada Y, Shioda N, et al. Cardioprotective effect of vanadyl sulfate on ischemia/reperfusion-induced injury in rat heart in vivo is mediated by activation of protein kinase B and induction of FLICE-inhibitory protein. Cardiovasc Ther. 2008;26(1):10-23.
Bhuiyan, M. S., Takada, Y., Shioda, N., Moriguchi, S., Kasahara, J., & Fukunaga, K. (2008). Cardioprotective effect of vanadyl sulfate on ischemia/reperfusion-induced injury in rat heart in vivo is mediated by activation of protein kinase B and induction of FLICE-inhibitory protein. Cardiovascular Therapeutics, 26(1), 10-23. https://doi.org/10.1111/j.1527-3466.2008.00039.x
Bhuiyan MS, et al. Cardioprotective Effect of Vanadyl Sulfate On Ischemia/reperfusion-induced Injury in Rat Heart in Vivo Is Mediated By Activation of Protein Kinase B and Induction of FLICE-inhibitory Protein. Cardiovasc Ther. 2008;26(1):10-23. PubMed PMID: 18466417.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Cardioprotective effect of vanadyl sulfate on ischemia/reperfusion-induced injury in rat heart in vivo is mediated by activation of protein kinase B and induction of FLICE-inhibitory protein. AU - Bhuiyan,Md Shenuarin, AU - Takada,Yoko, AU - Shioda,Norifumi, AU - Moriguchi,Shigeki, AU - Kasahara,Jiro, AU - Fukunaga,Kohji, PY - 2008/5/10/pubmed PY - 2008/6/5/medline PY - 2008/5/10/entrez SP - 10 EP - 23 JF - Cardiovascular therapeutics JO - Cardiovasc Ther VL - 26 IS - 1 N2 - Here we explored the mechanism of cardioprotective action of a tyrosine phosphatase inhibitor vanadyl sulfate on myocardial infarction and cardiac functional recovery in rats subjected to myocardial ischemia/reperfusion (MI/R) in vivo. Male Sprague-Dawley rats underwent 30 min heart ischemia by left coronary artery occlusion followed by 24-h reperfusion. Rats were randomized to receive either vehicle or vanadyl sulfate (1 and 5 mg/kg) intraperitoneally 0 min and 30 min after the start of reperfusion. Posttreatment with vanadyl sulfate significantly reduced the infarct size and significantly decreased the elevated left ventricular end diastolic pressure, improved left ventricular developed pressure, and left ventricular contractility (+/- dP/dt) after 72-h reperfusion in a dose-dependent manner. Moreover, treatment with vanadyl sulfate also significantly inhibited the apoptosis-related Caspase-3 and Caspase-9 processing, thereby elicited the antiapoptotic effect. The cardioprotective effect of vanadyl sulfate was closely associated with restoration of reduced protein kinase B (Akt) activity following MI/R injury. The recovered Akt activity correlated with increased phosphorylation of forkhead transcription factors, FKHR and FKHRL-1, thereby inhibiting apoptotic signaling. Furthermore, treatment with vanadyl sulfate significantly increased FLICE-inhibitory protein (FLIP) expression, and decreased expression of Fas ligand and Bim in cardiomyocytes. Taken together, rescue of cardiomyocytes by posttreatment with vanadyl sulfate from MI/R injury was mediated by increased FLIP expression and decreased Fas ligand and Bim expression via activation of Akt. These results demonstrate that treatment with vanadyl sulfate exerts significant cardioprotective effects along with cardiac functional recovery. SN - 1755-5914 UR - https://www.unboundmedicine.com/medline/citation/18466417/Cardioprotective_effect_of_vanadyl_sulfate_on_ischemia/reperfusion_induced_injury_in_rat_heart_in_vivo_is_mediated_by_activation_of_protein_kinase_B_and_induction_of_FLICE_inhibitory_protein_ L2 - https://doi.org/10.1111/j.1527-3466.2008.00039.x DB - PRIME DP - Unbound Medicine ER -