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目的:探讨链脲佐菌素(STZ)诱导的糖尿病树鼩胰岛β细胞再生与Bax、Bcl-2表达的关系。方法:将32只树鼩随机分为正常对照组和STZ处理组。根据血糖的变化将STZ处理组又分为4个亚组:血糖正常组(A组)、血糖先升高后恢复正常组(B组)、糖耐量减低组(C组)、糖尿病组(血糖≥11.1mmol/L,D组)。苏木精—伊红(HE)染色观察各组胰岛细胞形态、数量,免疫组织化学染色法检测各组树鼩胰腺胰岛素、胰腺十二指肠同源框蛋白1(Pdx-1)、神经元素蛋白3(Ngn3)、Bax、Bcl-2的表达。结果:与正常对照组相比,STZ处理组胰岛素、Pdx-1、Ngn3、Bcl-2蛋白表达量均明显降低(均P<0.05);A组、B组胰岛素、Pdx-1、Ngn3、Bcl-2表达均高于C组和D组,而Bax表达低于C组和D组(均P<0.05)。HE染色结果显示,B组胰岛细胞与正常对照组较为相似,数量较多,而D组胰岛细胞出现萎缩,数量显著减少。胰岛Pdx-1、Ngn3与Bcl-2蛋白表达呈正相关关系(r=0.830,r=0.803;均P<0.001),而与Bax蛋白表达呈负相关关系(r=-0.678,r=-0.643;均P<0.001)。结论:STZ诱导的糖尿病树鼩血糖恢复正常的机制可能是通过上调胰腺发育相关的转录因子Pdx-1、Ngn3的表达,同时调节Bcl-2和Bax的表达,使得胰岛β细胞数量及胰岛素分泌增加,从而实现胰岛再生,改善血糖代谢。
Objective: To investigate the relationship between streptozotocin (STZ) -induced pancreatic β-cell regeneration and the expression of Bax and Bcl-2 in diabetic tree gall. Methods: 32 trees were randomly divided into normal control group and STZ treatment group. According to the changes of blood glucose, STZ treatment group was divided into four subgroups: normal blood glucose group (group A), blood glucose first increased and returned to normal group (group B), impaired glucose tolerance group (group C), diabetes mellitus group (blood glucose ≥11.1mmol / L, group D). Hematoxylin-eosin (HE) staining was used to observe the morphology and quantity of islet cells in each group. The contents of insulin, pancreatic duodenal homeobox 1 (Pdx-1), neuronal Protein 3 (Ngn3), Bax, Bcl-2 expression. Results: Compared with normal control group, the expression of insulin, Pdx-1, Ngn3 and Bcl-2 protein in STZ group were significantly decreased (all P <0.05); the insulin, Pdx- -2 expression were higher than those in group C and group D, while the expression of Bax was lower than those in group C and group D (all P <0.05). The results of HE staining showed that the islet cells in group B were more similar to the normal control group, while the number of islet cells in group D was significantly reduced. The expressions of Pdx-1, Ngn3 and Bcl-2 were positively correlated (r = 0.830, r = 0.803; all P <0.001) All P <0.001). CONCLUSIONS: The mechanism of STZ-induced normalization of blood glucose in the tree may be through up-regulating the expression of pancreatic development-related transcription factors Pdx-1 and Ngn3 and simultaneously regulating the expression of Bcl-2 and Bax to increase the number of pancreatic β-cells and insulin secretion , In order to achieve islet regeneration, improve blood sugar metabolism.