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目的:建立大鼠胃热证的病理模型。方法:采用辣椒汁加60度白酒灌胃两周,最后3 d夹尾激怒引发胃热证模型。观察每只大鼠体温、食量、饮水量、大小便性状并检测血浆中白细胞素8(IL-8)、白细胞素2(IL-2)、肿瘤坏死因子α(TNFα)、血栓烷(TXB2)和6-酮-前列腺素F1α(6-keto-PGF 1α)含量及胃的组织学变化。结果:两周后可见模型组大鼠体温体重减少,饮水量增加,食量减少,大便量减少等主要症状体征,血浆中IL-8,IL-2,TNFα,TXB2和6-keto-PGF 1α含量明显增加,胃粘膜弥漫性充血,炎性损伤等的胃热证的变化特征;左金丸治疗后,胃热证的生化和组织学检查等均有所改善。结论:该方法能成功地建立大鼠胃热证的病理模型。
Objective: To establish a pathological model of stomach heat syndrome in rats. Methods: Chili juice with 60 degrees of white wine gavage for two weeks, the last 3 d folder tail anger provoked stomach heat syndrome model. The body temperature, food intake, water intake, urine and stool traits of each rat were observed and the contents of IL-8, TXB2, TNFα, TXB2, And 6-keto-prostaglandin F1α (6-keto-PGF 1α) content and gastric histological changes. Results: After two weeks, the main symptoms and signs such as IL-8, IL-2, TNFα, TXB2 and 6-keto-PGF 1α in plasma were decreased in body weight, water intake, Markedly increased gastric mucosal diffuse hyperemia, inflammatory lesions such as stomach heat syndrome characteristics; Zuo Jin Wan treatment, stomach heat syndrome biochemical and histological examination were improved. Conclusion: This method can successfully establish the pathological model of stomach heat syndrome in rats.