摘要
目的:观察灵芝多糖对甲氨蝶呤(MTX)造成的肠黏膜损伤的保护作用。方法:通过给小鼠连续2d、每天1次腹腔注射MTX模拟临床上化疗药物损伤肠黏膜屏障的模型,在注射MTX之前先给小鼠灌胃灵芝多糖7d,在最后一次注射MTX后的第3天取材。取空肠组织进行HE染色观察形态学变化,电镜观察超微结构的变化。取肠匀浆上清检测丙二醛(MDA)和总超氧化物歧化酶(T-SOD)活性变化。结果:MTX模型组的小肠绒毛变短、融合、隐窝细胞消失,杯状细胞减少。电镜结果表明肠上皮细胞的超微结构为微绒毛紊乱、变短,有些有缺失,核膜和线粒体肿胀。灵芝多糖治疗组小鼠的形态学变化比MTX模型组要轻。MTX模型组T-SOD活性降低,MDA增高。灵芝多糖给药组可以提高T-SOD活性,降低MDA含量。结论:灵芝多糖给药组可以改善MTX所致的小鼠肠道黏膜损伤。
AIM:To observe the protective effects of ganoderan on methotrexate (MTX)-induced intestinal damage in BALB/C mice.METHODS:The mouse model of intestinal damage was established by intraperitoneal injection of MTX once daily for two consecutive days,and this was to simulate clinical chemotherapy-induced intestinal injury.Intragastric administration of ganoderan was executed for 7 days before MTX injection,and the animals were sacrificed in 3 days after the last injection.The morphological and ultrastructural changes were observed to the jejunum segments by HE staining and electron microscope.The level of malondialdehyde(MDA)and the activity of total superoxide dismutase(T-SOD)were detected in intestinal homogenate supernatant.RESULTS:Compared with the normal group,the intestinal villus in the MTX group became shorter and fused,and the crypt cells were disappeared,the goblet cells were decreased.Ultrastructure showed that microvilli were irregularly arranged,variable short,and some were missing,and the nuclear membrane and mitochondria swelling.Morphological changes in the ganoderan group were smaller than those in MTX group.The T-SOD activity was decreased and the level of MDA was increased in MTX group,but the T-SOD activity was increased and the level of MDA was decreased in ganoderan group.CONCLUSION:The present study shows that ganoderan can protect the small intestine of mice from the MTX-induced damage.
出处
《中国临床药理学与治疗学》
CAS
CSCD
2009年第10期1110-1114,共5页
Chinese Journal of Clinical Pharmacology and Therapeutics