论文部分内容阅读
为了拓展藤黄在中医临床的应用,研究其内服的毒性及炮制减毒的机制是必要的。通过巨噬细胞RAW264.7释放炎症介质(一氧化氮NO、肿瘤坏死因子TNF-α和白细胞介素IL-6)和灌胃给予藤黄生品和炮制品后大鼠胃和十二指肠组织的病理表现,判断其毒性作用;采用免疫组化和实时荧光定量PCR技术检测灌胃给药后,大鼠胃和十二指肠组织AQP3,AQP4蛋白和m RNA的表达,研究藤黄炮制减毒的机制。结果表明,藤黄生品可促进炎症介质NO,TNF-α和IL-6的释放,且与剂量呈相关性;藤黄制品组与生品组比较,NO和IL-6的释放量降低,TNF-α的释放量增加;藤黄生品可引起大鼠腹泻、白细胞升高、淋巴细胞降低,使胃黏膜充血水肿,肠黏膜坏死和炎细胞浸润,从多个角度证明内服生藤黄对胃和十二指肠组织的毒性为致炎毒性,致炎毒性与给药剂量呈相关性,炮制后藤黄的致炎毒性降低。在藤黄对胃和十二指肠组织致炎的同时,藤黄生品高剂量组大鼠胃和十二指肠组织水通道蛋白AQP3,AQP4 m RNA和蛋白表达量显著增加(P<0.05),相应剂量藤黄制品组大鼠AQP3,AQP4表达量较生藤黄组低,说明AQP3,AQP4蛋白和m RNA表达量的高低与藤黄的致炎作用强弱有一致性。通过降低AQP3,AQP4的表达水平可能是藤黄炮制减毒的作用机制之一。
In order to expand the clinical application of Garcinia Cambogia in traditional Chinese medicine, it is necessary to study its oral toxicity and the mechanism of attenuating it. After the release of inflammatory mediators (NO, TNF-α and IL-6) by macrophage RAW264.7 and gavage of rat ganhuang and duodenal tissues Pathological findings, to determine its toxic effects; using immunohistochemistry and real-time fluorescent quantitative PCR technology to detect gastric and duodenal AQP3, AQP4 protein and m RNA expression in rats after gavage administration study Garcinia cambogia processing attenuated Mechanisms. The results showed that Garcinia cambogiae could promote the release of NO, TNF-αand IL-6in the inflammatory mediators, and had a dose-dependent relationship. Compared with the control group, the release of NO and IL- α release increased; Garcinia cambogia products can cause diarrhea in rats, leukocytosis, lymphocyte reduction, congestion and edema of the gastric mucosa, intestinal mucosal necrosis and inflammatory cell infiltration, from a variety of perspectives that oral administration of Garcinia on the stomach and twelve Toxicity of nosocomial tissue was induced by inflammatory cytokines. The inflammatory cytotoxicity was related to the dose of ganciclovir. At the same time, the AQP3, AQP4 mRNA and protein expressions in the gastric and duodenal tissues of the high-dose group were significantly increased (P <0.05) while the inflammation of the stomach and duodenum was induced by Garcinia cambogia. Correspondingly, the expression of AQP3 and AQP4 was lower in the rat of Garcinia glutinosa group than that of the group, which indicated that the expression of AQP3, AQP4 protein and m RNA were consistent with that of Garcinia cambogia. By reducing the expression level of AQP3 and AQP4, it may be one of the mechanisms of attenuated treatment by Garcinia cambogia.