Mohan Kumar M, Joshi M C, Prabha T, Dorababu M, Goel R K
Department of Pharmacology, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India.
Indian J Exp Biol. 2006 Apr;44(4):292-9.
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.
研究了香蕉（Musa sapientum var. Paradisiaca）甲醇提取物（MSE，100毫克/千克）对正常和非胰岛素依赖型糖尿病（NIDDM）大鼠的抗溃疡作用及黏膜防御因子。通过给5日龄大鼠幼崽腹腔注射链脲佐菌素（STZ，70毫克/千克）诱导NIDDM。在给予STZ 12周后，血糖水平>140毫克/分升的动物被视为NIDDM阳性。将MSE的作用与已知的溃疡保护药物硫糖铝（SFT，500毫克/千克）和抗糖尿病药物格列本脲（GLC，0.6毫克/千克）进行比较，它们均口服给药，每日一次，连续6天，用于对抗由冷束缚应激（CRS）和乙醇诱导的胃溃疡（GU），并观察随后胃黏膜糖蛋白、细胞增殖、自由基（脂质过氧化和一氧化氮）、抗氧化酶（超氧化物歧化酶和过氧化氢酶）以及谷胱甘肽（GSH）水平的变化。在CRS诱导的GU中，与SFT和GLC相比，MSE在NIDDM大鼠中显示出更好的溃疡保护作用。NIDDM导致胃黏膜糖蛋白水平显著降低，而对细胞增殖无影响。然而，所有受试药物都能逆转NIDDM大鼠中糖蛋白水平的降低，但仅MSE能增强细胞增殖。单独的CRS或NIDDM都会增加胃黏膜脂质过氧化（LPO）、一氧化氮（NO）和超氧化物歧化酶（SOD）水平，但会降低过氧化氢酶（CAT）水平，而CRS加NIDDM大鼠会使LPO和NO水平进一步升高，而SOD和CAT水平无进一步变化。MSE预处理比GLC更能逆转上述所有参数的水平变化。乙醇会导致谷胱甘肽水平降低，在NIDDM - 乙醇大鼠中会进一步降低。MSE在正常大鼠和NIDDM大鼠中均能显著逆转上述变化，而GLC仅能在NIDDM大鼠中逆转。然而，SFT在逆转CRS或乙醇诱导的变化或在NIDDM - CRS或NIDDM - 乙醇大鼠中给药时无效。结果表明，MSE的溃疡保护作用可能归因于其对黏膜糖蛋白、细胞增殖、自由基和抗氧化系统的主要作用。
