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Inhibition 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 PDFEvaluation of the potential efficacy of the nitric oxide donor molsidomine for the treatment of schizophrenia.
Med Gas Res
November 2024
Department of Pharmacology, Faculty of Medicine, School of Health Sciences, University of Thessaly, Larissa, Greece.
Schizophrenia is a chronic devastating psychiatric disease characterized by a high recurrence rate. Pharmacological management of this disorder appears disappointing since it is associated with a lack of efficacy for negative symptoms and cognitive deficits, typical features of schizophrenia, and the presence of severe undesired side effects. Thus, novel molecules with high efficacy and low toxicity for the treatment of schizophrenia are urgently needed.
View Article and Find Full Text PDFHistamine H receptor antagonist/nitric oxide donors as novel promising therapeutic hybrid-tools for glaucoma and retinal neuroprotection.
Biomed Pharmacother
November 2024
Department of Neurosciences, Psychology, Drug Research and Child Health (NEUROFARBA), University of Florence, Florence, Italy. Electronic address:
Glaucoma is a degenerative optic neuropathy in which the degeneration of optic nerve and blindness occur. The main cause is a malfunction of ciliary processes (protrusions of the ciliary bodies) resulting in increased intraocular pressure (IOP). Ocular hypertension (OHT) causes ischemic events leading to retinal ganglion cell (RGC) depletion and blindness.
View Article and Find Full Text PDFTherapeutic Potential of Molsidomine-Loaded Liquid Crystal Nanoparticles for the Treatment and Management of Niacin-Induced Varicose Veins: and Studies.
ACS Appl Bio Mater
November 2024
Infectious Disease Biology Laboratory, Chemical Biology Unit, Institute of Nano Science and Technology, Knowledge City, Sector-81, Mohali 140306, Punjab, India.
Varicose vein therapy has historically relied significantly on invasive surgical procedures, which frequently resulted in poor compliance among patients. The tendency could stem from the past use of abrasive surgical procedures and a lack of documented drug-induced animal models. To address this challenge, we envisaged an innovative approach for animal model development that uses niacin-induced recurrent flushing.
View Article and Find Full Text PDFInhibition of Sirtuin Deacylase Activity by Peroxynitrite.
Biochemistry
October 2024
Department of Biochemistry, Medical College of Wisconsin, Milwaukee, Wisconsin 53226, United States.
Sirtuins are a class of enzymes that deacylate protein lysine residues using NAD as a cosubstrate. Sirtuin deacylase activity has been historically regarded as protective; loss of sirtuin deacylase activity potentially increases susceptibility to aging-related disease development. However, which factors may inhibit sirtuins during aging or disease is largely unknown.
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