Nephroprotective effect of arjunolic acid on cytosolic lipids and mitochondrial enzymes against cyclosporine induced renal complications in rats



  • Vasanthi Palani

  • C. S. Parameswari

    Government Arts and Science College, Ramanathapuram



Root canal, Endodontic therapy, Surgical and non- surgical treatment


Cyclosporine (CsA) has considerably modified the graft survival in solid organ and bone marrow transplantations. Renal toxicity is the major adverse effect of chronic CsA administration. Deterioration of renal function and renal histopathology are the basic elements of the diagnosis. The present study aimed at investigating the protective effects of Arjunolic acid (10mg/kg body weight) against Cyclosporine (25mg/kg body weight) on the activities of TCA cycle enzymes – SDH (succinate dehydrogenase), MDH (malate dehydrogenase) Acotinase, Citrate synthase and examined the activities of respiratory chain complexes I, II, III, and IV. Mitochondrial enzymes of NADH DH, ICDH and ?KG DH activities in cytosol, Lysosomal enzymes of ?-Cathepsin, ?-Glucuronidase, ?-Galactosidase, ?-D-N-Acetyl Glucosaminidase in cytosol, lipids of Cholesterol, Triglycerides (TG), Free fatty acids (FFA), and phospholipids were estimated. Urea, Uric acid, and Creatinine were also estimated in 24hrs urinary sample. Results showed that CsA caused a marked decrease in the level of SDH, MDH, Acotinase, Citrate synthase, Respiratory chain complexes of I, II, III, IV, NADH DH, ICDH, ?KG DH, in the kidney mitochondrial tissue homogenate and also urea, uric acid and creatinine in urine sample. The lysosomal enzymes of ?-Cathepsin, ?-Glucuronidase, ?-Galactosidase, ?-D-N-Acetyl Glucosaminidase in cytosol, lipids of Cholesterol, Triglycerides (TG), Free fatty acids (FFA), and phospholipids were found to be increased in the cytosol of kidney tissue homogenates. But AA successfully prevented the alterations of these effects in the experimental animals. Our study demonstrated that AA could protect the mitochondrial kidney tissues against CsA induced oxidative stress probably by increasing antioxidative defense activities.


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How to Cite

Palani V, Parameswari CS. . Int J of Pharmc Res [Internet]. 2015Dec.5 [cited 2020Jul.5];5(11):276-87. Available from:


Vol. 5 No. 11 (2015): Nov


Research Articles

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