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Related Experiment Video

Updated: Jan 1, 2026

Author Spotlight: Network Pharmacology and Molecular Docking to Decipher the Action of Jiawei Shengjiang San Against Diabetic Kidney Disease
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Sulforaphane improves voiding function via the preserving mitochondrial function in diabetic rats.

Chia-Fa Lin1, Tsung-Hung Chueh1, Cheng-Hsun Chung1

  • 1School of Life Science, National Taiwan Normal University, Taipei, 11677, Taiwan.

Journal of the Formosan Medical Association = Taiwan Yi Zhi
|December 16, 2019
PubMed
Summary

Sulforaphane, an Nrf-2 activator, ameliorates diabetes-induced voiding dysfunction by reducing oxidative stress, endoplasmic reticulum stress, and apoptosis in the bladder. This antioxidant treatment improves bladder function in diabetic models.

Keywords:
Diabetic bladderMitochondriaNF-E2-related nuclear factor erythroid-2Voiding function

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Urology

Background:

  • Hyperglycemia in diabetes mellitus (DM) causes oxidative stress, leading to bladder dysfunction.
  • The antioxidant sulforaphane, a nuclear factor erythroid-2 (Nrf-2) activator, was investigated for its potential to mitigate DM-induced bladder issues.

Purpose of the Study:

  • To determine if sulforaphane can ameliorate oxidative stress and improve bladder function in a diabetic model.
  • To investigate the molecular mechanisms underlying sulforaphane's effects on the Nrf-2/HO-1 pathway, mitochondrial function, endoplasmic reticulum stress, and apoptosis.

Main Methods:

  • Diabetes mellitus was induced using streptozotocin, with sulforaphane administered prior to induction.
  • Key markers including reactive oxygen species (ROS), mitochondrial function (Bax, cytochrome c), Nrf-2/HO-1 antioxidant pathway, endoplasmic reticulum stress (ATF-6/CHOP), and apoptosis (caspase 3/PARP) were assessed.

Main Results:

  • Diabetic bladders showed increased ROS, impaired mitochondrial function, elevated endoplasmic reticulum stress, and apoptosis, resulting in voiding dysfunction.
  • Sulforaphane treatment significantly increased Nrf-2/HO-1 expression, reduced ROS, protected mitochondria, decreased endoplasmic reticulum stress and apoptosis, and improved voiding function.

Conclusions:

  • Sulforaphane activates the Nrf-2/HO-1 pathway, preserving mitochondrial function and suppressing oxidative stress, endoplasmic reticulum stress, and apoptosis.
  • These effects collectively ameliorate diabetes-induced voiding dysfunction, highlighting sulforaphane's therapeutic potential.