Low-Intensity Extracorporeal Shock Wave Therapy Alleviates Detrusor Muscle Apoptosis and Extracellular Matrix Dysregulation in the Bladder of Diabetic Rats

TL;DR

Low-intensity shock wave therapy helps reverse bladder damage in diabetic rats by reducing muscle cell death and fibrosis.

Contribution

This study reveals the molecular mechanisms by which Li-ESWT improves diabetic bladder dysfunction in rats.

Findings

Li-ESWT reduces muscle atrophy, apoptosis, and fibrosis in diabetic rat bladders.

Li-ESWT restores α-smooth muscle actin expression and lowers cleaved caspase-3, TGF-β1, and collagen I levels.

Li-ESWT shows potential to reverse structural and functional bladder abnormalities in diabetes.

Abstract

Diabetic bladder dysfunction (DBD) affects 80% of diabetic patients, especially women. Yet, the management of DBD remains inconclusive. Building on our previous findings in animal models, low-intensity extracorporeal shock wave therapy (Li-ESWT) seems to be a promising potential therapy for DBD. However, the molecular mechanisms underlying the therapeutic effect of Li-ESWT on DBD still need to be clarified. To elucidate the molecular pathways involved in the therapeutic effect of Li-ESWT on DBD, a diabetic rat model was established using a high-fat diet in combination with streptozotocin (STZ) induction. Female Sprague-Dawley rats were randomly assigned to three groups: control, diabetes mellitus (DM), and DM treated with Li-ESWT for four weeks. To induce diabetes, the rats received a high-fat diet followed by two intraperitoneal injections of STZ (30 mg/kg), administered one week apart. Li-ESWT was delivered once weekly for four weeks, using an energy flux density of 0.03 mJ/mm², 500 shocks per session, at a frequency of 3 Hz. Our findings indicate that Li-ESWT significantly ameliorates pathological bladder changes, including muscle atrophy, apoptosis, and fibrosis, in diabetic rats. The expression of α-smooth muscle actin, a key component of the smooth muscle cytoskeleton, was markedly reduced in diabetic bladders but was partially restored following Li-ESWT treatment. Additionally, elevated levels of cleaved caspase-3, transforming growth factor-β1, and collagen I observed in diabetic bladders were attenuated by Li-ESWT. In summary, Li-ESWT exerts restorative effects on the detrusor smooth muscle, suggesting its potential to reverse structural and functional abnormalities in diabetic bladder dysfunction.

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