BACKGROUND: Phikud Navakot (PN) is a set of nine medicinal plants and the main ingredient of "Yahom Navakot", a traditional Thai herbal formula for treatment of cardiovascular symptoms. OBJECTIVE: To investigate the cardioprotective effects of PN on myocardial ischemia/reperfusion (IR) in male Sprague Dawley rats. MATERIAL AND METHOD: Rats were randomly divided into 7 groups: sham, IR, and IR orally pretreated with PN (10, 50, 100, 200, and 400 mg/kg B W)for 7 days. After treatment, IR induction was performed by left coronary artery (LCA) ligation for 30 min, followed by reperfusion for 24 h. At the end of the experiment, blood was collected for hematological and biochemical parameters, and hearts were immediately removed for histopathological examination and Western blot analysis. RESULTS: IR induction caused ST elevation in the electrocardiogram and an increase in serum troponin I (TnI), confirming myocardial damage. In addition, histopathological changes of ischemic myocardium showed inflammation, infiltration, and edema. Oral administration of PN (10, 50, 100, 200, and 400 mg/kg BW) for 7 days prior to IR simulation showed no change on serum TnI and histopathology ofcardiac tissues, when compared to IR group. However Western blot analysis showed that IR rats pretreated with PN (10 mg/kg BW) significantly increased (p < 0.05) pERK/ERK ratio, meanwhile pretreated with PN (50-200 mg/kg BW) up-regulated (p < 0.05) the protein expression of HO-1, when compared with IR group. CONCLUSION: The present study implied that 7-day pretreatment of PN failed to protect cardiac tissues against IR injury induced by LCA ligation. Investigation at molecular level found however that PN up-regulated the expression of protective proteins pERK/ERK ratio and HO-1 in cardiac tissues, suggesting molecular mechanism of PN in cardioprotection against IR injury.
BACKGROUND: Phikud Navakot (PN) is a set of nine medicinal plants and the main ingredient of "Yahom Navakot", a traditional Thai herbal formula for treatment of cardiovascular symptoms. OBJECTIVE: To investigate the cardioprotective effects of PN on myocardial ischemia/reperfusion (IR) in male Sprague Dawley rats. MATERIAL AND METHOD:Rats were randomly divided into 7 groups: sham, IR, and IR orally pretreated with PN (10, 50, 100, 200, and 400 mg/kg B W)for 7 days. After treatment, IR induction was performed by left coronary artery (LCA) ligation for 30 min, followed by reperfusion for 24 h. At the end of the experiment, blood was collected for hematological and biochemical parameters, and hearts were immediately removed for histopathological examination and Western blot analysis. RESULTS: IR induction caused ST elevation in the electrocardiogram and an increase in serum troponin I (TnI), confirming myocardial damage. In addition, histopathological changes of ischemic myocardium showed inflammation, infiltration, and edema. Oral administration of PN (10, 50, 100, 200, and 400 mg/kg BW) for 7 days prior to IR simulation showed no change on serum TnI and histopathology ofcardiac tissues, when compared to IR group. However Western blot analysis showed that IR rats pretreated with PN (10 mg/kg BW) significantly increased (p < 0.05) pERK/ERK ratio, meanwhile pretreated with PN (50-200 mg/kg BW) up-regulated (p < 0.05) the protein expression of HO-1, when compared with IR group. CONCLUSION: The present study implied that 7-day pretreatment of PN failed to protect cardiac tissues against IR injury induced by LCA ligation. Investigation at molecular level found however that PN up-regulated the expression of protective proteins pERK/ERK ratio and HO-1 in cardiac tissues, suggesting molecular mechanism of PN in cardioprotection against IR injury.