Cardioprotective effect of root extract of Picrorhiza kurroa (Royle Ex Benth) against isoproterenol-induced cardiotoxicity in rats.

Normal rats pre-treated with P. kurroa (200 mg/kg) alone did not showed significant change, however, isoproterenol (ISP) administration resulted in hemodynamic and left ventricular dysfunction, oxidative stress, and lipid peroxidation. Such cardiac dysfunction was significantly prevented by P. kurroa root extract pre-treatment. Pre-treatment significantly attenuated the ISP-induced oxidative stress by restoring myocardial superoxide dismutase, catalase, and glutathione peroxidase enzymes except reduced glutathione content. P. kurroa pre-treatment markedly attenuated the ISP-induced rise in lipid peroxidation, thereby prevented leakage of myocyte creatine kinase-MB and lactate dehydrogenase enzymes. The results suggest that P. kurroa root extract possesses significant cardioprotective effect, which may be attributed to its antioxidant, anti-peroxidative, and myocardial preservative properties.

Protective effect of hydroalcoholic extract of Andrographis paniculata on ischaemia-reperfusion induced myocardial injury in rats.

Background & objectives: Protecting myocardium from ischaemia-reperfusion (I-R) injury is important to reduce the complication of myocardial infarction (MI) and interventional revascularization procedures. In the present study, the cardioprotective potential of hydroalcoholic extract of Andrographis paniculata was evaluated against left anterior descending coronary artery (LADCA) ligation-induced I-R injury of myocardium in rats. Methods: MI was induced in rats by LADCA ligation for 45 min followed by reperfusion for 60 min. The rats were divided into five experimental groups viz., sham (saline treated, but LADCA was not ligated), I-R control (saline treated + I-R), benazepril (30 mg/kg + I-R), A. paniculata (200 mg/kg per se) and A. paniculata (200 mg/kg + I-R). A. paniculata was administered orally for 31 days. On day 31, rats were subjected to the I-R and cardiac function parameters were recorded. Further, rats were sacrificed and heart was excised for biochemical and histopathological studies. Results: In I-R control group, LADCA ligation resulted in significant cardiac dysfunction evidenced by reduced haemodynamic parameters; mean arterial pressure (MAP) and heart rate (HR). The left ventricular contractile function was also altered. In I-R control group, I-R caused decline in superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reduced glutathione (GSH) as well as leakage of myocytes injury marker enzymes, creatine phosphokinase-MB (CK-MB) isoenzyme and lactate dehydrogenase (LDH), and enhanced lipid peroxidation product, malonaldialdehyde (MDA). However, rats pretreated with A. paniculata 200 mg/kg showed favourable modulation of haemodynamic and left ventricular contractile function parameters, restoration of the myocardial antioxidants and prevention of depletion of myocytes injury marker enzymes along with inhibition of lipid peroxidation. Histopathological observations confirmed the protective effects of A. paniculata. The cardioprotective effects of A. paniculata were found comparable to that of benazepril treatment. Interpretation & Conclusions: Our results showed the cardioprotective effects of A. paniculata against I-R injury likely result from the suppression of oxidative stress and preserved histoarchitecture of myofibrils along with improved haemodynamic and ventricular functions.

Cardioprotective effects of Commiphora mukul against isoprenaline-induced cardiotoxicity: A biochemical and histopathological evaluation.

Commiphora mukul commonly known as Guggul is one of the oldest and commonly consumed herb for promoting heart and vascular health. Present study was undertaken to evaluate cardioprotective potential of Commiphora mukul against isoprenaline-induced myocardial necrosis in rats. Wistar albino rats were divided into three main groups: sham (saline only), isoprenaline control (saline and isoprenaline) and Commiphora mukul treated (Commiphora mukul and isoprenaline) groups. Commiphora mukul was administered in three doses 100, 200 and 400 mg kg-1 p.o. for 30 days. On 29th and 30th day, the animals of isoprenaline control and Commiphora mukul pretreatment groups were administered isoprenaline (85 mg kg-1; s.c.), consecutively at an interval of 24 hr. Isoprenaline administration produced a significant (p<0.05) decrease in myocardial antioxidants; superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSHPx), reduced glutathione (GSH), and myocyte injury marker enzymes creatine- phosphokinase - MB (CK-MB) and lactate dehydrogenase (LDH) along with enhanced lipid peroxidation; malondialdehyde (MDA) in heart. Commiphora mukul pretreatment reversed the isoprenaline-induced oxidative changes in rat myocardium by significant (p<0.05) increase in SOD, CAT, GSHPx, GSH and reduction of MDA. In addition to improving myocardial antioxidant status, Commiphora mukul also prevented the leakage of LDH and CK-MB from heart. Further, histopathological examination showed the reduction of necrosis, edema and inflammation following Commiphora mukul pretreatment. Based on present findings, it is concluded that Commiphora mukul may be a potential preventive and therapeutic agent against the oxidative stress associated ischemic heart disease owing to antioxidant and antiperoxidative activity.

Effect of Inula racemosa root extract on cardiac function and oxidative stress against isoproterenol-induced myocardial infarction.

The cardioprotective potential of Inula racemosa root hydroalcoholic extract against isoproterenol-induced myocardial infarction was investigated in rats. The rats treated with isoproterenol (85 mg/kg, s.c.) exhibited myocardial infarction, as evidenced by significant (P<0.05) decrease in mean arterial pressure, heart rate, contractility, relaxation along with increased left ventricular end diastolic pressure, as well as decreased endogenous myocardial enzymatic and non-enzymatic antioxidants. Isoproterenol also significantly (P<0.05) induced lipid peroxidation and increased leakage of myocyte injury marker enzymes. Pretreatment with I. racemosa extract (50, 100 or 200 mg/kg per day, p.o.) for 21 consecutive days, followed by isoproterenol injections on days 19th and 20th significantly (P<0.05) improved cardiac function by increasing the heart rate, mean arterial pressure, contractility and relaxation along with decreasing left ventricular end diastolic pressure. Pretreatment with I. racemosa also significantly (P<0.05) restored the reduced form of glutathione and endogenous antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase from the heart, which were depleted after isoproterenol administration. In addition to restoration of antioxidants, I. racemosa significantly (P<0.05) inhibited lipid peroxidation and prevented the leakage of myocytes specific marker enzymes creatine phosphokinase-MB and lactate dehydrogenase from the heart. Thus, it is concluded that I. racemosa protects heart from isoproterenol-induced myocardial injury by reducing oxidative stress and modulating hemodynamic and ventricular functions of the heart. Present study findings demonstrate the cardioprotective effect of I. racemosa and support the pharmacological relevance of its use and cardioprotection mechanism in ischemic heart disease as well as substantiate its traditional claim

Hydroalcoholic extract of Emblica officinalis Gaertn. affords protection against PTZ-induced seizures, oxidative stress and cognitive impairment in rats.

The cognitive impairment seen in epileptics may be a consequence of either the underlying epileptogenic process alone or it could manifest on account of the use of antiepileptic drugs that cause cognitive impairment as an adverse effect or both. Thus, there is a need for drugs that can suppress epileptogenesis without contributing to or , if possible, by acting to prevent the development of cognitive impairment. Emblica officinalis, an Indian medicinal plant, has marked antioxidant property. The effect of seven days pretreatment of 300, 500 and 700 mg/kg doses of hydroalcoholic extract of E. officinalis (HAEEO) administered intraperitoneally to rats was evaluated on pentylenetetrazole (PTZ) induced seizures, cognitive deficit and oxidative stress markers viz malondialdehyde (MDA) and glutathione. The 500 and 700 mg/kg ip doses of HAEEO completely abolished the generalized tonic seizures and also improved the retention latency in passive avoidance task. Further, HAEEO dose-dependently ameliorated the oxidative stress induced by PTZ. These findings suggest the potential of HAEEO to be used as an adjuvant to treatment with antiepileptic drugs.