Please use this identifier to cite or link to this item: https://dspace.iiti.ac.in/handle/123456789/4024
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dc.contributor.authorSaqib, Uzmaen_US
dc.contributor.authorBaig, Mirza Saqiben_US
dc.date.accessioned2022-03-17T01:00:00Z-
dc.date.accessioned2022-03-17T15:31:23Z-
dc.date.available2022-03-17T01:00:00Z-
dc.date.available2022-03-17T15:31:23Z-
dc.date.issued2018-
dc.identifier.citationSaqib, U., Sarkar, S., Suk, K., Mohammad, O., Baig, M. S., & Savai, R. (2018). Phytochemicals as modulators of M1-M2 macrophages in inflammation. Oncotarget, 9(25), 17937-17950. doi:10.18632/oncotarget.24788en_US
dc.identifier.issn1949-2553-
dc.identifier.otherEID(2-s2.0-85044833784)-
dc.identifier.urihttps://doi.org/10.18632/oncotarget.24788-
dc.identifier.urihttps://dspace.iiti.ac.in/handle/123456789/4024-
dc.description.abstractMacrophages are critical mediators of the innate immune response against foreign pathogens, including bacteria, physical stress, and injury. Therefore, these cells play a key role in the "inflammatory pathway" which in turn can lead to an array of diseases and disorders such as autoimmune neuropathies and myocarditis, inflammatory bowel disease, atherosclerosis, sepsis, arthritis, diabetes, and angiogenesis. Recently, more studies have focused on the macrophages inflammatory diseases since the discovery of the two subtypes of macrophages, which are differentiated on the basis of their phenotype and distinct gene expression pattern. Of these, M1 macrophages are pro-inflammatory and responsible for inflammatory signaling, while M2 are anti-inflammatory macrophages that participate in the resolution of the inflammatory process, M2 macrophages produce anti-inflammatory cytokines, thereby contributing to tissue healing. Many studies have shown the role of these two subtypes in the inflammatory pathway, and their emergence appears to decide the fate of inflammatory signaling and disease progression. As a next step in directing the pro-inflammatory response toward the anti-inflammatory type after an insult by a foreign pathogen (e. g., bacterial lipopolysaccharide), investigators have identified many natural compounds that have the potential to modulate M1 to M2 macrophages. In this review, we provide a focused discussion of advances in the identification of natural therapeutic molecules with anti-inflammatory properties that modulate the phenotype of macrophages from M1 to M2. © Saqib et al.en_US
dc.language.isoenen_US
dc.publisherImpact Journals LLCen_US
dc.sourceOncotargeten_US
dc.subjectaloe emodinen_US
dc.subjectapigeninen_US
dc.subjectapocyninen_US
dc.subjectbacterium lipopolysaccharideen_US
dc.subjectberberineen_US
dc.subjectchrysinen_US
dc.subjectcurcuminen_US
dc.subjectepigallocatechin gallateen_US
dc.subjectforskolinen_US
dc.subjectgamma interferonen_US
dc.subjectgeraniinen_US
dc.subjectinterleukin 10en_US
dc.subjectinterleukin 1betaen_US
dc.subjectinterleukin 2en_US
dc.subjectinterleukin 8en_US
dc.subjectlupeolen_US
dc.subjectmalibatol Aen_US
dc.subjectmonocyte chemotactic protein 1en_US
dc.subjectnaringeninen_US
dc.subjectpaeoniflorinen_US
dc.subjectpaeoniflorin 6' o benzene sulfonic aciden_US
dc.subjectpeonolen_US
dc.subjectprocyanidinen_US
dc.subjectquercetinen_US
dc.subjectresveratrolen_US
dc.subjectstilbene derivativeen_US
dc.subjectterpinen 4 olen_US
dc.subjecttriptolideen_US
dc.subjecttumor necrosis factoren_US
dc.subjectunclassified drugen_US
dc.subjectunindexed drugen_US
dc.subjectcytokine releaseen_US
dc.subjectdisease courseen_US
dc.subjectenzyme activationen_US
dc.subjectenzyme inhibitionen_US
dc.subjecthumanen_US
dc.subjectin vivo studyen_US
dc.subjectmacrophageen_US
dc.subjectnonhumanen_US
dc.subjectphenotypeen_US
dc.subjectphytochemistryen_US
dc.subjectprotein bindingen_US
dc.subjectprotein expressionen_US
dc.subjectReviewen_US
dc.subjectSalsolaen_US
dc.subjectSalsola tuberculatiformisen_US
dc.subjectsignal transductionen_US
dc.subjectupregulationen_US
dc.titlePhytochemicals as modulators of M1-M2 macrophages in inflammationen_US
dc.typeReviewen_US
dc.rights.licenseAll Open Access, Gold, Green-
Appears in Collections:Department of Biosciences and Biomedical Engineering

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