Abstract
Diabetic kidney disease (DKD) is an inflammatory disease caused by metabolic disorder. As an important signaling pathway in the inflammatory response, the JNK signaling pathway plays an crucial role in kidney injury in DKD. Vitamin D3 can reduce the inflammatory reaction and delay or even reverse DKD progression. Unfortunately, the mechanism by which vitamin D3 regulates DKD pathogenesis is unclear. This research established a DKD rat model and vitamin D3 and irbesartan were used as interventions. Then, urine and blood biochemistry; and inflammatory cytokine (IL-1 and IL-6), phosphorylated JNK pathway protein (MEK-4 and JNK1/2/3) and downstream factor (AP-1 and ATF-2) expression were assessed. We found that the DKD group showed body weight and insulin secretion were significantly decreased; significantly increased FPG, HOMA-IR and blood lipids; and significantly increased 24-h urinary protein (UPro) compared with normal group. Additionally, the levels of IL-1 and IL-6 and phosphorylated JNK pathway proteins were significantly elevated. These changes were improved by vitamin D3, especially at a low dosage. These results suggest that active vitamin D3 protects against DKD in rats by reducing IL-6 and IL-1 release, downregulating the JNK inflammatory signaling pathway, and inhibiting downstream transcription factor AP-1- and ATF-2-mediated kidney damage. This research provides a new theoretical support for vitamin D3 treatment of diabetic nephropathy.
Highlights
Diabetic kidney disease (DKD) is one of the most common and serious complications of diabetes
In order to evaluate the effects of vitamin D3 on body weight, blood glucose, insulin secretion, renal function (24-h urinary protein (UPro)), and blood lipids (TC, TG, and low-density lipoprotein cholesterol (LDL-c)) in DKD rats
The DKD model group showed significantly increased Fasting plasma glucose (FPG), Homeostatic Model Assessment of Insulin Resistance (HOMA-IR), total cholesterol (TC), TG and 24-h UPro (p
Summary
Diabetic kidney disease (DKD) is one of the most common and serious complications of diabetes. The number of diabetes patients worldwide will increase to 366 million, and the number of DKD patients will exceed 100 million by 2030. Glomerular hypertrophy, glomerulosclerosis and interstitial fibrosis caused by extracellular matrix protein deposition and progressive renal insufficiency are important characteristics of DKD. DKD may eventually cause end-stage renal disease (ESRD) [2,3,4,5]. With the increasing incidence of diabetes, DKD has become the main cause of ESRD worldwide [6,7,8]. Because of its high morbidity and mortality and because it severely impacts the quality of life of patients, ESRD has become a serious public-health issues
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