Research Paper Volume 11, Issue 22 pp 10409—10421
The anti-inflammation, anti-oxidative and anti-fibrosis properties of swertiamarin in cigarette smoke exposure-induced prostate dysfunction in rats
- 1 The Gerontology Research Center of Jianghan University, The Sixth Hospital of Wuhan (Affiliated Hospital of Jianghan University), Jianghan University, Wuhan, China
- 2 Medical College, Jianghan University, Wuhan, China
- 3 Department of Pharmacy, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
received: July 21, 2019 ; accepted: November 8, 2019 ; published: November 17, 2019 ;https://doi.org/10.18632/aging.102467
How to Cite
Copyright © 2019 Chen et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Chronic cigarette smoke (CS) exposure induces prostate deficits. We previously found that swertiamarin had prostatic protective potential. This study was to investigate the possible protective effect of swertiamarin against CS-induced prostate dysfunction on human prostate epithelial cells, stromal cells and rats. Rat prostate collagen deposition and fibrosis were assessed by sirius red staining and measuring hydroxyproline content, as well as by qPCR and western blot analysis for fibrotic extracellular matrix components. Prostatic levels of oxidative stress and inflammatory-related factors were also analyzed. In order to explore its underling mechanisms, the activities of Hedgehog signaling pathway and epithelial-mesenchymal transition of human prostate cells and rat prostate tissue were estimated. It was found that swertiamarin ameliorated CS-induced prostatic collagen deposition, relieved oxidative stress and local inflammation, inhibited the activation of Hedgehog signaling pathway and attenuated epithelial-mesenchymal transition. It indicated that swertiamarin could ameliorate CS-induced prostatic fibrosis by inhibiting epithelial-mesenchymal transition and Hedgehog pathway.
α-SMA: α-smooth muscle actin; BPH: benign prostatic hyperplasia; CAT: catalase; Col: collagen; COX: cyclooxygenase; CS: cigarette smoke; E-cad: E-cadherin; ECM: extracellular matrix; EMT: epithelial-mesenchymal transition; GLI: glioma-associated oncogene homolog; GPx: glutathione peroxidase; GSH/GSSG: reduced glutathione/oxidized glutathione; Hyp: hydroxyproline; IHH: indian hedgehog; IL: interleukin; iNOS: inducible nitric oxide synthase; MDA: malondialdehyde; QYD: Qing Ye Dan; RWPE-1: human prostate epithelial cells; SHH: sonic hedgehog; SMO: smoothened; SOD: superoxide dismutase; TAOC: total antioxidant capacity; TGF: transforming growth factor; TNF: tumor necrosis factor; T-SH: total sulfhydryl; Vim: vimentin; WPMY-1: human prostate stromal cells.