Coompo Research Chemicals

Cycloart-23-ene-3,25-diol was tested for anti-inflammatory activity using the cyclooxygenase assays (COX-1 and COX-2), anti-cholinesterase activity using the microplate assay and investigated for potential mutagenic effects using the Ames test. In the cyclooxygenase assays, cycloart-23-ene-3,25-diol showed inhibitory activity against COX-2 (80%) at a concentration of 100 uM (IC50 was 40 uM). At the same concentration, the compound showed weak activity against COX-1 (56%) with an IC50 value of 97 uM. In the anti-cholinesterase test, the compound had a weak inhibitory effect against acetylcholinesterase (53%) when tested at a concentration of 0.4 mM. No potential mutagenic effects were observed in the Salmonella microsome assay (TA 98).

Cycloart-23-ene-3,25-diol has ability to protect vital organs from the toxic effects persuaded in diabetic conditions in streptozotocin- nicotinamide induced diabetic mice. Cycloart-23-ene-3,25-diol treated diabetic mice showed minimum neuronal degeneration, which confirmed their protective activity against streptozotocin induced toxicity. Further molecular and cellular level study should be performed to understand the exact mechanism of Cycloart-23-ene-3,25-diol which may lead to development of new antidiabetic agent.

Both glybenclamide and Cycloart-23-ene-3,25-diol increased serum and pancreatic insulin. Glycosylated haemoglobin, serum cholesterol, triglycerides, aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, globulin, bilirubin, lactate dehydrogenase, urea and uric acid were decreased significantly after Cycloart-23-ene-3,25-diol treatment. Cycloart-23-ene-3,25-diol treatment decreased liver malondialdehyde but increased superoxidase dismutase and reduced glutathione. Histologically, focal necrosis was observed in the diabetic mouse pancreata but was less obvious in treated groups. The mechanism of Cycloart-23-ene-3,25-diol appears to be due to increased pancreatic insulin secretion and antioxidant activity.