Data on Prostatic Hyperplasia Reported by Researchers at Pusan National University (6-Sialyllactose Ameliorates Dihydrotestosterone-induced Benign Prostatic Hyperplasia through Suppressing VEGF-mediated Angiogenesis)
2019 AUG 15 (NewsRx) -- By a News Reporter-Staff News Editor at Angiogenesis Daily -- Current study results on Urogenital Diseases and Conditions - Prostatic Hyperplasia have been published. According to news reporting out of Yangsan, South Korea, by NewsRx editors, research stated, “Benign prostatic hyperplasia (BPH), a common disease in elderly males, is accompanied by non-malignant growth of prostate tissues, subsequently causing hypoxia and angiogenesis. Although VEGF-related angiogenesis is one of the therapeutic targets of prostate cancer, there is no previous study targeting angiogenesis for treatment of BPH.”
Our news journalists obtained a quote from the research from Pusan National University, “Dihydrotestosterone (DHT)-induced expressions of vascular endothelial growth factor (VEGF) in prostate epithelial RWPE-1 cells and human umbilical vascular endothelial cells (HUVECs). Conditioned media (CM) from DHT-treated RWPE-1 cells were transferred to HUVECs. Then, 6SL inhibited proliferation, VEGFR-2 activation, and tube formation of HUVECs transferred with CM from DHT-treated RWPE-1 cells. In the rat BPH model, 6SL reduced prostate weight, size, and thickness of the prostate tissue. Formation of vessels in prostatic tissues were also reduced with 6SL treatment. We found that 6SL has an ameliorative effect on in vitro and in vivo the BPH model via inhibition of VEGFR-2 activation and subsequent angiogenesis.”
According to the news editors, the research concluded: “These results suggest that 6SL might be a candidate for development of novel BPH drugs.”
For more information on this research see: 6-Sialyllactose Ameliorates Dihydrotestosterone-induced Benign Prostatic Hyperplasia through Suppressing VEGF-mediated Angiogenesis. Bmb Reports, 2019;():.
Our news journalists report that additional information may be obtained by contacting K.T. Ha, Dept. of Korean Medical Science, School of Korean Medicine and Korean Medical Research Center for Healthy Aging, Pusan National University, Yangsan, Gyeongsangnam-do 50612, South Korea. Additional authors for this research include B.R. Jin, T.W. Chung, S.J. Bae, H. Park, D. Ryu, L. Jin, H.J. An and K.T Ha.
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