Nitric oxide-mediated pathways and its role in the degenerative diseases

Zhang, Nan; Diao, Yu; Hua, Rongrong; Wang, Jun; Han, Song; Li, Junfa; Yin, Yanling

doi:10.2741/4519

Cited by 21 publications

(3 citation statements)

References 58 publications

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“…Next to NO synthesis, L-arginine serves as the substrate for the enzymatic transformation of agmatine, creatine and urea in the human body [4, 5]. As the only precursor and nitrogen donor for nitric oxide (NO), L-arginine plays a central role in the form of a messenger in several physiological and pathophysiological processes [6-9]. Thus, L-arginine can be considered as a signaling molecule, which is responsible for the maintenance of essential cellular functions e.g.…”

Section: Introductionmentioning

confidence: 99%

Activation of Secretagogue Independent Gastric Acid Secretion via Endothelial Nitric Oxide Synthase Stimulation in Rats

Kitay

Link

Geibel

2017

Cell Physiol Biochem

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Background/Aims: L-arginine is an important mediator of cell division, wound healing, and immune function. It can be transformed by the nitric oxide synthase (NOS) to nitric oxide (NO), an important cell signaling molecule. Recent studies from our laboratory demonstrate specific effects of L-arginine (10mM) exposure on gastric acid secretion in rat parietal cells. Methods: Studies were performed with isolated gastric glands and the pH sensitive dye BCECF-AM +/- L-arginine to examine its effects on acid secretion. The direct NO-donor diethylamine NONOate sodium salt hydrate, was also used while monitoring intracellular pH. The specific inhibitor of the intracellular NO signal cascade ODQ was also used. Results: We found that gastric proton extrusion was activated with application of L-arginine (10mM), in a separate series when L-arginine (10mM) + L-NAME (30µM) were added there was no acid secretion. Addition of the NO-donor diethylamine NONOate sodium salt hydrate (10µM) also induced acid secretion. When the selective sGC-inhibitor ODQ was added with NONOate we did not observe acid secretion. Conclusion: We conclude that L-arginine is a novel secretagogue, which can mediate gastric acid secretion. Furthermore, the intake of L-arginine causes direct activation of the H⁺, K⁺ ATPase and increased proton extrusion from parietal cells resulting in the increased risk for acid-related diseases. The NO/sGC/cGMP pathway has never been described as a possible intracellular mechanism for H⁺, K⁺ ATPase activation before and presents a completely new scientific finding. Moreover, our studies demonstrate a novel role for L-NAME to effectively eliminate NOS induced acid secretion and thereby reducing the risk for L-arginine inducible ulcer disease.

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Section: Introductionmentioning

confidence: 99%

Activation of Secretagogue Independent Gastric Acid Secretion via Endothelial Nitric Oxide Synthase Stimulation in Rats

Kitay

Link

Geibel

2017

Cell Physiol Biochem

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“…Nitric oxide (NO) is a free radical with very short half-life during which it mediates many physiological processes that include enhancement of the tumoricidal and microbicidal activities through the activated macrophages. Excessive formation of NO in the tissue could have detrimental effect, cause tissue damage, and also activate the pro-inflammatory mediators (Jorens et al, 1995;Tripathi et al, 2007;Zhang et al, 2017). The murine monocytic macrophage (RAW 264.7) cell line was used in the present work to determine the anti-inflammatory effects of E. hyssopifolium methanolic extract by inhibiting the formation of excessive NO by the macrophage.…”

Section: Discussionmentioning

confidence: 99%

In vitro anti-inflammatory and comparative cytotoxicity studies on methanolic extract of Enicostemma hyssopifolium

Komal,

Berlin Grace,

Hussain

et al. 2023

IFRJ

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Enicostemma hyssopifolium is a perineal herb widely used as an antidiabetic agent in folklore medicine. The present work was focused on the assessment of its anti-inflammatory and cytotoxic properties. Its methanolic extract was evaluated for anti-inflammatory activity using murine monocytic macrophage RAW 264.7 cells, and screened for its cytotoxic property in different cancer cell lines. The methanolic extract was able to potentially inhibit the bacterial lipopolysaccharides-induced inflammatory response in RAW 264.7 cells. Results of the cytotoxicity studies revealed that the methanolic extract effectively induced the cytotoxicity at considerably lower concentration in MCF-7, A-549, and COLO-205 cell lines, while the viability of HeLa, CasKi, and HT-29 cells were inhibited at comparatively higher concentrations. Results thus indicated that E. hyssopifolium possessed potent anti-inflammatory and cytotoxic properties. This necessitates further exploration of bioactive phytochemical compounds responsible for these properties for therapeutic applications.

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“…Dubey et al [ 98 ] demonstrated the decisive role of inducible NO synthase in neutrophil apoptosis through enhanced generation of reactive oxygen species and caspase-8-mediated activation of the mitochondrial death pathway. NO increases Fas expression on SMCs, which enhances their apoptosis under these conditions [ 99 , 100 ].…”

Section: Apoptosis Markersmentioning

confidence: 99%

Apoptosis and Cell Proliferation Markers in Inflammatory-Fibroproliferative Diseases of the Vessel Wall (Review)

et al. 2020

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Apoptosis is the main feature of inflammatory-fibroproliferative disorders of the vessel wall. Studies in animal models have shown that smooth muscle cells (SMCs) cultured from endarterectomy specimens from the affected area proliferate more slowly and display higher apoptotic indices than SMCs derived from the normal vessel wall. Apoptotic cells were found in the destabilized atherosclerotic plaques, as well as in the samples with restenosis of the reconstruction area. Injury to the vessel wall causes two waves of apoptosis. The first wave is the rapid apoptosis in the media that occurs within a few hours after injury and leads to a marked reduction in the number of vascular wall cells. The second wave of apoptosis occurs much later (from several days to weeks) and is limited by the SMCs within the developing neointima. Up to 14% of the neointimal SMCs undergo apoptosis 20 days after balloon angioplasty. Ligation of the external carotid artery in a rabbit model led to a marked decrease in blood flow in the common carotid artery, which correlated with the increased apoptosis of endothelial cells and SMCs. Angioplasty-induced death of SMCs is regulated by a redox-sensitive signaling pathway, and topical administration of antioxidants can minimize vascular cell loss. On the whole, studies show that apoptosis is prevalent in vascular lesions, controlling the viability of both inflammatory and vascular cells, determining the cellular composition of the vessel wall. The main markers of apoptosis (Fas, Fas ligand, p53, Bcl-2, Bax) and cell proliferation (toll receptor) have been considered in the current review.

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Nitric oxide-mediated pathways and its role in the degenerative diseases

Cited by 21 publications

References 58 publications

Activation of Secretagogue Independent Gastric Acid Secretion via Endothelial Nitric Oxide Synthase Stimulation in Rats

Activation of Secretagogue Independent Gastric Acid Secretion via Endothelial Nitric Oxide Synthase Stimulation in Rats

In vitro anti-inflammatory and comparative cytotoxicity studies on methanolic extract of Enicostemma hyssopifolium

Apoptosis and Cell Proliferation Markers in Inflammatory-Fibroproliferative Diseases of the Vessel Wall (Review)

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