Slomiany B L, Piotrowski J, Ismail A, Klibaner M, Murty V L, Slomiany A
Research Center, New Jersey Dental School, University of Medicine and Dentistry of New Jersey, Newark 07013-2400.
Alcohol Clin Exp Res. 1991 Mar;15(2):196-204. doi: 10.1111/j.1530-0277.1991.tb01855.x.
The gastroprotective properties of GM1-ganglioside, an indigenous component of epithelial cell membrane, was investigated. The experiments were conducted with groups of rats with and without indomethacin pretreatment. The animals received intragastrically either a dose of GM1 as emulsion in 5% gum arabic or vehicle alone, followed by ethanol given at various time intervals up to 3 h after the GM1. The animals were sacrificed 30 min after the ethanol dose and their gastric mucosa subjected to macroscopic and histologic assessment, and physicochemical measurements. In the absence of GM1, ethanol caused extensive gastric hemorrhagic lesions which were significantly reduced by pretreatment with GM1 at dose as low as 70 micrograms/100 g body weight. Removal of sialic acid from GM1 led to the loss of gastroprotection. Furthermore, the effect of GM1 was not thwarted by indomethacin. The maximal protection was achieved 1 h following GM1 dose and this protective effect persisted at least 2.5 hr. The results of physicochemical measurements revealed that GM1 was capable of preventing the detrimental effect of indomethacin on the adherent mucus gel dimension, and on its content of sulfo- and sialomucins, protein, and phospholipids. The effects brought by GM1 were also accompanied by a significant (40-60%) increase in mucus gel viscosity, hydrogen ion retardation capacity (35-46%) and hydrophobicity (70-94%). The results indicate that the gastroprotective action of GM1 occurs through the enhancement of the physicochemical characteristics of the mucus layer, and does not appear to be mediated by endogenous prostaglandins.
对神经节苷脂GM1（上皮细胞膜的一种内源性成分）的胃保护特性进行了研究。实验在预先给予或未给予消炎痛的大鼠组中进行。动物经胃给予GM1乳剂（以5%阿拉伯胶配制）或仅给予赋形剂，随后在给予GM1后的不同时间间隔内直至3小时给予乙醇。在给予乙醇剂量30分钟后处死动物，对其胃黏膜进行大体和组织学评估以及物理化学测量。在没有GM1的情况下，乙醇导致广泛的胃出血性病变，而预先给予低至70微克/100克体重的GM1可显著减少这种病变。从GM1上去除唾液酸会导致胃保护作用丧失。此外，消炎痛不会削弱GM1的作用。在给予GM1剂量1小时后可达到最大保护作用，且这种保护作用至少持续2.5小时。物理化学测量结果表明，GM1能够防止消炎痛对附着黏液凝胶尺寸及其硫黏蛋白、唾液黏蛋白、蛋白质和磷脂含量的有害影响。GM1带来的这些作用还伴随着黏液凝胶黏度显著增加（40 - 60%）、氢离子阻滞能力增加（35 - 46%）和疏水性增加（70 - 94%）。结果表明，GM1的胃保护作用是通过增强黏液层的物理化学特性实现的，且似乎不是由内源性前列腺素介导的。
