Американское общество гирудотерапии

Hirudin-based treatment of diabetes-induced erectile dysfunction through inhibition of the HIF-1α to regulate RhoA/ROCK signaling pathway

Mechanism study published in American Journal of Men's Health (2025)

Последнее обновление: June 18, 2026Рецензент: ASH Editorial Board
Research article — evidence reviewArticle reference
Evidence: Preclinical (animal)Разработка лекарственных препаратовФармакология секрета слюнных желёзSun L et al. · American journal of men's health, 2025

Abstract

Diabetes-induced erectile dysfunction (DIED) is a type of refractory erectile dysfunction which can be clinically treated using the traditional Chinese medicine leech whose main ingredient is hirudin. Oxidative stress can damage vascular endothelial cells, affect blood circulation, and induce fibrosis of smooth muscle cells. This study assessed the efficacy of hirudin in treating DIED before exploring its potential mechanism of action. DIED was induced in rats using streptozotocin, while experimental apomorphine was used to screen for erectile dysfunction models. The rats were then divided into four groups: a blank control group (NC group), a model group (M group), a hirudin group (H group), and an inhibitor group (YC group). After 2 weeks, the serum levels of malondialdehyde (MDA), superoxide dismutase (SOD), and nitric oxide (NO) were determined. The histological features and HIF-1α/RhoA/ROCK signaling pathway-related proteins of the penile corpus cavernosum were detected. Erectile function improved in the H and YC groups without significantly affecting body weight and blood glucose levels, with histopathological analysis also showing improvement in penile structure in these groups. In addition, the expression of HIF-1α/RhoA/ROCK signaling pathway-related proteins was lower in the penile cavernous tissue of rats in the H and YC groups (p < .05), with the serum levels of NO and SOD also being higher in these groups (p < .05). The serum level of MDA decreased in the YC and H groups (p < .05). In this study, only animal experiments were conducted to investigate the regulation of Rho/ROCK pathway by HIF-1α. Cellular studies of the underlying mechanisms are lacking.

Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.

Publication typeJournal ArticleResearch Support, Non-U.S. Gov't
Indexed MeSH termsAnimalsMaleErectile DysfunctionRatsSignal TransductionHypoxia-Inducible Factor 1, alpha Subunitrho-Associated KinasesDiabetes Mellitus, ExperimentalHirudinsRats, Sprague-DawleyDisease Models, AnimalPenis

Резюме

Hirudin improves erectile function in diabetic rat model via HIF-1α inhibition and RhoA/ROCK pathway modulation — extends leech-hirudin pharmacology into urology/andrology.

Почему это важно для гирудотерапии

This study examined hirudin's efficacy and mechanism in diabetes-induced erectile dysfunction (DIED) using a streptozotocin-induced rat model, finding improved erectile function, reduced oxidative stress markers (lower MDA, higher SOD and NO), improved penile histology, and downregulation of the HIF-1α/RhoA/ROCK signaling pathway after two weeks of treatment. The rationale connects to traditional Chinese medicinal use of leeches whose main ingredient is hirudin. For ASH's domain, this is relevant as an animal study of a leech-derived bioactive compound. However, it is strictly preclinical (rats only), with no cellular studies of the underlying mechanism and no human data; clinical relevance to hirudotherapy remains unestablished.

Цитирование

Hirudin-based treatment of diabetes-induced erectile dysfunction through inhibition of the HIF-1α to regulate RhoA/ROCK signaling pathway.

Sun L et al. · American journal of men's health, 2025

Связанный клинический контекст

Добавлено в библиотеку ASH: May 27, 2026 · Последнее обновление сайта: June 18, 2026

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