Abstract

Thymosin β4 (Tβ4) treatment was known to show the potential therapeutic effects on diabetic complications. This study was performed to determine if Tβ4 expression is changed in both serum and tissues under diabetic conditions and can be a serum biomarker. Type 1 diabetic mice were induced in C57/BL6J mice by intraperitoneal injection of streptozotocin (STZ) at a dose of 50 mg/kg body weight. The mice were sacrificed at 16 weeks after STZ injection. Tissues and plasmas were obtained to determine the expression levels of Tβ4 using ELISA, real time RT-PCR, and immunohistochemistry. The average serum glucose level was increased to approximately 400 mg/dL beginning 2 weeks after the five injections of STZ and lasting for at least 13 weeks until sacrifice. The plasma and tissue levels of Tβ4 in the age-matched control mice were not significantly different from those of the diabetic mice. In conclusion, the Tβ4 expression level in the plasmas and tissues of diabetic mice was not affected by diabetic conditions. It indirectly suggests that the therapeutic effect of Tβ4 on diabetic complications is due to its regenerative effects on damaged tissue but not to the changed expression level of Tβ4 in plasma and tissues of diabetes.

Highlights

  • Thymosin β4 (Tβ4), a 4.9 kDa peptide with 43 amino acids, has a number of active sites

  • Relative T 4 mRNA level Relative T 4 mRNA level Relative T 4 mRNA level (a). These results indirectly suggest that diabetic conditions such as hyperglycemia do not significantly affect the serum and tissue levels of Tβ4 in type 1 diabetic mice

  • The STZ-induced type 1 diabetic mice were under hyperglycemic conditions for at least 13 weeks because they were not treated with any blood glucose lowering agents and were sacrificed 16 weeks after the final injection of STZ

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Summary

Introduction

Thymosin β4 (Tβ4), a 4.9 kDa peptide with 43 amino acids, has a number of active sites. The Tβ4 containing amino acids 1-4 has anti-inflammatory activity, residues 1-15 have anti-apoptotic and cytoprotective activity, and residues 1723 affect cell migration, actin biding, dermal wound healing, angiogenesis, and hair growth [1]. It binds to G-actin to regulate the formation of F-actin, which in turn regulates the dynamics of cytoskeletal rearrangement [2], leading to effects on cell mobility, cell division, and differentiation. Tβ4 treatment has been used to alleviate the symptoms of various diseases of animal models.

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