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Ginsenoside Rb1 mitigates diabetes-induced erectile dysfunction in rats by reducing oxidative stress and modulating
Zong-Hai Liu1, Wei-Bo Chen1, Jian-Zheng Li2
1Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan 250021, China.
Asian Journal of Andrology
|August 5, 2025
Summary
Ginsenoside Rb1 (Rb1) shows promise for treating diabetes mellitus-related erectile dysfunction (DMED). This study found Rb1 improved erectile function in rats by reducing oxidative stress, inflammation, and fibrosis, while activating key cellular pathways.
Area of Science:
- Biomedical Science
- Pharmacology
- Urology
Background:
- Diabetes mellitus-related erectile dysfunction (DMED) is a prevalent complication with limited effective treatments.
- Oxidative stress, fibrosis, and apoptosis are key pathological mechanisms in DMED.
- Ginsenoside Rb1 (Rb1) possesses antioxidant properties and therapeutic potential for DMED.
Purpose of the Study:
- To evaluate the therapeutic efficacy of Rb1 in a rodent model of streptozotocin-induced DMED.
- To investigate the underlying mechanisms of Rb1's action on erectile function and penile tissue.
Main Methods:
- A streptozotocin-induced DMED rat model was established.
- Rats were treated with Rb1 via gavage for 8 weeks.
- Erectile function was assessed, and penile tissues were analyzed using western blot, qPCR, ELISA, immunofluorescence, TUNEL, and Masson's trichrome staining.
Main Results:
- Rb1 significantly improved erectile function in DMED rats.
- Rb1 treatment reduced corpus cavernosum fibrosis (collagen content) and increased smooth muscle content.
- Rb1 modulated inflammatory markers, enhanced antioxidant enzyme activity and nitric oxide (NO) levels, and decreased lipid peroxidation.
- Rb1 activated the PI3K/AKT/eNOS signaling pathway and inhibited apoptosis in penile tissues.
Conclusions:
- Ginsenoside Rb1 effectively ameliorates erectile dysfunction in a diabetic rodent model.
- Rb1 exerts its therapeutic effects by reducing oxidative stress, inflammation, and fibrosis, and inhibiting apoptosis.
- Activation of the PI3K/AKT/eNOS pathway is a key mechanism underlying Rb1's beneficial effects in DMED.

