ArticleOxidative medicine and cellular longevity2019
Effect of Sulforaphane on Bladder Compliance in a Rat Model of Partial Bladder Outlet Obstruction.
Article in Oxidative medicine and cellular longevity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed, 5 citations in OpenAlex.
- Sulforaphane and bladder cancer: a potential novel antitumor compound.Frontiers in pharmacology · 2023Review
- Urinary exosomal vitronectin predicts vesicoureteral reflux in patients with neurogenic bladders and spinal cord injuries.Experimental and therapeutic medicine · 2022Article
- Bladder Hyperactivity Induced by Oxidative Stress and Bladder Ischemia: A Review of Treatment Strategies with Antioxidants.International journal of molecular sciences · 2021Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsTo investigate the effect of Nrf2 activator sulforaphane (SFN) on bladder compliance and the underlying mechanisms in a rat model of partial bladder outlet obstruction (BOO).
methodsMale 8-week-old Sprague-Dawley rats were divided into three groups. BOO rats were given daily 0.5 mg/kg sulforaphane (BOO+SFN) or vehicle (BOO) intraperitoneally for 4 weeks, while sham-operated rats were treated with vehicle (Sham). Bladder compliance, histological alteration, and collagen deposition were evaluated. The expression levels of collagen I, collagen III, MMP-1, and TIMP-1 were measured by immunohistochemistry and western blotting.
resultsBOO led to a significant decrease in bladder compliance. The change was partially restored by SFN treatment. The expression of MMP-1 was significantly decreased accompanying with increased TIMP-1 expression in BOO rats compared with that in Sham rats, which was ameliorated by SFN treatment. Moreover, the increased collagen I/collagen III ratio in the BOO group was reversed by SFN treatment.
conclusionsSulforaphane suppressed collagen deposition by regulating the MMP-1 and TIMP-1 expression and decreasing the collagen I/III expression ratio in BOO rats and improved bladder compliance.
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