ArticleNaunyn-Schmiedeberg's archives of pharmacology2017
Fasudil ameliorates endothelial dysfunction in streptozotocin-induced diabetic rats: a possible role of Rho kinase.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 17 citations in OpenAlex.
- Neoprzewaquinone A Inhibits Breast Cancer Cell Migration and Promotes Smooth Muscle Relaxation by Targeting PIM1 to Block ROCK2/STAT3 Pathway.International journal of molecular sciences · 2023Article
- RhoA/ROCK Signaling Is Involved in Pathological Retinal Neovascularization.Journal of vascular research · 2023Article
- Rho-kinase inhibition ameliorates non-alcoholic fatty liver disease in type 2 diabetic rats.Physiological research · 2022Article
- Sevoflurane and isoflurane inhibit KCl-induced, Rho kinase-mediated, and PI3K-participated vasoconstriction in aged diabetic rat aortas.BMC anesthesiology · 2021Article
- Targeting Small GTPases and Their Prenylation in Diabetes Mellitus.Journal of medicinal chemistry · 2021Review
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
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Abstract
Endothelial dysfunction is a major contributor to the pathogenesis of vascular disease in diabetes mellitus and RhoA/Rho-kinase (ROCK) system appears to play a crucial role in this setting. The present study was conducted to investigate the effect of the selective ROCK inhibitor, fasudil, on diabetes-related endothelial dysfunction and elucidated its underlying mechanism(s). Diabetes was induced by a single intraperitoneal injection of streptozotocin (STZ, 50 mg/kg), and fasudil (5 mg/kg per day) was orally administered for 8 weeks. Our results showed that fasudil administration attenuated the increased activity/expression of ROCK (627.5 ± 27 vs. 247.8 ± 19.1) and the NADPH oxidase subunits, NOX2 and p47phox, in diabetic rat aorta. Fasudil could reduce the elevated tumor necrosis factor (TNF)-α (70.2 ± 14.1 vs. 25.3 ± 5.2) and transforming growth factor (TGF-β) levels and restored the deficit in antioxidant level of the diabetic aorta. Additionally, fasudil markedly improved the endothelial dysfunction in the diabetic aorta (73.8 ± 8.1 vs. 47.42 ± 8.69) and corrected the dysregulated endothelial nitric oxide (eNOS) expression. In conclusion, the present study demonstrates that fasudil effectively ameliorates the endothelial dysfunction in STZ-induced diabetic rats through inhibition of the Rho/ROCK pathway and thereby reducing the TNF-α-mediated NADPH oxidase activation.
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