OBJECTIVE:
To evaluate the vulnerability of gastric mucosa to ulceration in non-insulin-dependent diabetes mellitus (NIDDM) rats
vis-à-
vis the protective effects of the methanolic extract of
Pterocarpus marsupium
heartwood (PMS, an antidiabetic herbal plant).
MATERIAL AND METHODS:
NIDDM was produced in 5-day-old rat pups by administering streptozotocin (70 mg/kg, i.p). The animals showing blood glucose level > 140 mg/dl after 12 weeks of STZ administration were considered as NIDDM positive rats. The effective hypoglycemic dose of PMS (750 mg/kg/day, p.o.) for 6 days was studied for its gastric ulcer (GU) protective effects against cold restraint stress (CRS), aspirin (ASP), ethanol (EtOH) and pylorus ligation (PL)-induced GU both in normal (NR) and NIDDM rats. To ascertain the mechanism of action, the effects of NIDDM and that of PMS treatment in NIDDM rats on mucosal offensive acid-pepsin, free-radicals (LPO,NO) and defensive mucin secretion, cell shedding, cell proliferation, glycoproteins and antioxidant enzymes (SOD and CAT) were studied.
RESULTS:
PMS (750 mg/kg) decreased the blood sugar level both in NR and NIDDM rats. NIDDM rats exhibited an increased propensity to GU, induced by CRS, ASP, EtOH and PL. Though, PMS did not protect the NR rats against GU induced by the above methods it reversed their increased propensity in NIDDM rats. NIDDM PL-rats showed an increase in acid-pepsin secretion, cell shedding and decrease in mucin secretion and mucosal glycoproteins with little effect on cell proliferation. PMS treatment in NIDDM rats reversed the acid-pepsin secretion, enhanced mucin and mucosal glycoproteins and decreased cell shedding without any effect on cell proliferation. NIDDM-CRS rats showed a significant increase in LPO and NO and a decrease in SOD and CAT levels, which were, reversed by PMS treatment.
CONCLUSION:
NIDDM increased the propensity to GU by affecting both offensive (increased) and defensive (decreased) mucosal factors. Though PMS, a hypoglycemic agent, did not show any protection against ulceration induced by CRS, ASP, EtOH and PL in normal rats, it protected the mucosa against the same in NIDDM rats by affecting the above mucosal offensive and defensive factors.
