Cilostazol protects vessels against hyperglycemic injury and accelerates healing after implantation of drug-eluting stent in a type 1 diabetes mellitus rat aorta stent model

Kwon, Jin-Sook; Kim, Yong Sook; Cho, Hyang Hee; Kee, Hae Jin; Hong, Moon Hwa; Kang, Won Yu; Jeong, Hyun‐Ja; Jeong, Myung Ho; Ahn, Youngkeun

doi:10.1016/j.atherosclerosis.2013.03.008

Cited by 6 publications

(3 citation statements)

References 24 publications

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“…It was reported that diabetes for 4 weeks increases apoptotic cell death in the tunica media of rat aorta. Severe and permanent hyperglycaemia can cause severe damage to the aortic wall (17). …”

Section: Discussionmentioning

confidence: 99%

“…It has been reported that insulin protects vascular smooth muscle cells from apoptosis in vitro (15) and that decreased insulin activity increases smooth muscle cell death in the arteries and can cause the formation of unstable plaque associated with diabetes (16). Diabetes has also been shown to cause apoptosis of vascular smooth muscle cells (17). …”

Section: Introductionmentioning

confidence: 99%

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Rheumatic involvement of the cleft mitral valve

Uygur¹

2016

Anatol J Cardiol

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Rheumatic involvement of the cleft mitral valve

Uygur¹

2016

Anatol J Cardiol

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“…It reportedly has no detectable effects on blood glucose levels but has been shown to be beneficial for modulating motor deterioration in patients with diabetes to a certain extent [ 10 , 11 , 12 ]. In other DM experimental models, cilostazol demonstrated the ability to reduce inflammatory burden and oxidative stress as well as protect cardiac vessels against hyperglycemia-induced injuries [ 10 , 11 , 13 , 14 , 15 , 16 ]. In vitro and in vivo studies have also shown the beneficial effects of the medication in reducing endothelial dysfunction and improving peripheral blood flow [ 10 , 17 , 18 , 19 ].…”

Section: Introductionmentioning

confidence: 99%

Peripheral Nerve Denervation in Streptozotocin-Induced Diabetic Rats Is Reduced by Cilostazol

Tseng

Wang

et al. 2023

Medicina

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Background and Objective: Our previous study demonstrated that consistent treatment of oral cilostazol was effective in reducing levels of painful peripheral neuropathy in streptozotocin-induced type I diabetic rats. As diabetic neuropathy is characterized by hyperglycemia-induced nerve damage in the periphery, this study aims to examine the neuropathology as well as the effects of cilostazol treatments on the integrity of peripheral small nerve fibers in type I diabetic rats. Materials and Methods: A total of ninety adult male Sprague-Dawley rats were divided into the following groups: (1) naïve (control) group; (2) diabetic rats (DM) group for 8 weeks; DM rats receiving either (3) 10 mg/kg oral cilostazol (Cilo10), (4) 30 mg/kg oral cilostazol (Cilo30), or (5) 100 mg/kg oral cilostazol (Cilo100) for 6 weeks. Pain tolerance thresholds of hind paws toward thermal and mechanical stimuli were assessed. Expressions of PGP9.5, P2X3, CGRP, and TRPV-1 targeting afferent nerve fibers in hind paw skin and glial cells in the spinal dorsal horn were examined via immunohistochemistry and immunofluorescence. Results: Oral cilostazol ameliorated the symptoms of mechanical allodynia but not thermal analgesia in DM rats. Significant reductions in PGP9.5-, P2X3-, CGRP, and TRPV-1-labeled penetrating nerve fibers in the epidermal layer indicated denervation of sensory nerves in the hind paw epidermis of DM rats. Denervation significantly improved in groups that received Cilo30 and Cilo100 in a dose-dependent manner. Cilostazol administration also suppressed microglial hyperactivation and increased astrocyte expressions in spinal dorsal horns. Conclusions: Oral cilostazol ameliorated hyperglycemia-induced peripheral small nerve fiber damage in the periphery of diabetic rats and effectively mitigated diabetic neuropathic pain via a central sensitization mechanism. Our findings present cilostazol not only as an effective option for managing symptoms of neuropathy but also for deterring the development of diabetic neuropathy in the early phase of type I diabetes.

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