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dc.contributor.authorZeng, Ling-Hui
dc.contributor.authorFatima, Mobeen
dc.contributor.authorSyed, Shahzada Khurram
dc.contributor.authorShaukat, Saira
dc.contributor.authorMahdy, Amina
dc.contributor.authorHussain, Nadia
dc.contributor.authorAl Haddad, Amal H. I.
dc.contributor.authorSaid, Amira S. A.
dc.contributor.authorAlqahtani, Ali
dc.contributor.authorAlqahtani, Taha
dc.contributor.authorMajeed, Abdul
dc.contributor.authorTariq, Muhammad
dc.contributor.authorHussain, Musaddique
dc.date.accessioned2023-03-27T07:11:36Z
dc.date.available2023-03-27T07:11:36Z
dc.date.issued2022en_US
dc.identifier.citationZeng, L.-H., Fatima, M., Syed, S. K., Shaukat, S., Mahdy, A., Hussain, N. ... Hussain, M. (2022). Anti-inflammatory and anti-oxidant properties of Ipomoea nil (Linn.) Roth significantly alleviates cigarette smoke (CS)-induced acute lung injury via possibly inhibiting the NF-KB pathway. Biomedicine & Pharmacotherapy, 155. https://dx.doi.org/10.1016/j.biopha.2022.113267en_US
dc.identifier.issn0753-3322
dc.identifier.issn1950-6007
dc.identifier.urihttps://dx.doi.org/10.1016/j.biopha.2022.113267
dc.identifier.urihttps://hdl.handle.net/20.500.12511/10699
dc.description.abstractAcute respiratory distress syndrome (ARDS), a serious manifestation of acute lung injury (ALI), is a debilitating inflammatory lung disease that is caused by multiple risk factors. One of the primary causes that can lead to ALI/ ARDS is cigarette smoke (CS) and its primary mode of action is via oxidative stress. Despite extensive research, no appropriate therapy is currently available to treat ALI/ARDS, which means there is a dire need for new potential approaches. In our study we explored the protective effects of 70 % methanolic-aqueous extract of Ipomoea nil (Linn.) Roth, named as In.Mcx against CS-induced ALI mice models and RAW 264.7 macrophages because Ipomoea nil has traditionally been used to treat breathing irregularities. Male Swiss albino mice (20-25 +/- 2 g) were subjected to CS for 10 uninterrupted days in order to establish CS-induced ALI murine models. Dexamethasone (1 mg/kg), In.Mcx (100 200, and 300 mg/kg) and normal saline (10 mL/kg) were given to respective animal groups, 1 h before CS-exposure. 24 h after the last CS exposure, the lungs and bronchoalveolar lavage fluid (BALF) of all euthanized mice were harvested. Altered alveolar integrity and elevated lung weightcoefficient, total inflammatory cells, oxidative stress, expression of pro-inflammatory cytokines (IL-10 and IL-6) and chemokines (KC) were significantly decreased by In.Mcx in CS-exposed mice. In.Mcx also revealed significant lowering IL-10, IL-6 and KC expression in CSE (4 %)-activated RAW 264.7 macrophage. Additionally, In.Mcx showed marked enzyme inhibition activity against Acetylcholinesterase, Butyrylcholinesterase and Lipoxygenase. Importantly, In.Mcx dose-dependently and remarkably suppressed the CS-induced oxidative stress via not only reducing the MPO, TOS and MDA content but also improving TAC production in the lungs. Accordingly, HPLC analysis revealed the presence of many important antioxidant components. Finally, In.Mcx showed a marked decrease in the NF-KB expression both in in vivo and in vitro models. Our findings suggest that In.Mcx has positive therapeutic effects against CS-induced ALI via suppressing uncontrolled inflammatory response, oxidative stress, lipoxygenase and NF-KB p65 pathway.en_US
dc.language.isoengen_US
dc.publisherElsevier Franceen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.rightsAttribution-NonCommercial-NoDerivatives 4.0 International*
dc.rights.urihttps://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subjectAcute Lung Injuryen_US
dc.subjectOxidative Stressen_US
dc.subjectPro-Inflammatory Cytokinesen_US
dc.subjectRAW 264.7 Macrophageen_US
dc.subjectLipoxygenase Pathwayen_US
dc.subjectNF-κB p65en_US
dc.titleAnti-inflammatory and anti-oxidant properties of Ipomoea nil (Linn.) Roth significantly alleviates cigarette smoke (CS)-induced acute lung injury via possibly inhibiting the NF-KB pathwayen_US
dc.typearticleen_US
dc.relation.ispartofBiomedicine & Pharmacotherapyen_US
dc.departmentİstanbul Medipol Üniversitesi, Uluslararası Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, Tıbbi Farmakoloji Ana Bilim Dalıen_US
dc.identifier.volume155en_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.identifier.doi10.1016/j.biopha.2022.113267en_US
dc.institutionauthorMahdy, Amina
dc.identifier.wosqualityQ1en_US
dc.identifier.wos000933892600001en_US
dc.identifier.scopus2-s2.0-85138992557en_US
dc.identifier.pmid36271539en_US
dc.identifier.scopusqualityQ1en_US


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