Intraperitoneal co-administration of thymosin alpha-1 ameliorates streptozotocin-induced pancreatic lesions and diabetes in C57BL/6 mice.
Intraperitoneal co-administration of thymosin alpha-1 ameliorates streptozotocin-induced pancreatic lesions and diabetes in C57BL/6 mice.
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DOI：
10.3892/ijmm_00000169
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发表时间：
2009-05
影响因子：
5.4
通讯作者：
Longxin Qiu;Cuilin Zhang;Jun Zhang;Jiaxin Liang;Jun Liu;Ci-Yu Ji;James Y. Yang
中科院分区：
文献类型：
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作者：
Longxin Qiu;Cuilin Zhang;Jun Zhang;Jiaxin Liang;Jun Liu;Ci-Yu Ji;James Y. Yang
我们研究了体内胸腺素α -1 （Talpha-1）对链脲佐菌素（STZ）诱导的胰腺病变和糖尿病的影响。将小鼠随机分为4个实验组：血糖控制正常组、STZ处理组、STZ + 0.1微克/公斤体重/天talpha -1处理组、STZ + 1微克/公斤体重/天talpha -1处理组。定期测定血糖，实验结束时用ELISA试剂盒测定血清胰岛素。采用乙醛品红染色对胰腺进行组织病理学检查。以胰腺丙二醛（MDA）水平、谷胱甘肽（GSH）含量、超氧化物歧化酶和过氧化氢酶活性为指标测定氧化应激参数。在开始Talpha-1治疗14天后，直到第35天停止治疗时，STZ和Talpha-1联合治疗的两组小鼠的血糖水平均显著低于STZ治疗但Talpha-1未治疗的小鼠，尽管两者仍高于正常血糖对照组。在talpha1治疗结束时，连续35天给予1微克/千克/天talpha1的stz治疗小鼠血清胰岛素水平是未给予talpha1治疗的stz -糖尿病小鼠的2倍（P<0.001），尽管没有完全恢复到正常水平。胰醛品红染色显示，STZ处理引起明显的胰腺炎，胰岛萎缩，胰腺β细胞数量明显减少。然而，1微克/千克/天的Talpha-1治疗35天后，这些组织学病变明显减轻。与未处理stz -糖尿病小鼠相比，1 μ g/kg/d处理stz -1诱导小鼠胰腺GSH水平是未处理stz -糖尿病小鼠的1.92倍（P<0.01），而胰腺MDA水平仅为未处理stz -糖尿病小鼠的81.9% （P<0.05）。综上所述，联合给予Talpha-1对stz诱导的胰腺损伤和糖尿病具有显著的保护作用，部分保护作用可能是通过增强胰腺抗氧化能力来实现的。
We investigated the effects of the in vivo administration of thymosin alpha-1 (Talpha-1) on streptozotocin (STZ)-induced pancreatic lesions and diabetes. Mice were randomly divided into four experimental groups: normoglycemic control, STZ-treated, STZ plus 0.1 microg/kg body weight/day Talpha-1-treated, and STZ plus 1 microg/kg/day Talpha-1-treated. Blood glucose was assayed periodically, and serum insulin was determined at the end of the experiment using the ELISA Kit. Aldehyde fuchsin staining was used for histopathological examination of the pancreas. Parameters for oxidative stress were measured with pancreatic malondialdehyde (MDA) level, glutathione (GSH) content and enzymatic activities of superoxide dismutase and catalase. Fourteen days after the initiation of Talpha-1 treatment and up to day 35 when the treatment was stopped, both of the two STZ and Talpha-1-co-treated mouse groups had significant lower levels of blood glucose than the STZ-treated but Talpha-1-untreated mice, although both remained higher than that of the normoglycemic controls. At the end of the Talpha-1 treatment, the serum insulin level for STZ-treated mice receiving 1 microg/kg/day Talpha-1 for 35 days was 2-fold (P<0.001) as much as that of the Talpha-1-untreated STZ-diabetic mice, although not completely restored to the normal level. Pancreatic aldehyde fuchsin staining showed that STZ treatment caused significant pancreatitis, islet atrophy, and a significant reduction in the number of pancreatic beta cells. These histological lesions, however, were significantly alleviated by 1 microg/kg/day Talpha-1 treatment for 35 days. Furthermore, compared with the Talpha-1- untreated STZ-diabetic mice, the pancreatic GSH level of the 1 microg/kg/day Talpha-1-treated STZ-induced mice was 1.92-fold that of the untreated STZ-induced mice (P<0.01), whereas the pancreatic MDA level was only 81.9% that of the untreated STZ-diabetic mice (P<0.05). Together these results demonstrate that co-administration of Talpha-1 leads to significant protection against STZ-induced pancreatic damage and diabetes, and part of the protection might be achieved through enhancing pancreatic antioxidative capability.