Polypeptide-K from bitter melon (Momordica charantia) seeds attenuates carrageenan-induced inflammation in streptozotocin-diabetic Sprague-Dawley rats
TL;DR
Polypeptide-K (PPK) significantly suppressed NO and PGE2-associated pathways, reducing acute inflammatory reactions in diabetic rats using the paw edema model.
Abstract
Purpose: To investigate the anti-inflammatory activity of orally administered Polypeptide-K (PPK) in streptozotocin (STZ)-induced diabetic Sprague-Dawley rats using the paw edema model.Methods: A total of 42 male rats were randomly assigned into 7 groups (n = 6 each). Group 1 was the inflammation group; group 2 was induced with diabetes; groups 3, 4, 5, 6, and 7 were induced with diabetes and treated with distilled water, indomethacin (10 mg/kg), and PPK at 50, 150, and 300 mg/kg, respectively. A plethysmometer was used to measure paw volume every hour for 5 h. Three hours after intraperitoneal carrageenan induction, peritoneal exudate was analyzed for Evans blue extravasation, nitrite (NO surrogate), total cyclooxygenase (COX) activity, and prostaglandin E2 (PGE2) levels.Results: In the paw edema model, PPK at 300 mg/kg significantly reduced edema at 5 h, achieving 78 % inhibition compared to indomethacin (81 %). In the peritonitis model, 300 mg/kg PPK significantly reduced Evans blue leakage, nitrite, and PGE2 (p < 0.05), while COX activity showed no significant change.Conclusion: Polypeptide-K (PPK) significantly suppressed NO and PGE2-associated pathways, reducing acute inflammatory reactions in diabetic rats.