Abstract:
OBJECTIVE To investigate the underlying mechanism of linarin on improving benign prostatic hyperplasia glandular fibrosis via observing its effects on inhibiting Hsa_circ_0001359 level and TGF-β1 expression.
METHODS Both the mice prostate hyperplasia model and human epithelial cell line proliferation model were established by testosterone. The glandular collagen deposition was evaluated by Masson and sirius red staining. The hydroxyproline content was detected using spectrophotometry. The expression of epithelial mesenchymal transition(EMT) markers were evaluated by immunohistochemical analysis. The levels of glandular EMT transcription factors and epithelial EMT markers mRNAs, as well as the Hsa_circ_0001359 were evaluated by real-time fluorescence quantitative PCR analysis. The expression of TGF-β1 was explored by Western blotting.
RESULTS At the animal level, compared with the normal control group, the model group mice showed prostate fibrosis, EMT characteristics, as well as significant higher content of hydroxyproline and mRNA level of TGF-β1(P<0.01). Compared with the model group, linarin inhibited glandular EMT and fibrosis, as well as significant reduced the content of hydroxyproline and mRNA level of TGF-β1(P<0.01). At the cellular level, 50 mg·L−1 linarin significantly inhibited testosterone-induced epithelial cell proliferation and EMT, reduced Hsa_circ_0001359 level and decreased TGF-β1 expression(P<0.01 or P<0.05).
CONCLUSION Linarin can attenuate prostatic fibrosis via inhibiting Hsa_circ_0001359/TGF-β1.
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