Effect of plantain banana on gastric ulceration in NIDDM rats: role of gastric mucosal glycoproteins, cell proliferation, antioxidants and free radicals.
Methanolic extract of Musa sapientum var. Paradisiaca (MSE, 100 mg/kg) was studied for its antiulcer and mucosal defensive factors in normal and non-insulin dependent diabetes mellitus (NIDDM) rats. NIDDM was induced by administering streptozotocin (STZ, 70 mg/kg, ip) to 5 days old rat pups. The animals showing blood glucose level >140mg/dL after 12 weeks of STZ administration were considered as NIDDM positive. Effects of MSE were compared with known ulcer protective drug, sucralfate (SFT, 500 mg/kg) and anti-diabetic drug glibenclamide (GLC, 0.6 mg/kg) when administered orally, once daily for 6 days against gastric ulcers (GU) induced by cold-restraint stress (CRS) and ethanol and subsequent changes in gastric mucosal glycoproteins, cell proliferation, free radicals (lipid peroxidation and nitric oxide) and anti-oxidants enzymes (super oxide dismutase and catalase) and glutathione (GSH) levels. MSE showed better ulcer protective effect in NIDDM rats compared with SFT and GLC in CRS-induced GU. NIDDM caused a significant decrease in gastric mucosal glycoprotein level without having any effect on cell proliferation. However, all the test drugs reversed the decrease in glycoprotein level in NIDDM rats, but cell proliferation was enhanced in case of MSE alone. Both CRS or NIDDM as such enhanced gastric mucosal LPO, NO and SOD, but decreased CAT levels while CRS plus NIDDM rats caused further increase in LPO and NO level without causing any further changes in SOD and CAT level. MSE pretreatment showed reversal in the levels of all the above parameters better than GLC. Ethanol caused a decrease in glutathione level which was further reduced in NIDDM-ethanol rats. MSE reversed the above changes significantly in both normal as well as in NIDDM rats, while GLC reversed it only in NIDDM rats. However, SFT was ineffective in reversing the changes induced by CRS or ethanol or when given in NIDDM-CRS or NIDDM-ethanol rats. The results indicated that the ulcer protective effect of MSE could be due to its predominant effect on mucosal glycoprotein, cell proliferation, free radicals and antioxidant systems.
Mohan Kumar
M
M
Department of Pharmacology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
Joshi
M C
MC
Prabha
T
T
Dorababu
M
M
Goel
R K
RK
D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D049109:Cell Proliferation; D003924:Diabetes Mellitus, Type 2; D005260:Female; D005609:Free Radicals / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism*; D008297:Male; D028521:Musa / Q000737:chemistry*; D010936:Plant Extracts / Q000737:chemistry / Q000627:therapeutic use; D051381:Rats; D013276:Stomach Ulcer / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology* / Q000517:prevention & control; D013311:Streptozocin / Q000494:pharmacology; D013392:Sucralfate / Q000627:therapeutic use
D000975:Antioxidants; D005609:Free Radicals; D006023:Glycoproteins; D010936:Plant Extracts; D013392:Sucralfate; D013311:Streptozocin; D005978:Glutathione