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Curcumin improves bladder dysfunction in diabetic rats by attenuating oxidative stress via the Keap1/NRF2/HO-1
Jun-Hao Zheng1, Dao-Feng Zhang1, Hao-Rui Li1
1Department of Urology, Shandong Provincial Hospital Affiliated to Shandong First Medical University, Jinan, China.
Background:
Diabetic bladder dysfunction (DBD) is a common urological complication of diabetes. Research suggests that oxidative stress (OS) is critically implicated in its development and progression. Curcumin (Cur), a natural polyphenol derived from turmeric, exhibits potent antioxidant properties and has been extensively investigated for treating OS-related disorders. Consequently, this study aims to explore the potential of Cur to mitigate DBD.
Methods:
In vitro, a high glucose (HG)-stimulated bladder smooth muscle cell (BSMC) model was established and treated with Cur. Cell viability was assessed by Cell Counting Kit-8 (CCK-8) assay. Intracellular reactive oxygen species (ROS) levels and the apoptosis rate were measured by flow cytometry. Protein expression was evaluated using Western blot (WB) and immunofluorescence. In vivo, rats were fed a high-fat and high-sugar diet and then induced into a diabetic rat model using streptozotocin. Subsequently, Cur was administered to these rats by oral gavage. Bladder function was assessed through urodynamic testing and histopathological examination. Protein expression in bladder tissue was analyzed by WB.
Results:
Cur demonstrated a protective effect against HG-induced injury in BSMC, enhancing cell viability and reducing ROS generation. It inhibited kelch-like ECH-associated protein 1 (Keap1) expression, thereby promoting the expression of nuclear factor erythroid 2-related factor 2 (NRF2) and its downstream effectors, heme oxygenase-1 (HO-1) and superoxide dismutase 1 (SOD1). Additionally, Cur decreased the apoptotic rate, suppressed the expression of B-cell lymphoma 2 (BCL-2)-associated X protein (BAX) and cysteine-aspartic acid protease 3 (caspase-3), and upregulated BCL-2. In diabetic rats, Cur ameliorated bladder dysfunction, as evidenced by reduced maximum micturition pressure and prolonged micturition intervals. Histological analyses revealed attenuated bladder tissue fibrosis and apoptosis, concomitant with suppressed Keap1 and elevated expression of NRF2, HO-1, and SOD1 in the bladder tissue.
Conclusions:
Cur alleviates OS and thereby ameliorates DBD in diabetic rats by regulating the Keap1/NRF2/HO-1 pathway, which highlights its therapeutic potential for DBD.