Icariin and icariside II (ICA II), two active components isolated from herba epimedii, have a closely structural relationship.
There is evidence that icariin may be useful in the treatment of erectile dysfunction (ED), however, the study on the therapeutic efficacy of ICA II on ED is currently scant. We investigated the effects of ICA II on improving erectile function of rats with streptozocin induced diabetes. Fifty 8 week-old Sprague-Dawley rats were randomly distributed into normal control and diabetic groups. Diabetes was induced by a one-time intraperitoneal injection of streptozocin (60mg/kg). Three days later, the diabetic rats were randomly divided into 4 groups including a saline treated placebo arm and 3 ICA II-treated models (1, 5, 10mg/kg/d). After three-months, penile hemodynamics was measured by cavernous nerve electrostimulation (CNE) with real time intracorporal pressure assessment. Penises were harvested with subsequent histological examination (picrosirius red stain, Hart's elastin stain and immunohistochemical stain) and Western blots to explore the expression of the NO-cGMP and TGFβ1/Smad2 signaling pathways. Diabetes significantly attenuated erectile responses to CNE. Diabetic rats had decreased corpus cavernous smooth muscle/collagen ratio and endothelial cell content relative to the control group. The ratio of collagen I to II was significantly lower in the corpora of diabetic rats; furthermore cavernous elastic fibers were fragmented in the diabetic animals. The nNOS, eNOS, and VEGF were lower expressed in diabetic group; ICA II treated diabetic rats had higher expression in the penis relative to placebo treated diabetic animals. Both the TGFβ1/Smad2/CTGF signaling pathway and apoptosis were down-regulated in the penis from ICA II-treated rats. ICA II treatment attenuates diabetes-related impairment of penile hemodynamics, likely by increasing smooth muscle, endothelial function, and nNOS expression. ICA II could alter corpus cavernosum fibrous-muscular pathological structure in DM rats which could be regulated by the TGFβ1/Smad2/CTGF and NO-cGMP signaling pathways.
Written by:
Zhou F, Xin H, Liu T, Li GY, Gao ZZ, Liu J, Li WR, Cui WS, Bai GY, Park NC, Xin ZC. Are you the author?
Reference: J Androl. 2012 Mar 8. Epub ahead of print.
doi: 10.2164/jandrol.111.015172
PubMed Abstract
PMID: 22403279
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