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目的:研究蝙蝠蛾拟青霉人工发酵虫草菌丝(Paecilomyces Hepiali Chen,PHC)对链佐霉素(Streptozotocin,STZ)所致大鼠1型糖尿病(Insulin dependent diabetes mellitus,IDDM)的防治作用。方法:一次性腹腔注射50 mg·kg-1 STZ溶液,建立大鼠IDDM模型。阳性对照组和预防组造模24 h前分别灌胃给予盐酸二甲双胍溶液和PHC,连续给药28 d;治疗组造模7 d后灌胃给予PHC,连续给药21 d。以大鼠饮水量、体重以及血糖值为观察指标,28 d后取胰腺组织HE染色,取血清进行SOD值检测。结果:PHC预防给药第7 d开始,IDDM大鼠的高血糖、多饮和体重减轻情况明显改善,28 d后测得血清SOD活力显著升高;胰腺病理形态学观察可见胰岛基本无炎性细胞浸润。治疗组IDDM大鼠高血糖症状无明显改善,但血清SOD活力升高。胰腺腺泡间有以淋巴细胞为主的炎性细胞,胰岛周围见数个淋巴细胞、单核细胞。结论:PHC预防给药对STZ所致大鼠IDDM有明显降低血糖作用,推测其降糖机制主要与其防止炎症细胞浸润,保护胰岛细胞免受损伤有关,与其清除自由基作用无明显相关性。
Objective: To study the preventive and therapeutic effect of Paecilomyces Hepiali Chen (PHC) against the development of type 1 diabetes mellitus (IDDM) induced by streptozotocin (STZ) in rats. METHODS: The rat IDDM model was established by intraperitoneal injection of 50 mg·kg-1 STZ solution. In the positive control group and the prevention group, the metformin hydrochloride solution and PHC were administered by gavage 24 hours before the model was established. The treatment group was given intragastric administration of PHC for 7 days after the model was established and continued for 21 days. The rats drinking water, body weight and blood glucose were used as observation indexes. 28 days later, pancreatic tissue was stained with HE and serum was taken for SOD detection. RESULTS: On the 7th day after prophylactic administration of PHC, the hyperglycemia, polydipsia, and weight loss of IDDM rats were significantly improved. The serum SOD activity was significantly increased after 28 days. The pathological changes of pancreas showed that the islets were almost noninflammation. Cell infiltration. The hyperglycemic symptoms of IDDM rats in the treatment group did not improve significantly, but the serum SOD activity increased. Between the pancreatic acinar cells are mainly inflammatory cells with lymphocytes, and several lymphocytes and monocytes are seen around the islets. Conclusion: PHC prophylactic administration can significantly reduce blood glucose in rats with IDDM induced by STZ. It is speculated that the mechanism of hypoglycemic is mainly related to preventing inflammatory cell infiltration and protecting islet cells from injury, and there is no obvious correlation with its effect of scavenging free radicals.