Cardioprotective activity of flax lignan concentrate extracted from seeds of Linum usitatissimum in isoprenalin induced myocardial necrosis in rats
Cardioprotective activity of flax lignan concentrate extracted from seeds of Linum usitatissimum in isoprenalin induced myocardial necrosis in rats
Year: 2011
Authors: Hedge, M.V. Bodhankar, S.L.
Publication Name: Interdiscip. Toxicol.
Publication Details: Volume 4; Number 2; Pages 90 – 97.
Abstract:
The objective of the study was to evaluate the cardioprotective activity of flax lignan concentrate (FLC) in isoprenalin (ISO) induced cardiotoxicity in rats. Male Wistar rats (200�230 g) were divided into three groups. Group I: control, Group II: isoprenalin, Group III: FLC (500 mg/kg, p.o.) orally for 8 days and in group II and III isoprenalin 5.25 mg/kg, s.c. on day 9 and 8.5 mg/kg on day 10. On day 10 estimation of marker enzymes in serum and haemodynamic parameters were recorded. Animals were sacrificed, histology of heart was performed. Isoprenalin showed cardiotoxicity, manifested by increased levels of marker enzymes and increased heart rate. FLC treatment reversed these biochemical changes significantly compared with ISO group. The cardiotoxic effect of isoprenalin was less in FLC pretreated animals, which was confirmed in histopathological alterations. Haemodynamic, biochemical alteration and histopathological results suggest a cardioprotective protective effect of FLC in isoprenalin induced cardiotoxicity
(Auhtors abstract)
Reactive oxygen species are known to play a major role of Ischaemic heart disease. Ischaemic tissue generates oxygen-derived free radicals and other reactive species which bring about oxidative damage of membrane lipids, proteins and carbohydrates leading to qualitative and quantitative alterations of the myocardium . Isoprenalin (ISO), a synthetic catecholamine and β-adrenergic agonist is documented to produce myocardial infarction due to generation of highly cytotoxic free radicals through its auto-oxidation.The pharmacologic effect of isoprenalin is believed to be associated with its β-adrenergic effect, which increases heart rate, decreases blood pressure and diminishes the oxygen supply to the myocardium. The objective of the present investigation was to study the effect of flax lignan concentrate (FLC) extracted from seeds of Linum usitatissimum on isoprenalin induced cardiotoxicity in Wistar rats. Following 10-day administration of FLC isoprenalin-induced tachycardia was reduced. Isoprenalin injection on the 9th and 10th day significantly increased the HR compared to that of the control group. Increased myocardial oxygen demand leads to ischaemic necrosis of the myocardium in rats. ISO+FLC produced a nonsignificant decrease in HR compared to that of ISO. After isoprenalin treatment, 24-h blood pressure measurement showed a non-significant decrease in MABP. FLC pretreatment attenuated the hypotensive effect of isoprenalin and tachycardia. Apart from haemodynamic parameters, several diagnostic marker enzymes like CK-MB isoenzyme and LDH present in the myocardium are used as predictor of pathological changes in the heart. These enzymes are released into the extracellular fluid during myocardial injury. In the isoprenalin group the significant increase in CK-MB indicated myocyte injury. A lesser increase in CK-MB after isoprenalin in the FLC-treated group indicated cardioprotective activity of FLC. Experimental data showed lowered activities of these enzymes in FLC-treated rats than in isoprenalin-treated rats, indicating protection against necrotic damage of the myocardial membrane. The lower LDH level in FLC-treated group, although is not significant, following isoprenalin insult, further supports the protective effect. Increase in the serum level of AST in the isoprenalin alone group compared to the control group indicates myocardial necrosis. FLC-treated rats had a lower level of AST, indicating cardioprotection. The activity of FLC also seems to preserve the structural and functional integrity of the myocardial membrane, as evident from the reduction in the elevated levels of these serum marker enzymes in rats pretreated with FLC when compared to the ISO alone group, establishing thus the cardioprotective effect of FLC. The antioxidant property of FLC as a scavenger of different free radicals, may be in part responsible for its cardioprotective effect. Histopathological finding of the FLC (500 mg/kg, p.o.) pre-treated myocardium showed reduction in necrosis and inflammation seen with isoproterenol treatment. FLC (500 mg/kg) treated normal rats showed only 0�30% cardiac necrotic architecture. These data further confirmed the cardioprotective action of oral administration of FLC. Protection from cardiotoxic effect of isoprenalin in FLC-pretreated animals was established by haemodynamic, biochemical, and histopathological results. The antioxidant effect appears to contribute to the cardioprotective effect of flax lignin concentrate in isoprenalin-induced cardiotoxicity. (Editors comments)
(Auhtors abstract)
Reactive oxygen species are known to play a major role of Ischaemic heart disease. Ischaemic tissue generates oxygen-derived free radicals and other reactive species which bring about oxidative damage of membrane lipids, proteins and carbohydrates leading to qualitative and quantitative alterations of the myocardium . Isoprenalin (ISO), a synthetic catecholamine and β-adrenergic agonist is documented to produce myocardial infarction due to generation of highly cytotoxic free radicals through its auto-oxidation.The pharmacologic effect of isoprenalin is believed to be associated with its β-adrenergic effect, which increases heart rate, decreases blood pressure and diminishes the oxygen supply to the myocardium. The objective of the present investigation was to study the effect of flax lignan concentrate (FLC) extracted from seeds of Linum usitatissimum on isoprenalin induced cardiotoxicity in Wistar rats. Following 10-day administration of FLC isoprenalin-induced tachycardia was reduced. Isoprenalin injection on the 9th and 10th day significantly increased the HR compared to that of the control group. Increased myocardial oxygen demand leads to ischaemic necrosis of the myocardium in rats. ISO+FLC produced a nonsignificant decrease in HR compared to that of ISO. After isoprenalin treatment, 24-h blood pressure measurement showed a non-significant decrease in MABP. FLC pretreatment attenuated the hypotensive effect of isoprenalin and tachycardia. Apart from haemodynamic parameters, several diagnostic marker enzymes like CK-MB isoenzyme and LDH present in the myocardium are used as predictor of pathological changes in the heart. These enzymes are released into the extracellular fluid during myocardial injury. In the isoprenalin group the significant increase in CK-MB indicated myocyte injury. A lesser increase in CK-MB after isoprenalin in the FLC-treated group indicated cardioprotective activity of FLC. Experimental data showed lowered activities of these enzymes in FLC-treated rats than in isoprenalin-treated rats, indicating protection against necrotic damage of the myocardial membrane. The lower LDH level in FLC-treated group, although is not significant, following isoprenalin insult, further supports the protective effect. Increase in the serum level of AST in the isoprenalin alone group compared to the control group indicates myocardial necrosis. FLC-treated rats had a lower level of AST, indicating cardioprotection. The activity of FLC also seems to preserve the structural and functional integrity of the myocardial membrane, as evident from the reduction in the elevated levels of these serum marker enzymes in rats pretreated with FLC when compared to the ISO alone group, establishing thus the cardioprotective effect of FLC. The antioxidant property of FLC as a scavenger of different free radicals, may be in part responsible for its cardioprotective effect. Histopathological finding of the FLC (500 mg/kg, p.o.) pre-treated myocardium showed reduction in necrosis and inflammation seen with isoproterenol treatment. FLC (500 mg/kg) treated normal rats showed only 0�30% cardiac necrotic architecture. These data further confirmed the cardioprotective action of oral administration of FLC. Protection from cardiotoxic effect of isoprenalin in FLC-pretreated animals was established by haemodynamic, biochemical, and histopathological results. The antioxidant effect appears to contribute to the cardioprotective effect of flax lignin concentrate in isoprenalin-induced cardiotoxicity. (Editors comments)
