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| http://dx.doi.org/10.2337/dc12-2702 | DOI Listing |
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Investigation of the protective effect of cilostazol on acute lung injury-mediated inflammation and in silico molecular modelling studies of inflammatory signalling pathway: a repurposing study.
Naunyn Schmiedebergs Arch Pharmacol
January 2025
Dr. Babasaheb Ambedkar Technological University, Lonere, Raigad, 402103, India.
Acute lung injury i.e. ALI and its serious form acute respiratory distress syndrome (ARDS) are incurable medical conditions associated with significant global mortality and morbidity.
View Article and Find Full Text PDFInhibition of nitric oxide synthase transforms carotid occlusion-mediated benign oligemia into large cerebral infarction.
Theranostics
January 2025
Department of neurology, Dongguk University Ilsan Hospital, Goyang 10326, Republic of Korea.
It remains unclear why unilateral proximal carotid artery occlusion (UCAO) causes benign oligemia in mice, yet leads to various outcomes (asymptomatic-to-death) in humans. We hypothesized that inhibition of nitric oxide synthase (NOS) both transforms UCAO-mediated oligemia into full infarction and expands pre-existing infarction. Using 900 mice, we i) investigated stroke-related effects of UCAO with/without intraperitoneal administration of the NOS inhibitor (NOSi) N-nitro-L-arginine methyl ester (L-NAME, 400 mg/kg); ii) examined the rescue effect of the NO-donor, molsidomine (200 mg/kg at 30 minutes); and iii) tested the impact of antiplatelet medications.
View Article and Find Full Text PDFCilostazol Alleviates Delayed Cerebral Ischemia After Subarachnoid Hemorrhage by Attenuating Microcirculatory Dysfunction.
Transl Stroke Res
November 2024
Department of Neurosurgery, Hirosaki General Medical Center, Hirosaki, Japan.
Cilostazol, a phosphodiesterase 3 (PDE3) inhibitor that exerts antiplatelet effects, has therapeutic potential for delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). However, its mechanism of action remains unclear. We hypothesized that cilostazol alleviates DCI by improving cerebral microcirculatory dysfunction, which is a component of early brain injury.
View Article and Find Full Text PDFCombination treatment with cilostazol and isosorbide mononitrate attenuates microemboli-mediated vascular cognitive impairment and improves imaging and plasma biomarkers in diabetic rats.
Exp Neurol
January 2025
Ralph H. Johnson VA Medical Center, Charleston, SC, United States of America; Department of Pathology & Laboratory Medicine, Medical University of South Carolina, Charleston, SC, United States of America.
Diabetes is a major risk factor for all types of dementia. The underlying reasons are not fully understood, and preventive therapeutic strategies are lacking. Previously we have shown that diabetic but not control rats developed a progressive cognitive decline in a microemboli (ME) model of vascular contributions to cognitive impairment & dementia (VCID).
View Article and Find Full Text PDFRenal microRNA-144-3p is associated with transforming growth factor-β1-induced oxidative stress and fibrosis by suppressing the NRF2 pathway in hypertensive diabetic kidney disease.
Free Radic Biol Med
November 2024
Department of Pharmacy and BK21FOUR Advanced Program for SmartPharma Leaders, Graduate School of The Catholic University of Korea, Gyeonggi-do, 14662, Republic of Korea; Integrated Research Institute for Pharmaceutical Sciences, The Catholic University of Korea, Gyeonggi-do, 14662, Republic of Korea; College of Pharmacy, The Catholic University of Korea, Gyeonggi-do, 14662, Republic of Korea. Electronic address:
Chronic kidney disease (CKD) is a global health problem characterized by progressive renal fibrosis and excessive extracellular matrix deposition. Oxidative stress and epigenetic regulation, particularly through microRNAs (miRNAs), play crucial roles in the pathogenesis of CKD. In this study, we investigated the role of urinary miR-144-3p, which is upregulated in rats with CKD induced by diabetes and hypertension, in renal fibrosis progression, particularly its regulation of the nuclear factor erythroid-2-related factor 2 (NRF2) pathway.
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