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Year : 2022  |  Volume : 18  |  Issue : 79  |  Page : 766-772

Schisandrin A ameliorates erectile dysfunction and regulates RhoA/ROCK1 pathway in rats with streptozotocin-induced type 1 diabetes

1 Department of Endocrinology, The Second Hospital of Hebei Medical University, Shijiazhuang, China
2 Department of Endocrinology, The Second Hospital of Shi Jiazhuang, Shijiazhuang, China
3 Department of Endocrinology, Tangshan Gongren Hospital, Tangshan, China

Correspondence Address:
Hao Yongmei
Department of Endocrinology, The Second Hospital of Hebei Medical University, No. 215, Heping West Road, Shijiazhuang - 050000, Hebei Province
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/pm.pm_454_21

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Introduction: Erectile dysfunction (ED) is a common complication of diabetes mellitus (DM) that severely affects the patient's quality of life. Schisandrin A, maybe a novel therapeutic option for patients with diabetes mellitus-induced erectile dysfunction (DIED). Materials and Methods: After induction by streptozotocin administration, rats were divided into four groups: Normal control (NC), DIED, low dosage (5 mg/kg/d), middle dosage (10 mg/kg/d), and high dosage (20 mg/kg/d) of schisandrin A treated DIED group. All groups were treated with normal saline or the relevant drug for 8 weeks. Body weight, erectile rate, intracavernosal pressure (ICP), mean arterial pressure (MAP), and serum glucose concentration were measured. The nitrate reductase method and nitric oxide synthase activity assay detected nitric oxide (NO) and endothelial nitric oxide synthase (eNOS) levels. Pulldown assay detected GTP-RhoA activity. Western blotting detected alpha-smooth muscle actin (α-SMA), transforming growth factor-β1 (TGF-β1), Collagen III, Collagen IV, RhoA, ROCK1, ROCK2, phospho-myosin phosphatase target subunit 1 (p-MYPT-1), MYPT-1, phospho-eNOS (p-eNOS), and eNOS expressions. Results: Compared with the NC group, schisandrin A alleviated the ED rate of DIED rats, and increased ICP and ICP/MAP in DIED + SA group. Schisandrin A increased NO level and activated p-eNOS in penile tissues of DIED group. The expression of α-SMA increased, whereas, TGF-β1, Collagen III, Collagen IV decreased in DIED + SA group compared to DIED group. Schisandrin A inhibited the levels of GTP-RhoA, RhoA, ROCK1, ROCK2, and p-MYPT1 in penile tissues from rats of DIED. Schisandrin A in the high dose group (20 mg/kg/d) had a better effective effect on DIED. Conclusion: Schisandrin A ameliorated erectile dysfunction in rats with DIED by promoting eNOS production, inhibiting fibrosis, and inhibiting the RhoA/ROCK1 pathway.

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