scholarly journals Literature-Based Drug Repurposing in Traditional Chinese Medicine: Reduced Inflammatory M1 Macrophage Polarization by Jisil Haebaek Gyeji-Tang Alleviates Cardiovascular Disease In Vitro and Ex Vivo

2020 ◽  
Vol 2020 ◽  
pp. 1-12
Author(s):  
Ga-Ram Yu ◽  
Seung-Jun Lee ◽  
Da-Hoon Kim ◽  
Dong-Woo Lim ◽  
Hyuck Kim ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Nuclear Translocation ◽  
Ex Vivo ◽  
Macrophage Polarization ◽  
Reducing Power ◽  
Mapk Signaling ◽  
Raw 264.7 ◽  
M1 Macrophage ◽  
Anti Inflammatory

Relatively high proportions of proinflammatory M1-like macrophages in tissues may lead to vascular impairment and trigger numerous diseases including atherosclerosis-related cardiovascular disease (CVD). Jisil Haebaek Gyeji-tang (JHGT), a polyherbal decoction, is traditionally used to treat various human ailments including chest pain, angina, and myocardial infarction. In the present study, we investigated the anti-inflammatory effects of JHGT on lipopolysaccharide- (LPS-) stimulated M1 macrophage polarization generated via the mitogen-activated protein kinases (MAPKs) pathway in RAW 264.7 mouse macrophages. The reducing power of JHGT was also investigated using DAF-FA DA in a zebrafish model. JHGT  significantly reduced inflammatory mediator levels, including iNOS, COX2, TNF-α, IL-6, and IL-1β, as compared with LPS-stimulated controls in vitro and ex vivo. Furthermore, JHGT suppressed the ERK1/2, JNK, and p38 MAPK pathways and reduced p-IκBα levels and the nuclear translocation of NF-κB in RAW 264.7 cells. In addition, treatment with JHGT significantly reduced the NO levels in LPS-treated zebrafish larva ex vivo. Our findings show the potent anti-inflammatory properties of JHGT are due to its suppression of MAPK signaling, NF-κB translocation, and M1 macrophage polarization.

scholarly journals Suppression of LPS-Induced Inflammation by Chalcone Flavokawain A through Activation of Nrf2/ARE-Mediated Antioxidant Genes and Inhibition of ROS/NFκB Signaling Pathways in Primary Splenocytes

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Hsin-Ling Yang ◽  
Ting-Yu Yang ◽  
Yugandhar Vudhya Gowrisankar ◽  
Chun-Huei Liao ◽  
Jiunn-Wang Liao ◽  
...  
Keyword(s):  
Proinflammatory Cytokine ◽  
Molecular Mechanisms ◽  
Nuclear Translocation ◽  
Ex Vivo ◽  
Root Extract ◽  
Piper Methysticum ◽  
Serum Lipase ◽  
Antioxidant Genes ◽  
Anti Inflammatory

Oxidative stress is an important contributing factor for inflammation. Piper methysticum, also known as Kava-kava, is a shrub whose root extract has been consumed as a drink by the pacific islanders for a long time. Flavokawain A (FKA) is a novel chalcone derived from the kava plant that is known to have medicinal properties. This study was aimed at demonstrating the antioxidant molecular mechanisms mediated by FKA on lipopolysaccharide- (LPS-) induced inflammation in BALB/c mouse-derived primary splenocytes. In vitro data show that the nontoxic concentrations of FKA (2-30 μM) significantly suppressed the proinflammatory cytokine (TNF-α, IL-1β, and IL-6) release but induced the secretion of interleukin-10 (IL-10), an anti-inflammatory cytokine. It was also shown that FKA pretreatment significantly downregulated the LPS-induced ROS production and blocked the activation of the NFκB (p65) pathway leading to the significant suppression of iNOS, COX-2, TNF-α, and IL-1β protein expressions. Notably, FKA favored the nuclear translocation of Nrf2 leading to the downstream expression of antioxidant proteins HO-1, NQO-1, and γ-GCLC via the Nrf2/ARE signaling pathway signifying the FKA’s potent antioxidant mechanism in these cells. Supporting the in vitro data, the ex vivo data obtained from primary splenocytes derived from the FKA-preadministered BALB/c mice (orally) show that FKA significantly suppressed the proinflammatory cytokine (TNF-α, IL-1β, and IL-6) secretion in control-, LPS-, or Concanavalin A- (Con A-) stimulated cells. A significant decrease in the ratios of pro- and anti-inflammatory cytokines (IL-6/IL-10; TNF-α/IL-10) showed that FKA possesses strong anti-inflammatory properties. Furthermore, BALB/c mice induced with experimental pancreatitis using cholecystokinin- (CCK-) 8 showed decreased serum lipase levels due to FKA pretreatment. We conclude that with its potent antioxidant and anti-inflammatory properties, chalcone flavokawain A could be a novel therapeutic agent in the treatment of inflammation-associated diseases.

scholarly journals microRNA-155 Is Decreased During Atherosclerosis Regression and Is Increased in Urinary Extracellular Vesicles During Atherosclerosis Progression

2020 ◽  
Vol 11 ◽  
Author(s):  
Stephen Fitzsimons ◽  
Silvia Oggero ◽  
Robyn Bruen ◽  
Cathal McCarthy ◽  
Moritz J. Strowitzki ◽  
...  
Keyword(s):  
Extracellular Vesicles ◽  
Ex Vivo ◽  
Macrophage Polarization ◽  
Chronic Inflammatory Disease ◽  
Cholesterol Diet ◽  
Human Coronary Artery ◽  
Inflammatory Signaling ◽  
Anti Inflammatory

BackgroundAtherosclerosis is a chronic inflammatory disease driven by macrophage accumulation in medium and large sized arteries. Macrophage polarization and inflammation are governed by microRNAs (miR) that regulate the expression of inflammatory proteins and cholesterol trafficking. Previous transcriptomic analysis led us to hypothesize that miR-155-5p (miR-155) is regulated by conjugated linoleic acid (CLA), a pro-resolving mediator which induces regression of atherosclerosis in vivo. In parallel, as extracellular vesicles (EVs) and their miR content have potential as biomarkers, we investigated alterations in urinary-derived EVs (uEVs) during the progression of human coronary artery disease (CAD).MethodsmiR-155 expression was quantified in aortae from ApoE−/− mice fed a 1% cholesterol diet supplemented with CLA blend (80:20, cis-9,trans-11:trans-10,cis-12 respectively) which had been previously been shown to induce atherosclerosis regression. In parallel, human polarized THP-1 macrophages were used to investigate the effects of CLA blend on miR-155 expression. A miR-155 mimic was used to investigate its inflammatory effects on macrophages and on ex vivo human carotid endarterectomy (CEA) plaque specimens (n = 5). Surface marker expression and miR content were analyzed in urinary extracellular vesicles (uEVs) obtained from patients diagnosed with unstable (n = 12) and stable (n = 12) CAD.ResultsHere, we report that the 1% cholesterol diet increased miR-155 expression while CLA blend supplementation decreased miR-155 expression in the aorta during atherosclerosis regression in vivo. CLA blend also decreased miR-155 expression in vitro in human THP-1 polarized macrophages. Furthermore, in THP-1 macrophages, miR-155 mimic decreased the anti-inflammatory signaling proteins, BCL-6 and phosphorylated-STAT-3. In addition, miR-155 mimic downregulated BCL-6 in CEA plaque specimens. uEVs from patients with unstable CAD had increased expression of miR-155 in comparison to patients with stable CAD. While the overall concentration of uEVs was decreased in patients with unstable CAD, levels of CD45+ uEVs were increased. Additionally, patients with unstable CAD had increased CD11b+ uEVs and decreased CD16+ uEVs.ConclusionmiR-155 suppresses anti-inflammatory signaling in macrophages, is decreased during regression of atherosclerosis in vivo and is increased in uEVs from patients with unstable CAD suggesting miR-155 has potential as a prognostic indicator and a therapeutic target.

scholarly journals Study of anti-inflammatory functions of HDL in experimental mouse models

2015 ◽  
Author(s):  
Περιστέρα-Ιωάννα Πετροπούλου
Keyword(s):  
Mouse Models ◽  
Ex Vivo ◽  
Raw 264.7 ◽  
Experimental Mouse ◽  
Anti Inflammatory

H υψηλής πυκνότητας λιποπρωτεΐνη (HDL) έχει σημαντικές ανοσορυθμιστικές ιδιότητες, συμπεριλαμβανομένης της εξασθένησης της φλεγμονώδους απόκρισης που επάγεται από τον λιποπολυσακχαρίτη (LPS). Σκοπός της παρούσας μελέτης ήταν να διερευνήσει την πιθανή συσχέτιση μεταξύ της δομής και της σύνθεσης της HDL και των αντι-φλεγμονωδών λειτουργίων της στην LPS-επαγόμενη φλεγμονή. Καθώς η λεκίθινο-χοληστερολική ακυλοτρανσφεράση (LCAT) είναι ένα κρίσιμο ένζυμο στην ωρίμανση της HDL ερευνήσαμε αν τα ποντίκια με ανεπάρκεια στο ένζυμο LCAT (Lcat-/-) που στερούνται ώριμης σφαιρικής HDL, παρουσιάζουν αυξημένη LPS-επαγόμενη φλεγμονώδη απόκριση. Η επίδραση του LPS στα Lcat-/-ποντίκια συγκρίθηκε με αυτή των ποντικιών με ανεπάρκεια στην απολιποπρωτεΐνη Α-Ι (Αροa1-/-) ποντίκια, τα οποία στερούνται κλασικής HDL και είναι γνωστό ότι έχουν αυξημένη απόκριση στο LPS, και με άγριου τύπου (WT) ποντίκια ελέγχου. Ο χαρακτηρισμός της απολιποπρωτεΐνικής σύνθεσης της HDL, αποκάλυψε ότι η HDL των Lcat-/- ποντικιών αποτελείται κατά κύριο λόγο από ΑροΕ, ενώ η HDL των Αροa1-/- ποντικιών είναι ιδιαίτερα εμπλουτισμένη σε ΑροΕ και ΑροΑ-ΙΙ. Περαιτέρω αναλύσεις έδειξαν σαφείς διαφορές στη σύνθεση των λιπιδίων της HDL μεταξύ των τριών ομάδων. Όπως αναμενόταν, η LPS-επαγόμενη (100 μg / kg βάρους σώματος) απόκριση κυτταροκινών τόσο των Lcat-/- όσο και των Αροa1-/- ποντικιών ήταν σημαντικά ενισχυμένη και παρατεταμένη σε σύγκριση με τα WT ποντίκια. Διέγερση ολικού αίματος με LPS (1-100 ng /mL) ex vivo έδειξε εναν παρόμοια ενισχυμένο προ-φλεγμονώδη φαινότυπο. Περαιτέρω χαρακτηρισμός σε RAW 264.7 μακροφάγα in vitro έδειξε ότι ο ορός και η HDL, αλλά όχι τα χυλομικρά και τα VLDL (πλούσιες σε τριγλυκερίδια λιποπρωτεΐνες - κλάσμα TRL) ή το κλάσμα απολιπιδιωμένων πρωτεΐνών των Lcat-/- ποντικιών, είχαν μειωμένη εξουδετερωτική ικανότητα της LPS-επαγόμενης απόκρισης του TNFα. Αντίθετα, η ανεπάρκεια για την ΑροΑ-Ι δεν επηρέασε την ικανότητα της HDL να εξουδετερωσει το LPS. Πρόσθετες μελέτες ανοσοφαινότυπησης έδειξαν ότι μόνο τα Lcat-/- και όχι τα Αροa1-/- ποντίκια, έχουν σημαντικά αυξημένους αριθμούς κυκλοφορούντων μονοκυττάρων, ως αποτέλεσμα της αύξησης των «ήπια προ-φλεγμονωδών» CD11b+LyCmid μονοκύτταρων, κι όχι λόγω των «έντονα προ-φλεγμονωδών» CD11b+LyChi μονοκύτταρων τα οποία παρουσίασαν αν μη τι αλλο μείωση. Σύμφωνα με αυτή την παρατήρηση, τα κύτταρα Kuppfer στο ήπαρ των Lcat-/- ποντικιών φαίνεται να έχουν έναν αντι-φλεγμονώδη, ρυθμιστικό φαινότυπο, ενώ τα περιτοναϊκά μακροφάγα των Lcat-/- έδειξαν επίσης μια αξιοσημείωτα μειωμένη LPS-επαγόμενη απόκριση του TNFα. Ωστόσο, μελέτες φθορίζουσας μικροσκοπίας έδειξαν οτι η περιεκτικότητα της μεμβράνης σε χοληστερόλη και η ρευστότητα της, δεν ήταν σε θέση να παράσχουν μία συσχέτιση μεταξύ αυτών των παραμέτρων, και της ανταπόκρισης των μακροφάγων στο LPS. Είναι σημαντικό ότι η επανεισαγωγή του ενζύμου LCAT με τη χρήση αδενοϊού (AdLCAT) στα Lcat-/- ποντίκια, επανέφερε το προφίλ λιπιδίων και την αναλογία Ly6Chi/Ly6Cmid των μονοκυττάρων στα επίπεδα των WT ποντικιών. Κατά συνέπεια, τα Lcat-/- ποντίκια στα οποία χορηγήθηκε ο αδενοϊος AdLCAT, παρουσίασαν σημαντική μείωση στα επίπεδα του TNFα μετά τη μόλυνση με LPS, σε σύγκριση με τα Lcat-/- ποντίκια που έλαβαν τον αδενοϊό ελέγχου AdGFP. Με βάση τα παραπάνω, καταλήγουμε στο συμπέρασμα ότι η ανεπάρκεια του ενζύμου LCAT στα ποντίκια, προκαλεί αύξηση της LPS-επαγόμενης φλεγμονής γεγονός που οφείλεται στη μειωμένη ικανότητα εξουδετέρωσης του LPS από την ανώριμη δισκοειδή HDL, καθώς και στον αυξημένο αριθμό των μονοκυττάρων, παρά τον διαταραγμένο φαινότυπο μονοκυττάρων/μακροφάγων.

scholarly journals In Vitro and Ex Vivo Effects of Silymarin Derivatives on Proinflammatory Cytokine Secretion Using a Murine Colonic Strip Model

2018 ◽  
Vol 5 (02) ◽  
pp. e55-e60
Author(s):  
Leo Fitzpatrick ◽  
Ella Mokrushin ◽  
George Talbott ◽  
Tibebe Woldermariam
Keyword(s):  
Cell Lines ◽  
Proinflammatory Cytokine ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Ex Vivo ◽  
Cytokine Secretion ◽  
Raw 264.7 ◽  
Tnf Α ◽  
Anti Inflammatory

AbstractSilymarin has anti-inflammatory properties and documented anti-colitis activity. Our prior study determined that in vitro treatment with certain extracted fractions of silymarin inhibited stimulated proinflammatory cytokine secretion from cell lines relevant to colitis. In this study, colitis was induced in mice by giving dextran sulfate sodium drinking water for 6 days. The ex vivo effects of crude silymarin extract, two different silymarin fractions, as well as commercially derived silibinin and isosilibinin were examined by determining the secretion of MIP-2, TNF-α, and IL-17 in cell culture media from colonic strips. Further, the effects of silymarin-derived treatments on IL-8 and TNF-α secretion induced by the colitis supernatant was characterized with HT-29 colonic epithelial and RAW 264.7 macrophage cell lines. Prominent inhibition of MIP-2 and TNF-α secretion from colonic strips of mice with/without dextran sulfate sodium-induced colitis was observed with various silymarin treatments. Further, inhibition of dual (IL-23+IL-1β) cytokine-stimulated secretion of IL-17 from colonic strips of mice was found with certain silymarin treatments. Significant attenuation of TNF-α secretion from colitis supernatant-stimulated RAW 264.7 cells was observed for crude silymarin extract and isosilibinin treatments. Finally, inhibition of IL-8 secretion from the colitis supernatant-stimulated HT29 colonic epithelial cell line was found with isosilibinin. These results contribute to the identification of silymarin-derived flavonoligans with optimal anti-inflammatory properties for further testing in colitis models.

scholarly journals Inhibition of Skin Inflammation by Scytonemin, an Ultraviolet Sunscreen Pigment

Marine Drugs ◽  
2020 ◽  
Vol 18 (6) ◽  
pp. 300
Author(s):  
Moo Rim Kang ◽  
Sun Ah Jo ◽  
Hyunju Lee ◽  
Yeo Dae Yoon ◽  
Joo-Hee Kwon ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Nuclear Translocation ◽  
Skin Inflammation ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Blue Green Algae ◽  
Tnf Α ◽  
Anti Inflammatory

Scytonemin is a yellow-green ultraviolet sunscreen pigment present in different genera of aquatic and terrestrial blue-green algae, including marine cyanobacteria. In the present study, the anti-inflammatory activities of scytonemin were evaluated in vitro and in vivo. Topical application of scytonemin inhibited 12-O-tetradecanoylphorbol-13-acetate (TPA)-induced ear swelling in BALB/c mice. The expression of tumor necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS) was also suppressed by scytonemin treatment in the TPA-treated ear of BALB/c mice. In addition, scytonemin inhibited lipopolysaccharide (LPS)-induced production of TNF-α and nitric oxide (NO) in RAW 264.7 cells, a murine macrophage-like cell line, and the mRNA expressions of TNF-α and iNOS were also suppressed by scytonemin in LPS-stimulated RAW 264.7 cells. Further study demonstrated that LPS-induced NF-κB activity was significantly suppressed by scytonemin treatment in RAW 264.7 cells. Our results also showed that the degradation of IκBα and nuclear translocation of the p65 subunit were blocked by scytonemin in LPS-stimulated RAW 264.7 cells. Collectively, these results suggest that scytonemin inhibits skin inflammation by blocking the expression of inflammatory mediators, and the anti-inflammatory effect of scytonemin is mediated, at least in part, by down-regulation of NF-κB activity. Our results also suggest that scytonemin might be used as a multi-function skin care ingredient for UV protection and anti-inflammation.

scholarly journals Anti-Inflammatory Effect of Curcumin on the Mouse Model of Myocardial Infarction through Regulating Macrophage Polarization

2021 ◽  
Vol 2021 ◽  
pp. 1-19
Author(s):  
Shaoxi Yan ◽  
Mo Zhou ◽  
Xiaoyun Zheng ◽  
Yuanyuan Xing ◽  
Juan Dong ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Ventricular Remodeling ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
M1 Macrophages ◽  
Macrophage Marker ◽  
M1 Macrophage ◽  
Anti Inflammatory

Inflammation causes tissue damage and promotes ventricular remodeling after myocardial infarction (MI), and the infiltration and polarization of macrophages play an important role in regulating inflammation post-MI. Here, we investigated the anti-inflammatory function of curcumin after MI and studied its relationship with macrophage polarization. In vivo, curcumin not only attenuated ventricular remodeling 3 months after MI but also suppressed inflammation during the first 7 days post-MI. Importantly, the results of qPCR and immunochemistry showed that curcumin decreased M1 (iNOS, CCL2, and CD86) but increased M2 macrophage (Arg1, CD163, and CD206) marker expression in the myocardium of MI mice during the first 7 days post-MI. And flow cytometry analysis indicated that curcumin suppressed M1 (CD45+Gr-1-CD11b+iNOS+ cells) but enhanced M2 macrophage (CD45+Gr-1-CD11b+Arg+ cells) expansion in the myocardium of MI mice during the first 7 days post-MI. In vitro, curcumin decreased LPS/IFNγ-elevated M1 macrophage marker (iNOS and CD86) expression and the proportion of M1 macrophages (iNOS+F4/80+ cells) but increased LPS/IFNγ-suppressed M2 macrophage marker (Arg1 and CD206) expression and the proportion of M2 macrophages (Arg1+F4/80+ cells). In addition, curcumin modulates M1/M2 macrophage polarization partly via AMPK. In conclusion, curcumin suppressed the MI-induced inflammation by modulating macrophage polarization partly via the AMPK pathway.

scholarly journals The Anti-Inflammatory Effect of KS23, A Novel Peptide Derived From Globular Adiponectin, on Endotoxin-Induced Uveitis in Rats

2021 ◽  
Vol 11 ◽  
Author(s):  
Xin Shi ◽  
Shaopin Zhu ◽  
Huiyi Jin ◽  
Junwei Fang ◽  
Xindan Xing ◽  
...  
Keyword(s):  
Aqueous Humor ◽  
Nuclear Translocation ◽  
Raw 264.7 Cells ◽  
Therapeutic Effects ◽  
Raw 264.7 ◽  
Tnf Α ◽  
Globular Adiponectin ◽  
Anti Inflammatory

Purpose: Adiponectin has been shown to exert potent anti-inflammatory activities in a range of systemic inflammatory diseases. This study aimed to investigate the potential therapeutic effects of KS23, a globular adiponectin-derived peptide, on endotoxin-induced uveitis (EIU) in rats and lipopolysaccharide (LPS)-stimulated mouse macrophage-like RAW 264.7 cells.Methods: EIU was induced in Lewis rats by subcutaneous injection of LPS into a single footpad. KS23 or phosphate-buffered saline (PBS) was administered immediately after LPS induction via intravitreal injection. Twenty-four hours later, clinical and histopathological scores were evaluated, and the aqueous humor (AqH) was collected to determine the infiltrating cells, protein concentration, and levels of inflammatory cytokines. In vitro, cultured RAW 264.7 cells were stimulated with LPS in the presence or absence of KS23, inflammatory cytokine levels in the supernatant, nuclear translocation of nuclear factor kappa B (NF-κB) subunit p65, and the expression of NF-kB signaling pathway components were analyzed.Results: KS23 treatment significantly ameliorated the clinical and histopathological scores of EIU rats and reduced the levels of infiltration cells, protein, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the aqueous humor. Consistently, KS23 decreased the expression of TNF-α and IL-6 in the supernatant of LPS-stimulated RAW 264.7 cells and inhibited the LPS-induced nuclear translocation of NF-κB p65 and the phosphorylation of IKKα/β/IκBα/NF-κB.Conclusion: The in vivo and in vitro results demonstrated the anti-inflammatory effects of the peptide KS23 and suggested that KS23 is a compelling, novel therapeutic candidate for the treatment of ocular inflammation.

scholarly journals Effect of Cocoa Polyphenolic Extract on Macrophage Polarization from Proinflammatory M1 to Anti-Inflammatory M2 State

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Laura Dugo ◽  
Maria Giovanna Belluomo ◽  
Chiara Fanali ◽  
Marina Russo ◽  
Francesco Cacciola ◽  
...  
Keyword(s):  
Macrophage Polarization ◽  
Total Phenolic ◽  
Macrophage Response ◽  
Beneficial Effects ◽  
Polyphenolic Extract ◽  
M1 Macrophage ◽  
Inflammatory State ◽  
M1 Phenotype ◽  
Anti Inflammatory

Polyphenols-rich cocoa has many beneficial effects on human health, such as anti-inflammatory effects. Macrophages function as control switches of the immune system, maintaining the balance between pro- and anti-inflammatory activities. We investigated the hypothesis that cocoa polyphenol extract may affect macrophage proinflammatory phenotype M1 by favoring an alternative M2 anti-inflammatory state on macrophages deriving from THP-1 cells. Chemical composition, total phenolic content, and antioxidant capacity of cocoa polyphenols extracted from roasted cocoa beans were determined. THP-1 cells were activated with both lipopolysaccharides and interferon-γfor M1 or with IL-4 for M2 switch, and specific cytokines were quantified. Cellular metabolism, through mitochondrial oxygen consumption, and ATP levels were evaluated. Here, we will show that cocoa polyphenolic extract attenuated in vitro inflammation decreasing M1 macrophage response as demonstrated by a significantly lowered secretion of proinflammatory cytokines. Moreover, treatment of M1 macrophages with cocoa polyphenols influences macrophage metabolism by promoting oxidative pathways, thus leading to a significant increase in O2consumption by mitochondrial complexes as well as a higher production of ATP through oxidative phosphorylation. In conclusion, cocoa polyphenolic extract suppresses inflammation mediated by M1 phenotype and influences macrophage metabolism by promoting oxidative pathways and M2 polarization of active macrophages.

Apigenin-7-O-β-d-glucuronide inhibits LPS-induced inflammation through the inactivation of AP-1 and MAPK signaling pathways in RAW 264.7 macrophages and protects mice against endotoxin shock

2016 ◽  
Vol 7 (2) ◽  
pp. 1002-1013 ◽  
Author(s):  
Weicheng Hu ◽  
Xinfeng Wang ◽  
Lei Wu ◽  
Ting Shen ◽  
Lilian Ji ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Mapk Signaling ◽  
Endotoxin Shock ◽  
Raw 264.7 ◽  
Raw 264.7 Macrophages ◽  
Anti Inflammatory ◽  
Mapk Signaling Pathways

In vitro and in vivo anti-inflammatory activities of apigenin-7-O-β-d-glucuronide.

scholarly journals Saponin from Periploca forrestii Schltr Mitigates Oxazolone-Induced Atopic Dermatitis via Modulating Macrophage Activation

2020 ◽  
Vol 2020 ◽  
pp. 1-13
Author(s):  
Luting Zeng ◽  
Yingqin Liu ◽  
Congcong Xing ◽  
Yijie Huang ◽  
Xin Sun ◽  
...  
Keyword(s):  
Atopic Dermatitis ◽  
Macrophage Activation ◽  
Skin Diseases ◽  
Nuclear Translocation ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Mouse Bone Marrow ◽  
Inflammatory Skin Diseases ◽  
M1 Macrophage

Atopic dermatitis (AD) is a relapsing, acute, and chronic skin disease featured by intractable itching, eczematous skin. Conventional therapies based on immunosuppression such as corticosteroids are associated with multiple adverse reactions. Periploca forrestii Schltr saponin (PFS) was shown to potently inhibit murine arthritis by protecting bone and cartilage injury and suppressing NF-κB activation. However, its therapeutic effect on oxazolone-induced atopic dermatitis (AD) and the underlying mechanisms on macrophage are still unclear. The AD-like dermatitis was induced by repeated oxazolone challenge to the skin of BALB/c mice in vivo. Blood and ears were biochemically or histologically processed. RT-PCR, western blotting, and ELISA were conducted to evaluate the expression of macrophage factors. Mouse bone marrow-derived macrophages (BMDMs) stimulated with lipopolysaccharide (LPS) were used as a model in vitro. PFS treatment inhibited AD-like dermatitis development. PFS downregulated epidermis thickness and cell infiltration, with histological analysis of the skin lesion. PFS alleviated plasma immunoglobulin (Ig) E, IgG2a, and IgG1 levels. PFS downregulated the expression of M1 macrophage factors, tumor necrosis factor- (TNF-) α, interleukin- (IL-) 6, monocyte chemotactic protein-1 (MCP-1), and nitric oxide synthase2 (NOS2), and M2 macrophage factors, IL-4, arginase1 (Arg1) and CD163 in AD-like skin, which were confirmed by western blot and ELISA analysis. In addition, PFS inhibited LPS-induced macrophage polarization via the inhibition of the phosphorylation of signal transducer and activator of transcription 3 (STAT3) and nuclear translocation of NF-κB p65. These results suggest that PFS exerted an antidermatitis effect against oxazolone by modulating macrophage activation. PFS administration might be useful in the treatment of AD and inflammatory skin diseases.

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