Holmium laser enucleation of the prostate for the treatment of lower urinary tract symptoms in men with benign prostatic hyperplasia

Sathianathen, Niranjan; Hwang, Eu Chang; Brown, Sarah Jane; Borofsky, Michael S.; Dahm, Philipp

doi:10.1002/14651858.cd013291

Cited by 1 publication

(1 citation statement)

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“…Benign prostatic hyperplasia (BPH) is the condition of an enlarged prostate that is caused by accelerated proliferation of stromal and epithelial cells, but which does not induce tumor production [ 3 ]. Abnormal overgrowth of the prostate causes various histological changes, such as increased epithelial thickness and penetration of epithelial tissue into the lumen region, leading to urinary diseases such as lower urinary tract symptoms (LUTS), acute urinary retention (AUR), and bladder outlet obstruction (BOO) [ 4 ]. Most BPH patients are >50 years of age and are known to have lower quality of life due to BPH-induced symptoms such as urinary intermittency, incomplete emptying, weak stream, staining, urgency, and nocturia [ 5 ].…”

Section: Introductionmentioning

confidence: 99%

Ellagic acid improves benign prostate hyperplasia by regulating androgen signaling and STAT3

et al. 2022

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AbstractsBenign prostate hyperplasia (BPH) is an age-related disease in men characterized by the growth of prostate cells and hyperproliferation of prostate tissue. This condition is closely related to chronic inflammation. In this study, we highlight the therapeutic efficacy of ellagic acid (EA) for BPH by focusing on the AR signaling axis and STAT3. To investigate the effect of EA on BPH, we used EA, a phytochemical abundant in fruits and vegetables, to treat testosterone propionate (TP)-induced BPH rats and RWPE-1 human prostate epithelial cells. The EA treatment reduced prostate weight, prostate epithelial thickness, and serum DHT levels in the TP-induced BPH rat model. In addition, EA improved testicular injury by increasing antioxidant enzymes in testis of the BPH rats. EA reduced the protein levels of AR, 5AR2, and PSA. It also induced apoptosis by regulating Bax, Bcl_xL, cytochrome c, caspase 9, and caspase 3 with increasing mitochondrial dynamics. Furthermore, EA reduced the expression of IL-6, TNF-α, and NF-κB, as well as phosphorylation of STAT3 and IκBα. These findings were also confirmed in TP-treated RWPE-1 cells. Overall, our data provide evidence of the role of EA in improving BPH through inhibition of AR and the STAT3 pathway.

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Section: Introductionmentioning

confidence: 99%