RESUMEN
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.