Objective To explore the effect and significance of glycogen synthase kinase-3β (GSK-3β) in the regulation of osteoprotegerin-related signal pathway in renal tissue of rats with diabetic kidney disease (DKD).

Methods Forty-five Sprague-Dawley (SD) rats were randomly divided into a normal control grope (NC), a DKD model grope and a GSK-3β inhibitor (lithium chloride, LiCl) treatment group. For all the rats, 24-hour urine protein was determined with coomassie brilliant blue method. Kidney tissue sections were stained by hematoxylin-eosin for observing pathological changes in the renal tissues. The protein and mRNA expression of β-catenin and osteoprotegerin (OPG) in renal tissues were detected with reverse transcription quantitative real-time polymerase chain reaction (RT-qPCR) and immunohistochemistry method.

Results Compared with those in the NC group, significantly increased blood glucose (22.63 ± 2.08 mmol/L), 24-hour protein urine (154.17 ± 20.65 g), and obvious pathological changes in renal tissues were observed in the DKD model group. In comparison to those of the DKD model grope, the blood glucose (17.98 ± 1.09 mmol/L) and 24-hour protein urine (107.2 ± 31.15 g) decreased significantly and pathological changes in renal tissues alleviated in LiCl treatment group. Compared to those of the NC group, the expression of β-catenin in the rats′ renal cell cytoplasm (2.2 ± 0.31) of model group and LiCl treatment group (2.0 ± 0.20) were significantly higher (both P < 0.05). Compared with that of NC group, the expression of OPG/ receptor activator of nuclear factor-kappa B ligand (RANKL) mRNA (0.6 ± 0.06) in rats′ renal tissues of model group was decreased; whereas, the expression of OPG/RANKL mRNA (1.6 ± 0.12) in the rats′ renal tissues of the LiCl treatnet group increased significantly compared to that of the DKD model grope (P < 0.05)

Conclusion LiCl could reduce renal pathological changes and alleviate the progression of diabetic kidney disease in rats; the mechanism of the effects may be related to the regulation of the Wnt/β-catenin signaling pathway and the increase of OPG expression.