ABSTRACT
Atherosclerosis is complex disease and the underlying cause of heart attack, stroke and peripheral vascular disease. It is the main cause of morbidity and mortality worldwide, characterized by an excessive inflammatory, fibro fatty, proliferative response to damage of the artery wall. The present study was designed to evaluate the cardioprotective role of Justicia tranquebareinsis Linn. leaf extract on isoproterenol induced myocardial infarction in Wistar albino rats. The rats were divided into five groups of six animals each. Group I served as a normal control, Group II rats were administered isoproterenol (20mg/kg, s.c) at the end of experimental period on the29th and 30th days. Group III and IV were pretreated with Justicia tranquebareinsis Linn. leaf extract (100 mg/kg, 200mg/kg ,respectively) for a period of 28 days and received a subcutaneous injection of isoproterenol (20mg/kg, b.w)at the end of experimental period for 2 consecutive days. Group V received aqueous extract of Justicia tranquebariensis Linn 200mg/kg b.w for 28 days. After the experimental period, blood was collected and serum was separated and used for the estimation of protein, cholesterol, triglycerides, phospholipids, and lipoproteins and the assay of marker enzymes. The heart homogenate was used for the assay lipid profile. Isoproterenol induced rats showed significant increase in the levels of triglycerides, total cholesterol and phospholipids in both serum and heart homogenate. A rise in the levels of LDL, VLDL with significant decrease in the level of HDL was also observed in the serum of isoproterenol-intoxicated rats. Significant increase in the level of myocardial marker enzymes (CK, LDH, ALT and AST) in serum was noted. The LDH & CK levels were low in the heart tissue. Oral administration of aqueous leaf extract of Justicia tranquebariensis Linn. (100 and 200mg/kg) to isoproterenol-induced rats daily for a period of 28 days proved the protective role of the aqueous extract of Justicia tranquebariensis Linn. The levels of the biochemical parameters in the plant treated groups were nearly the same as that of the normal control.
ABSTRACT
The improper functioning of the antioxidant defense system of our body results in the damage of macromolecules such as DNA, protein and lipids. This forms the basis of pathology of various diseases. Antioxidants prevent the accumulation of the free radicals and protect the body from diseases. The present study was designed to assess the antioxidant potential of Musa paradisiaca L in acetaminophen induced damage. The experimental models were grouped into six groups comprising of six rats each. Group I served as normal control, Group II was induced with acetaminophen at a dose of 2g/kg BW as a single dose. Group III was induced with acetaminophen and orally administered aqueous extract of Musa paradisiaca L at a dose of 100mg/Kg BW for 15 days. Group IV was induced with acetaminophen and orally administered aqueous extract of Musa paradisiaca L at a dose of 200mg/Kg BW for 15 days. Group V received the aqueous extract of Musa paradisiaca L alone at a dose of 200mg/Kg BW for 15 days. Group VI was induced with acetaminophen and administered silymarin at a dose of 25mg/KgBW for 15 days. At the end of the experimental period the animals were sacrificed. Serum and hepatic tissue were used for the study. The following parameters were analysed in the hepatic tissue – Lipid peroxidation (LPO), Superoxide Dismutase (SOD), Reduced Glutathione(GSH) and protein. The serum protein level was also measured. The induction of hepatic damage with acetaminophen resulted in increased lipid peroxidation and reduced scavenging activity of the defense system of the body. On treatment with the aqueous extract of Musa paradisiaca L the antioxidant system was activated reducing the lipid peroxidation and accumulation of free radicals, thereby protecting the hepatic tissue from oxidative damage.