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Published on: April 25, 2017
Peucedani Radix ameliorates bladder overactivity induced by partial bladder outlet obstruction via Nos3-mediated
Liang Zhao1, Jiang Tan2, Qingtao Hou3
1Department of Urology, The people's Hospital of Yubei District of Chongqing, Chongqing, China.
Background:
Overactive bladder (OAB) is a prevalent global clinical challenge with limited effective treatments. This study aimed to investigate the therapeutic effects and underlying molecular mechanisms of Peucedani Radix (PR), the dried root of Peucedanum praeruptorum Dunn, on a rat model of overactive bladder (OAB) induced by partial bladder outlet obstruction (pBOO), and to clarify the functional roles of its active components.
Methods:
A pBOO-induced OAB rat model was established. Urodynamic assessments and histological analyses were conducted to evaluate bladder function and structure. Integrated transcriptomic and network pharmacological analyses were used to identify key pathways and targets. UPLC-MS analysis identified the principal active component of PR. Molecular docking, molecular dynamics simulations, cellular thermal shift assay (CETSA), drug affinity responsive target stability (DARTS) assays, and surface plasmon resonance (SPR) were performed to investigate compound-target interaction. Functional cellular experiments using human and rat bladder smooth muscle cells, including gene knockdown, were conducted to validate the mechanism.
Results:
PR significantly ameliorated bladder overactivity, detrusor hypercontractility, and the abnormal smooth muscle-to-collagen ratio in rats with pBOO. Integrated transcriptomic and network pharmacological analyses identified the cGMP-PKG signaling pathway as the core pathway and Nos3 as a potential key molecular target. Furthermore, PR was confirmed to upregulate Nos3 expression and activate the cGMP-PKG pathway. In addition, dl-praeruptorin A was identified as the principal bioactive component of PR, which directly binds to Nos3. Cellular experiments demonstrated that dl-praeruptorin A inhibited hydrostatic pressure-induced contraction of bladder smooth muscle cells via Nos3-mediated activation of the cGMP-PKG pathway, an effect abolished by Nos3 knockdown. Corresponding changes in intracellular nitric oxide levels, Nos3 expression, and cGMP-PKG pathway-related proteins were observed.
Conclusion:
PR alleviates pBOO-induced OAB through its active component dl-praeruptorin A, which directly targets Nos3 to activate the cGMP-PKG signaling pathway, ultimately promoting bladder smooth muscle relaxation. This study provides a promising therapeutic candidate and mechanistic evidence supporting the use of PR for OAB treatment.
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