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The Role of SOCS1 in Tubulointerstitium Injury of Mice with Diabetes
Li Kejun1, Du Yunxia2, Feng Xiaojuan2, Zhang Wei2, Liu Qingjuan2*
1Department of Ophthalmology, People’s Hospital of Hebei Province, Shijiazhuang 050000, China;
2Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China
2Department of Pathology, Hebei Medical University, Shijiazhuang 050017, China
Abstract: The aim of this study is to investigate the role of SOCS1 on diabetic renal injury. The diabetic mice were induced by intraperitoneal injection of STZ at a dose of 150 mg/kg body weight. The mice of transfection group were received an injection of SOCS1 plasmid or empty vector every 7 days. At 12 weeks after STZ injection， specimens were collected to detect the blood glucose and 24 hours urine protein. RT-PCR analysis was used to detecte the expression of SOCS1， CK18 and α-SMA mRNA. Immunohistochemistry or Western blot analysis was used to determine the expression of SOCS1， CK18， α-SMA and FN. The expression of CD68 was detected by flow cytometry. The secretion level of IL-1β and TGF-β1 was detected by ELISA. The results suggested that overexpression of SOCS1 in kidney ameliorated excretion of urine protein and inhibited the expression of CD68， IL-1β， TGF-β1 and FN. In addition， SOCS1 overexpression increased the expression of CK18 and decreased the expression of α-SMA in tubular epithelial cells. All of the results indicated that overexpression of SOCS1 could reduce the inflammatory response and inhibit the tubular epithelial-mesenchymal transdifferentiation in renal tissue of diabetic mice and relieve renal tubular interstitial damage.
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