Akarca-Dizakar S O, Aktuğ H, Oltulu F, Öktem G, Yavaşoğlu A, Açikgöz E, Yiğittürk G, Demir K, Uysal A
a Department of Histology and Embryology , Gazi University Medical Faculty , Ankara , Turkey.
b Department of Histology and Embryology , Ege University Medical Faculty , İzmir , Turkey.
Biotech Histochem. 2018;93(5):328-335. doi: 10.1080/10520295.2018.1439532. Epub 2018 Apr 13.
Diabetes mellitus (DM) affects many organs including kidney. Tyrosine kinase can cause hypoglycemia and sunitinib is an inhibitor of tyrosine kinase. We investigated the possible effects of sunitinib on the kidney of streptozotocin (STZ) induced type 1 diabetic mice. We used 28 CD 1 type male mice divided into four groups of seven. Type 1 diabetes was induced by injection of STZ. Group 1 was the untreated control. Group 2 comprised non-diabetic mice + sunitinib. Both groups 1 and 2 exhibited normal blood glucose levels. Group 3 comprised STZ treated diabetic mice + saline. Group 4 were diabetic mice + sunitinib treatment. Kidneys were removed after 8 weeks. The immunoreactivities of vimentin, E-cadherin and S100 were assessed. Immunostaining of vimentin, E-cadherin and S100 was located in both the glomeruli and tubules of the kidney. We found that the number of vimentin and E-cadherin positive glomeruli and tubules were increased after sunitinib treatment compared to saline treated diabetic mice. The number of vimentin labeled tubules was decreased in the sunitinib treated group compared to diabetic + saline groups. Differences in the number of S100 positive tubules and glomeruli between groups 3 and 4 were not statistically significant. The effect of sunitinib on experimental diabetic mice appears to be related to levels of vimentin, E-cadherin and S100 in the glomeruli and tubules of the kidney, and sunitinib may protect against renal damage from DM.
糖尿病（DM）会影响包括肾脏在内的许多器官。酪氨酸激酶可导致低血糖，而舒尼替尼是一种酪氨酸激酶抑制剂。我们研究了舒尼替尼对链脲佐菌素（STZ）诱导的1型糖尿病小鼠肾脏的可能影响。我们使用了28只CD1型雄性小鼠，分为四组，每组7只。通过注射STZ诱导1型糖尿病。第1组为未治疗的对照组。第2组包括非糖尿病小鼠+舒尼替尼。第1组和第2组的血糖水平均正常。第3组包括经STZ治疗的糖尿病小鼠+生理盐水。第4组为糖尿病小鼠+舒尼替尼治疗。8周后取出肾脏。评估波形蛋白、E-钙黏蛋白和S100的免疫反应性。波形蛋白、E-钙黏蛋白和S100的免疫染色位于肾脏的肾小球和肾小管中。我们发现，与生理盐水治疗的糖尿病小鼠相比，舒尼替尼治疗后波形蛋白和E-钙黏蛋白阳性的肾小球和肾小管数量增加。与糖尿病+生理盐水组相比，舒尼替尼治疗组中波形蛋白标记的肾小管数量减少。第3组和第4组之间S100阳性肾小管和肾小球数量的差异无统计学意义。舒尼替尼对实验性糖尿病小鼠的作用似乎与肾脏肾小球和肾小管中波形蛋白、E-钙黏蛋白和S100的水平有关
