C.Maheswari
RVS College of Pharmaceutical Sciences, India
Title: Combined Effect Of Orthosiphon Stamineus And Coccinia Grandis Leaf Extracts On Cyclosporine A Induced Chronic Progressive Renal Interstitial Fibrosis
Biography
Biography: C.Maheswari
Abstract
Interstitial fibrosis is characterized by destruction of renal tubules and interstitial capillaries as well as by the accumulation of extracellular matrix proteins. The severity of tubulointerstitial fibrosis has long been considered as a crucial determinant of progressive renal injury in both human and experimental glomerulonephritis. One of the major adverse effects of long term cyclosporine-A (CyA) administration is chronic nephrotoxicity. Cyclosporine-A (CyA)-induced chronic nephrotoxicity is characterized by renal dysfunction and interstitial fibrosis. Early and progressive renal macrophage influx, correlating with latter interstitial fibrotic areas, has been associated with CyA treatment. Nephrotoxicity is induced by 7.5 mg/kg per day of cyclosporine is injected for 21 days causes Renal Interstitial Fibrosis. Administration of Coccinia grandis (CG) and Orthosiphon stamineus (OS) methanolic leaf extracts protected renal tissues from nephrotoxic effects of Cyclosporine A as evidenced from reduced level of kidney biochemical parameters. Nephrotoxic effect of Cyclosporine A was decreased in the animals treated with methanol extracts of OS and CG (100mg/kg and 200 mg/kg) and lowest concentration fractions of OS and CG (10mg/kg) by reducing the levels of the kidney biochemical parameters. Lowest concentration (100 mg/kg) tested was the least effective whereas at highest concentration tested dose 200mg/kg the drug effectively inhibited Cyclosporine-A induced interstitial fibrosis. Fractions of highest concentrations of OS ( 20mg/kg ) and CG ( 20mg/kg ) produced significant activity against Cyclosporine-A induced interstitial fibrosis. Combined activity of methanol extracts of OS and CG and its combined fractions of highest concentrations produced excellent activity against Cyclosporine A induced interstitial fibrosis.