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IR-61 Improves Voiding Function via Mitochondrial Protection in Diabetic Rats.

Jianwu Wang1, Linyong Dai1, Xiaofeng Yue1

  • 1Department of Urology, The Third Affiliated Hospital (Gener Hospital) of Chongqing Medical University, Chongqing, China.

Frontiers in Pharmacology
|May 3, 2021
PubMed
Summary

IR-61, a novel dye, shows promise in treating diabetic bladder dysfunction (DBD). It protects bladder mitochondria from oxidative stress, improving voiding function in diabetic rats by activating the Nrf2 pathway.

Keywords:
IR-61bladder smooth muscle cellsdiabetic bladder dysfunctionmitochondrianuclear factor erythroid 2-related factor 2

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Area of Science:

  • Biomedical Science
  • Pharmacology
  • Cell Biology

Background:

  • Diabetic bladder dysfunction (DBD) affects nearly half of diabetic patients, with limited effective treatments.
  • Oxidative stress and mitochondrial damage in bladder smooth muscle cells (BSMCs) are key contributors to DBD.
  • Novel therapeutic strategies targeting oxidative stress are needed for DBD management.

Purpose of the Study:

  • To investigate the efficacy of IR-61, a novel heptamethine cyanine dye, in alleviating diabetic bladder dysfunction (DBD) in a rat model.
  • To determine the distribution and cellular localization of IR-61 in the bladder.
  • To elucidate the underlying mechanisms of IR-61's therapeutic effects, focusing on oxidative stress and mitochondrial protection.

Main Methods:

  • Diabetes was induced in rats using streptozotocin; IR-61 or vehicle was administered intraperitoneally.
  • Tissue distribution and subcellular localization of IR-61 were assessed using confocal fluorescence and NIR imaging.
  • Bladder function was evaluated using filling cystometry; histomorphometry, apoptosis assays, and protein expression analysis were performed.
  • Reactive oxygen species (ROS) levels, mitochondrial morphology, and Nrf2 pathway activation were examined.

Main Results:

  • IR-61 accumulated in the bladders of diabetic rats, primarily in mitochondria of BSMCs.
  • IR-61 significantly improved bladder function and mitigated pathological changes in diabetic rat bladders.
  • IR-61 reduced BSMC apoptosis, decreased levels of pro-apoptotic proteins, and lowered ROS production.
  • IR-61 preserved mitochondrial integrity and upregulated the Nrf2 antioxidant pathway in BSMCs.

Conclusions:

  • IR-61 effectively improves voiding function in a rat model of diabetic bladder dysfunction (DBD).
  • The therapeutic effects of IR-61 are attributed to the protection of BSMC mitochondria against oxidative stress.
  • Activation of the Nrf2 pathway appears to be a key mechanism underlying IR-61's beneficial actions in DBD.