Low-Energy Extracorporeal Shock Wave Therapy Ameliorates Kidney Function in Diabetic Nephropathy

Abstract

Background. Diabetic nephropathy is the most common cause of end-stage renal disease. Traditional therapy for diabetic nephropathy has focused on supportive treatment, and there is no significant effective therapy. We investigated the effect of low-energy extracorporeal shock wave therapy on a diabetic nephropathy rat model. Methods. Streptozotocin-induced diabetic nephropathy rats were treated with six sessions of low-energy extracorporeal shock wave therapy (weekly for six consecutive weeks) or left untreated. We assessed urinary creatinine and albumin, glomerular volume, renal fibrosis, podocyte number, renal inflammation, oxidative stress, and tissue repair markers (SDF-1 and VEGF) six weeks after the completion of treatment. Results. The six-week low-energy extracorporeal shock wave therapy regimen decreased urinary albumin excretion as well as reduced glomerular hypertrophy and renal fibrosis in the rat model of diabetic nephropathy. Moreover, low-energy extracorporeal shock wave therapy increased podocyte number in diabetic nephropathy rats. This was likely primarily attributed to the fact that low-energy extracorporeal shock wave therapy reduced renal inflammation and oxidative stress as well as increased tissue repair potency and cell proliferation. Conclusions. Low-energy extracorporeal shock wave therapy preserved kidney function in diabetic nephropathy. Low-energy extracorporeal shock wave therapy may serve as a novel noninvasive and effective treatment of diabetic nephropathy.

Low-Energy Extracorporeal Shock Wave Ameliorates Streptozotocin Induced Diabetes and Promotes Pancreatic Beta Cells Regeneration in a Rat Model

“…This study showed that low-energy SW increased anti-inflammatory M2 macrophages. Low-energy SW is also reported to enhance anti-inflammatory M2 macrophage infiltration in a rat model of diabetic nephropathy [17] as well as acute myocardial infarction [24]. Low-energy SW might inhibit inflammation by polarizing pro-inflammatory M1 macrophages to anti-inflammatory M2 macrophages.…”

“…Low-energy SW might inhibit inflammation by polarizing pro-inflammatory M1 macrophages to anti-inflammatory M2 macrophages. Low-energy SW has an anti-inflammatory effect against various diseases [17,29,33].…”

“…This study demonstrated that low-energy SW significantly reduced apoptosis markers cleaved-caspase 3, and TUNEL but enhanced beta cells marker Nkx6.1, cell proliferation marker PCNA, tissue repair marker SDF-1 and GLP-1, which may contribute to increase beta cells regeneration potency. Interestingly, our previous study also demonstrated that low-energy SW can enhance podocyte regeneration [17] and activate axonal regeneration [21].…”

“…It is a single pressure pulse with a short needle-like positive spike and followed by a tensile part of several microseconds at a lower amplitude [14,15]. A low-energy extracorporeal shock wave (SW) exerts its effects through other mechanisms, such as increased angiogenesis [16], increased cell proliferation [17], anti-inflammation [17,18,19,20], inhibition of oxidative stress [17,20], anti-apoptotic [17], enhanced podocyte regeneration [17], activating axonal regeneration [21], improved nerve regeneration [22,23], and enhanced tissue repair [17]. Low-energy SW might inhibit inflammation by polarizing M1 macrophages to M2 macrophages [17,24].…”

Sitagliptin ameliorates renal tubular injury in diabetic kidney disease via STAT3‐dependent mitochondrial homeostasis through SDF‐1α/CXCR4 pathway

“…In addition, several studies have shown that DPP4 inhibitors improve oxidative stress and protect against mitochondrial membrane depolarization in diabetic patients and diabetic rats 23,24 . Other studies suggest that DPP4 inhibition contributes to diabetic kidney protection partly through SDF‐1α‐dependent antioxidative and antifibrotic effects and through the amelioration of adverse renal hemodynamic 25,26 . Conversely, blockade of SDF‐1α/CXCR4 signaling with the antagonist AMD3100 in diabetic mice accelerates renal functional deterioration and aggravates glomerular hypertension 25 .…”