Effect of 3-substituted 1,4-benzodiazepin-2-ones on bradykinin-induced smooth muscle contraction

Virych, Pavlo; Shelyuk, O.; Kabanova, T. A.

doi:10.15407/ubj89.01.031

Cited by 5 publications

(1 citation statement)

References 15 publications

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“…Bradykinin, a pro‐inflammatory nonapeptide, is released by the action of plasma or tissue kallikreins on kininogens (Drouin et al 1979; Kakoki and Smithies 2009). Signaling by bradykinin is mainly mediated through B2R, a receptor of the seven‐transmembrane GPCR family, which are capable of generating a broad spectrum of physiological responses such as vasodilation, fluid balance and retention, smooth muscle contraction, and algesia on target cells (Khasar et al 1995; Virych et al 2017). Bradykinin/B2R induces the activation of MAPK1/3 via PKC and c‐Src pathways, which up‐regulates matrix metalloproteinase (MMP)‐9 and increases the conventional outflow facility in human trabecular meshwork cells (Webb et al 2011).…”

Section: Description Of the Bradykinin Signaling Pathwaymentioning

confidence: 99%

A modular map of Bradykinin-mediated inflammatory signaling network

Rex

Deepak

Vaid

et al. 2021

J. Cell Commun. Signal.

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Bradykinin, a member of the kallikrein‐kinin system (KKS), is associated with an inflammatory response pathway with diverse vascular permeability functions, including thrombosis and blood coagulation. In majority, bradykinin signals through Bradykinin Receptor B2 (B2R). B2R is a G protein‐coupled receptor (GPCR) coupled to G protein family such as Gαqs, Gαq/Gα11, Gαi1, and Gβ1γ2. B2R stimulation leads to the activation of a signaling cascade of downstream molecules such as phospholipases, protein kinase C, Ras/Raf‐1/MAPK, and PI3K/AKT and secondary messengers such as inositol‐1,4,5‐trisphosphate, diacylglycerol and Ca2+ ions. These secondary messengers modulate the production of nitric oxide or prostaglandins. Bradykinin‐mediated signaling is implicated in inflammation, chronic pain, vasculopathy, neuropathy, obesity, diabetes, and cancer. Despite the biomedical importance of bradykinin, a resource of bradykinin‐mediated signaling pathway is currently not available. Here, we developed a pathway resource of signaling events mediated by bradykinin. By employing data mining strategies in the published literature, we describe an integrated pathway reaction map of bradykinin consisting of 233 reactions. Bradykinin signaling pathway events included 25 enzyme catalysis reactions, 12 translocations, 83 activation/inhibition reactions, 11 molecular associations, 45 protein expression and 57 gene regulation events. The pathway map is made publicly available on the WikiPathways Database with the ID URL: https://www.wikipathways.org/index.php/Pathway:WP5132. The bradykinin‐mediated signaling pathway map will facilitate the identification of novel candidates as therapeutic targets for diseases associated with dysregulated bradykinin signaling.

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Section: Description Of the Bradykinin Signaling Pathwaymentioning

confidence: 99%

A modular map of Bradykinin-mediated inflammatory signaling network

Rex

Deepak

Vaid

et al. 2021

J. Cell Commun. Signal.

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Analysis of decay kinetics of the cytosolic calcium transient induced by oxytocin in rat myometrium smooth muscle cells

Karakhim

Шлыков

Babich

et al. 2021

J Muscle Res Cell Motil

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Anti-Inflammatory Effects of Propoxazepam on Different Models of Inflammation

Golovenko¹,

Kabanova²,

Андронати³

et al. 2020

IJMMR

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Background. Propoxazepam, 7-bromo-5-(2-chlorophenyl)-3-propoxy-1H-benzo[e][1,4]diazepin-2(3H)-one, is a promising analgesic and anticonvulsant and is on preclinical trial. Objective. The aim of the research was to study the anti-inflammatory and analgesic action of Propoxazepam. Methods. The anti-inflammatory action was evaluated by carrageenan induced rat paw edema, formalin-induced paw licking response in mice and bradykinin-induced pain response in rat models. Results. It was established for the first time that the administration of Propoxazepam caused a significant anti-inflammatory activity when tested in different in vivo chemical experimental models of induced inflammation, i.e. carrageenan-, bradykinin- and formalin-induced inflammation tests. Conclusions. Propoxazepam significantly reduced acute and sub-acute inflammation and proved its efficacy and similar to anti-inflammatory action.

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Effect of 3-substituted 1,4-benzodiazepin-2-ones on bradykinin-induced smooth muscle contraction

Cited by 5 publications

References 15 publications

A modular map of Bradykinin-mediated inflammatory signaling network

A modular map of Bradykinin-mediated inflammatory signaling network

Analysis of decay kinetics of the cytosolic calcium transient induced by oxytocin in rat myometrium smooth muscle cells

Anti-Inflammatory Effects of Propoxazepam on Different Models of Inflammation

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