Nitrate Metabolism and Ischemic Cerebrovascular Disease: A Narrative Review

Wang, Yicong; Chen, Weiqi; Zhou, Jian; Wang, Yongjun; Wang, Hao; Wang, Yilong

doi:10.3389/fneur.2022.735181

Cited by 5 publications

(6 citation statements)

References 122 publications

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“…Oxidative stress disturbs Nitric oxide signalling and induces inflammation. 43 Ischemic condition activates iNOS which in turn elevates nitric oxide which oxides the lipids, and protein causing cell injury. 44 In this study, the MCAO-performed rats showed increased levels of nitrate in cortex and striatum regions of the brain and also showed an increased level of lipid peroxidation confirming the cell infarct.…”

Section: Discussionmentioning

confidence: 99%

Nerolidol Attenuates Cerebral Ischemic Injury in Middle Cerebral Artery Occlusion-Induced Rats via Regulation of Inflammation, Apoptosis, and Oxidative Stress Markers

Zhang

Zhou

2023

Pharmacognosy Magazine

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Background Cerebral ischemia is a syndrome that occurs due to the restricted flow of oxygen-rich blood to the brain, causing damage to the brain cells. Globally, ischemia ranks second in causing mortality and third in causing disability in stroke patients. Nerolidol is a bioactive compound present in the essential oil of plants with a floral odour. It is a natural sesquiterpene alcohol used in cosmetics, perfumes, and as a food flavouring agent. It also possesses antioxidant, antimicrobial, anti-inflammatory, and anticancer properties. Materials and Methods In this study, we assessed the anti-ischemic property of nerolidol in cerebral ischemia-induced mice. Healthy male Wistar rats were induced into cerebral ischemia with middle cerebral artery occlusion (MCAO) and treated with 10 mg and 20 mg nerolidol for 21 days. The brain morphometric, antioxidant, and MMP levels were estimated in the brain tissue of MCAO-performed and nerolidol-treated rats. The cerebral infarct-alleviating potency of nerolidol was analysed by estimating the levels of inflammatory cytokines and apoptotic proteins. It was further confirmed by assessing the levels of COX-2/PGE-2 signalling proteins in brain tissue from MCAO-performed in rats. Results Nerolidol significantly reduced the cerebral infarct volume and brain edema via increased antioxidant levels and decreased MMPs. It also decreased the pro-inflammatory cytokines and proapoptotic proteins in brain tissue. The inflammatory signalling proteins NFκB, COX-2, and PGE-2 were significantly decreased in nerolidol-treated MCAO-performed rats, confirming the antiischemic property of nerolidol. Conclusion Our results prove nerolidol significantly alleviates cerebral ischemia in rats, and it can be subjected to further trials to be formulated as an anti-ischemic drug.

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Section: Discussionmentioning

confidence: 99%

Nerolidol Attenuates Cerebral Ischemic Injury in Middle Cerebral Artery Occlusion-Induced Rats via Regulation of Inflammation, Apoptosis, and Oxidative Stress Markers

Zhang

Zhou

2023

Pharmacognosy Magazine

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“…In the tumour microenvironment, low to moderate levels of NO (NO) derived from tumour and endothelial cells can activate angiogenesis, promoting an aggressive phenotype. Conversely, high levels of NO derived from M1 macrophages and Th1 lymphocytes can exert an anti-tumoural effect, providing protection against cancer [1,8,15,16]. Therefore, identifying the NO equilibrium state is particularly important for ccRCC biology.…”

Section: The Disruption Of No Homeostasis In Ccrccmentioning

confidence: 99%

“…Three isoforms of NO synthetases (NOSs) are known to be involved in NO synthesis: endothelial (NOS1 or eNOS), inducible (NOS2 or iNOS), and neuronal (NOS3 or nNOS) [16,26].…”

Section: The Disruption Of No Signaling In Ccrccmentioning

confidence: 99%

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Disturbances in Nitric Oxide Cycle and Related Molecular Pathways in Clear Cell Renal Cell Carcinoma

Ene,

Tampa,

Georgescu

et al. 2023

Cancers

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It is important to note that maintaining adequate levels of nitric oxide (NO), the turnover, and the oxidation level of nitrogen are essential for the optimal progression of cellular processes, and alterations in the NO cycle indicate a crucial step in the onset and progression of multiple diseases. Cellular accumulation of NO and reactive nitrogen species in many types of tumour cells is expressed by an increased susceptibility to oxidative stress in the tumour microenvironment. Clear cell renal cell carcinoma (ccRCC) is a progressive metabolic disease in which tumour cells can adapt to metabolic reprogramming to enhance NO production in the tumour space. Understanding the factors governing NO biosynthesis metabolites in ccRCC represents a relevant, valuable approach to studying NO-based anticancer therapy. Exploring the molecular processes mediated by NO, related disturbances in molecular pathways, and NO-mediated signalling pathways in ccRCC could have significant therapeutic implications in managing and treating this condition.

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“…Тому за фізіологічних умов окиснення NO до нітритів можна розглядати як безпечний шлях утилізації надлишкового NO. Проте за умов ацидозу та накопичення великої кількості речовин із високим редоксним потенціалом (НАДН відновлений, ФАДН відновлений, тощо) можливе зменшення інтенсивності окиснення нітритів до нітратів та навіть відновлення нітритів до оксиду азоту (за допомогою нітратнітритредуктазних систем) [9]. Накопичення великої кількості нітритів, особливо при наявності АФК, створює умови для нітрування (приєднання простетичної групи NO2 -) білків, що змінює їхню активність та може надати їм антигенних властивостей [10].…”

Section: результати та їх обговоренняunclassified

The Role of Ap-1 Transcription Factor Activation in the Changes of Production and Utilization of Nitric Oxide in the Gastric Mucosa of Rats Under Conditions of Chronic Fluoride Intoxication

Акімов¹

2022

Med. and Ecol. probl.

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Millions of people are affected by excessive fluoride intake. The effect of fluorides on the activation or inhibition of redox-sensitive transcription factors remains poorly understood. The aim of this research is to examine the effect of activation of the transcription factor AP-1 on changes in the activity of inducible NO synthase and constitutive isoforms of NO synthase, concentrations of peroxynitrites of alkali and alkaline earth metals, concentrations of nitrites and nitrosothiols in the gastric mucosa of rats under conditions of chronic fluoride intoxication. The study was conducted on 18 adult male Wistar rats weighing 220-260 g. Experimental animals were randomly divided into 3 groups of 6 animals each: control, chronic fluoride intoxication group and AP-1 transcription factor blockade group. Chronic fluoride intoxication was simulated by the administration of sodium fluoride at a dose of 10 mg / kg for 30 days. AP-1 blockade was performed by administering SR11302 at a rate of 15 mg / kg twice a week. In the gastric mucosa, the following was studied: the activities of constitutive and inducible isoforms of NO synthase, the concentration of nitrites, peroxynitrites and nitrosothiols. Chronic fluoride intoxication reduces the activity of constitutive NO synthases by 37.73% and increases the activity of inducible NO synthase by 1.61 times. The concentration of peroxynitrites increases by 2.68 times, nitrites – by 1.74 times, and nitrosothiols – by 1.88 times. Blockade of AP-1 reduces the activity of inducible isoform by 2.11, does not affect the activity of constitutive isoforms, and reduces the concentration of peroxynitrites by 1.98 times, nitrites – by 2.10 times, and nitrosothiols – by 2.37 times. Activation of the transcription factor AP-1 under conditions of chronic excessive fluoride intake leads to increased production of nitric oxide in the gastric mucosa of rats, enhances its oxidation to nitrites, promotes the formation of nitrosyl groups in the reaction with low molecular weight donors of thiol groups and increases the peroxidation of nitric oxide with the formation of peroxynitrite.

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Nitrate Metabolism and Ischemic Cerebrovascular Disease: A Narrative Review

Cited by 5 publications

References 122 publications

Nerolidol Attenuates Cerebral Ischemic Injury in Middle Cerebral Artery Occlusion-Induced Rats via Regulation of Inflammation, Apoptosis, and Oxidative Stress Markers

Nerolidol Attenuates Cerebral Ischemic Injury in Middle Cerebral Artery Occlusion-Induced Rats via Regulation of Inflammation, Apoptosis, and Oxidative Stress Markers

Disturbances in Nitric Oxide Cycle and Related Molecular Pathways in Clear Cell Renal Cell Carcinoma

The Role of Ap-1 Transcription Factor Activation in the Changes of Production and Utilization of Nitric Oxide in the Gastric Mucosa of Rats Under Conditions of Chronic Fluoride Intoxication

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