scholarly journals A therapeutic oxygen carrier isolated from Arenicola marina decreased P. gingivalis induced inflammation and tissue destruction

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Fareeha Batool ◽  
Céline Stutz ◽  
Catherine Petit ◽  
Nadia Benkirane-Jessel ◽  
Eric Delpy ◽  
...  
Keyword(s):  
Gene Expression ◽  
Oxygen Carrier ◽  
Tissue Destruction ◽  
Biofilm Growth ◽  
Immune Modulators ◽  
Arenicola Marina ◽  
Oral Epithelial Cells ◽  
Inflammatory Score ◽  
Tnf Α

Abstract The control of inflammation and infection is crucial for periodontal wound healing and regeneration. M101, an oxygen carrier derived from Arenicola marina, was tested for its anti-inflammatory and anti-infectious potential based on its anti-oxidative and tissue oxygenation properties. In vitro, no cytotoxicity was observed in oral epithelial cells (EC) treated with M101. M101 (1 g/L) reduced significantly the gene expression of pro-inflammatory markers such as TNF-α, NF-κΒ and RANKL in P. gingivalis-LPS stimulated and P. gingivalis-infected EC. The proteome array revealed significant down-regulation of pro-inflammatory cytokines (IL-1β and IL-8) and chemokine ligands (RANTES and IP-10), and upregulation of pro-healing mediators (PDGF-BB, TGF-β1, IL-10, IL-2, IL-4, IL-11 and IL-15) and, extracellular and immune modulators (TIMP-2, M-CSF and ICAM-1). M101 significantly increased the gene expression of Resolvin-E1 receptor. Furthermore, M101 treatment reduced P. gingivalis biofilm growth over glass surface, observed with live/dead analysis and by decreased P. gingivalis 16 s rRNA expression (51.7%) (p < 0.05). In mice, M101 reduced the clinical abscess size (50.2%) in P. gingivalis-induced calvarial lesion concomitant with a decreased inflammatory score evaluated through histomorphometric analysis, thus, improving soft tissue and bone healing response. Therefore, M101 may be a novel therapeutic agent that could be beneficial in the management of P. gingivalis associated diseases.

scholarly journals Modulatory Effects of Osthole on Lipopolysaccharides-Induced Inflammation in Caco-2 Cell Monolayer and Co-Cultures with THP-1 and THP-1-Derived Macrophages

Nutrients ◽  
2020 ◽  
Vol 13 (1) ◽  
pp. 123
Author(s):  
Natalia K. Kordulewska ◽  
Justyna Topa ◽  
Małgorzata Tańska ◽  
Anna Cieślińska ◽  
Ewa Fiedorowicz ◽  
...  
Keyword(s):  
Gene Expression ◽  
Inflammatory Reaction ◽  
Wide Spectrum ◽  
Cell Monolayer ◽  
In Vivo Studies ◽  
Dependent Manner ◽  
Concentration Dependent Manner ◽  
Tnf Α

Lipopolysaccharydes (LPS) are responsible for the intestinal inflammatory reaction, as they may disrupt tight junctions and induce cytokines (CKs) secretion. Osthole has a wide spectrum of pharmacological effects, thus its anti-inflammatory potential in the LPS-treated Caco-2 cell line as well as in Caco-2/THP-1 and Caco-2/macrophages co-cultures was investigated. In brief, Caco-2 cells and co-cultures were incubated with LPS to induce an inflammatory reaction, after which osthole (150–450 ng/mL) was applied to reduce this effect. After 24 h, the level of secreted CKs and changes in gene expression were examined. LPS significantly increased the levels of IL-1β, -6, -8, and TNF-α, while osthole reduced this effect in a concentration-dependent manner, with the most significant decrease when a 450 ng/mL dose was applied (p < 0.0001). A similar trend was observed in changes in gene expression, with the significant osthole efficiency at a concentration of 450 ng/μL for IL1R1 and COX-2 (p < 0.01) and 300 ng/μL for NF-κB (p < 0.001). Osthole increased Caco-2 monolayer permeability, thus if it would ever be considered as a potential drug for minimizing intestinal inflammatory symptoms, its safety should be confirmed in extended in vitro and in vivo studies.

scholarly journals LPS-induced expression of CD14 in the TRIF pathway is epigenetically regulated by sulforaphane in porcine pulmonary alveolar macrophages

2016 ◽  
Vol 22 (8) ◽  
pp. 682-695 ◽  
Author(s):  
Qin Yang ◽  
Maren J Pröll ◽  
Dessie Salilew-Wondim ◽  
Rui Zhang ◽  
Dawit Tesfaye ◽  
...  
Keyword(s):  
Gene Expression ◽  
Alveolar Macrophages ◽  
Methylation Status ◽  
Gene Body ◽  
Gene Body Methylation ◽  
Tnf Α ◽  
Pulmonary Alveolar Macrophages ◽  
Cluster Of Differentiation ◽  
Cd14 Gene

Pulmonary alveolar macrophages (AMs) are important in defense against bacterial lung inflammation. Cluster of differentiation 14 (CD14) is involved in recognizing bacterial lipopolysaccharide (LPS) through MyD88-dependent and TRIF pathways of innate immunity. Sulforaphane (SFN) shows anti-inflammatory activity and suppresses DNA methylation. To identify CD14 epigenetic changes by SFN in the LPS-induced TRIF pathway, an AMs model was investigated in vitro. CD14 gene expression was induced by 5 µg/ml LPS at the time point of 12 h and suppressed by 5 µM SFN. After 12 h of LPS stimulation, gene expression was significantly up-regulated, including TRIF, TRAF6, NF-κB, TRAF3, IRF7, TNF-α, IL-1β, IL-6, and IFN-β. LPS-induced TRAM, TRIF, RIPK1, TRAF3, TNF-α, IL-1β and IFN-β were suppressed by 5 µM SFN. Similarly, DNMT3a expression was increased by LPS but significantly down-regulated by 5 µM SFN. It showed positive correlation of CD14 gene body methylation with in LPS-stimulated AMs, and this methylation status was inhibited by SFN. This study suggests that SFN suppresses CD14 activation in bacterial inflammation through epigenetic regulation of CD14 gene body methylation associated with DNMT3a. The results provide insights into SFN-mediated epigenetic down-regulation of CD14 in LPS-induced TRIF pathway inflammation and may lead to new methods for controlling LPS-induced inflammation in pigs.

scholarly journals Febrile-range temperature modifies cytokine gene expression in LPS-stimulated macrophages by differentially modifying NF-κB recruitment to cytokine gene promoters

2010 ◽  
Vol 298 (1) ◽  
pp. C171-C181 ◽  
Author(s):  
Zachary A. Cooper ◽  
Arundhati Ghosh ◽  
Aditi Gupta ◽  
Tapan Maity ◽  
Ivor J. Benjamin ◽  
...  
Keyword(s):  
Gene Expression ◽  
Receptor Activation ◽  
Cytokine Gene Expression ◽  
Raw 264.7 Cells ◽  
Raw 264.7 ◽  
Heat Shock Factor 1 ◽  
Gene Promoters ◽  
Cytokine Gene ◽  
Tnf Α

We previously showed that exposure to febrile-range temperatures (FRT, 39.5–40°C) reduces LPS-induced TNF-α expression, in part through the direct interaction of heat shock factor-1 (HSF1) with the TNF-α gene promoter. However, it is not known whether exposure to FRT also modifies more proximal LPS-induced signaling events. Using HSF1-null mice, we confirmed that HSF1 is required for FRT-induced repression of TNF-α in vitro by LPS-stimulated bone marrow-derived macrophages and in vivo in mice challenged intratracheally with LPS. Exposing LPS-stimulated RAW 264.7 mouse macrophages to FRT reduced TNF-α expression while increasing IL-1β expression despite the two genes sharing a common myeloid differentiation protein-88 (MyD88)-dependent pathway. Global activation of the three LPS-induced signaling intermediates that lead to cytokine gene expression, ERK and p38 MAPKs and NF-κB, was not affected by exposing RAW 264.7 cells to FRT as assessed by ERK and p38 phosphorylation and NF-κB in vitro DNA-binding activity and activation of a NF-κB-dependent synthetic promoter. However, chromatin immunoprecipitation (ChIP) analysis demonstrated that exposure to FRT reduced LPS-induced recruitment of NF-κB p65 to the TNF-α promoter while simultaneously increasing its recruitment to the IL-1β promoter. These data suggest that FRT exerts its effects on cytokine gene expression in a gene-specific manner through distal effects on promoter activation rather than proximal receptor activation and signal transduction.

Determinants of leptin gene expression in fat depots of lean mice

2002 ◽  
Vol 282 (1) ◽  
pp. R226-R234 ◽  
Author(s):  
Yiying Zhang ◽  
Kai-Ying Guo ◽  
Patricia A. Diaz ◽  
Moonseong Heo ◽  
Rudolph L. Leibel
Keyword(s):  
Gene Expression ◽  
Glucocorticoid Receptor ◽  
Insulin Receptor ◽  
Physiological Role ◽  
Mrna Levels ◽  
Strongly Correlated ◽  
Fat Depots ◽  
Tnf Α ◽  
Adipocyte Volume

The relationship of leptin gene expression to adipocyte volume was investigated in lean 10-wk-old male C57BL/6J mice. mRNA levels for leptin, insulin receptor, glucocorticoid receptor, and tumor necrosis factor (TNF)-α in inguinal, epididymal, and retroperitoneal adipose tissues were quantified and related to adipocyte volume. Leptin mRNA levels were highly correlated with adipocyte volume within each fat depot. Multiple regression analysis of pooled data from the three depots showed that leptin mRNA levels were strongly correlated with adipocyte volumes (β = 0.84, P < 0.001) and, to a smaller degree, with glucocorticoid receptor mRNA levels (β = 0.36, P < 0.001). Depot of origin had no effect ( P > 0.9). Rates of leptin secretion in vitro were strongly correlated with leptin mRNA levels ( r = 0.89, P < 0.001). mRNA levels for TNF-α, insulin receptor, and glucocorticoid receptor showed no significant correlation with adipocyte volume. These results demonstrate that depot-specific differences in leptin gene expression are mainly related to the volumes of the constituent adipocytes. The strong correlation between leptin gene expression and adipocyte volume supports leptin's physiological role as a humoral signal of fat mass.

Cell-specific posttranscriptional regulation of CFTR gene expression via influence of MAPK cascades on 3′UTR part of transcripts

2005 ◽  
Vol 289 (5) ◽  
pp. C1240-C1250 ◽  
Author(s):  
Maryvonne Baudouin-Legros ◽  
Alexandre Hinzpeter ◽  
Amandine Jaulmes ◽  
Franck Brouillard ◽  
Bruno Costes ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Lines ◽  
Posttranscriptional Regulation ◽  
P38 Map Kinase ◽  
Cftr Gene ◽  
Control Of Gene Expression ◽  
Cytosolic Proteins ◽  
Tnf Α ◽  
Ht 29

Expression of the cystic fibrosis (CF) transmembrane conductance regulator (CFTR) gene, which contains the mutations responsible for CF, is regulated by cytokines (TNF-α and IL-1β) in a cell-specific manner. TNF-α decreases CFTR mRNA in human colon cell lines (HT-29), but not in pulmonary cell lines (Calu-3), and IL-1β increases it only in Calu-3 cells. We looked for the cytokine-induced posttranscriptional regulation of CFTR gene expression and studied the modulation of CFTR mRNA stability linked to its 3′ untranslated sequence (3′UTR) in HT-29 and Calu-3 cells. The stability of CFTR mRNA was analyzed by Northern blot after in vitro incubation of total RNAs from CFTR-expressing cells with cytosolic proteins extracted from control or cytokine-treated HT-29 and Calu-3 cells. CFTR mRNA was degraded only by extracts of TNF-α-treated HT-29 cells and not by cytosolic proteins from untreated or IL-1β-treated HT-29 cells. In contrast, extracts of untreated Calu-3 cells enhanced CFTR mRNA degradation, and IL-1β treatment inhibited this; TNF-α had no significant effect. The 3′UTR part of CFTR mRNA was found to be required for this posttranscriptional regulation. The 5′ part of the 3′UTR (the 217 first bases), which contains two AUUUA sequences, was implicated in CFTR mRNA destabilization and the following 136 bases, containing several C-repeats in U-rich environment, in its protection. The proteins, which reacted with the U- and C-repeats of CFTR mRNA 3′UTR, were mainly controlled by stimulation of the p42/p44 and p38 MAP kinase cascades with interaction between these pathways. This posttranscriptional control of gene expression is a common feature of CFTR and many proteins of inflammation.

Anti Human CX3CR1 VHH Molecule Attenuates Venous Neointimal Hyperplasia of Arteriovenous Fistula in Mouse Model

2021 ◽  
pp. ASN.2020101458
Author(s):  
Sanjay Misra ◽  
Sreenivasulu Kilari ◽  
Binxia Yang ◽  
Amit Sharma ◽  
Chih-Cheng Wu ◽  
...  
Keyword(s):  
Gene Expression ◽  
Arteriovenous Fistula ◽  
Neointimal Hyperplasia ◽  
Rna Seq ◽  
Humanized Mouse ◽  
Fractalkine Receptor ◽  
Tnf Α ◽  
And Migration ◽  
Proliferation And Migration

BackgroundFractalkine receptor 1 (CX3CR1) mediates macrophage infiltration and accumulation, causing venous neointimal hyperplasia (VNH)/venous stenosis (VS) in arteriovenous fistula (AVF). The effect of blocking CX3CR1 using an anti–human variable VHH molecule (hCX3CR1 VHH, BI 655088) on VNH/VS was determined using a humanized mouse in which the human CX3CR1 (hCX3CR1) gene was knocked in (KI).MethodsWhole-transcriptomic RNA sequencing with bioinformatics analysis was used on human stenotic AVF samples, C57BL/6J, hCX3CR1 KI mice with AVF and CKD, and in in vitro experiments to identify the pathways involved in preventing VNH/VS formation after hCX3CR1 VHH administration.ResultsAccumulation of CX3CR1 and CD68 was significantly increased in stenotic human AVFs. In C57BL/6J mice with AVF, there was increased Cx3cr1, Cx3cl1, Cd68, and Tnf-α gene expression, and increased immunostaining of CX3CR1 and CD68. In hCX3CR1-KI mice treated with hCX3CR1 VHH molecule (KI-A), compared with vehicle controls (KI-V), there was increased lumen vessel area and patency, and decreased neointima in the AVF outflow veins. RNA-seq analysis identified TNF-α and NF-κB as potential targets of CX3CR1 inhibition. In KI-A–treated vessels compared with KI-V, there was decreased gene expression of Tnf-α, Mcp-1, and Il-1β; with reduction of Cx3cl1, NF-κB, and Cd68; decreased M1, Ly6C, smooth muscle cells, fibroblast-activated protein, fibronectin, and proliferation; and increased TUNEL and M2 staining. In cell culture, monocytes stimulated with PMA and treated with hCX3CR1 VHH had decreased TNF-α, CD68, proliferation, and migration.ConclusionsCX3CR1 blockade reduces VNH/VS formation by decreasing proinflammatory cues.

P3112The oral administration of colchicine prevents the progression of aortic aneurysm

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
H Okawa ◽  
A Yamawaki-Ogata ◽  
Y Narita ◽  
H Munakata ◽  
R Hashizume ◽  
...  
Keyword(s):  
Gene Expression ◽  
Aortic Aneurysm ◽  
Oral Administration ◽  
Inflammatory Cytokines ◽  
Nlrp3 Inflammasome ◽  
Aortic Aneurysms ◽  
Aortic Diameter ◽  
Tnf Α

Abstract Objective The pathogenesis of aortic aneurysm (AA) is characterized by the chronic inflammation of the aortic wall with the accumulation of macrophages and the degradation of the extracellular matrix (ECM) including elastin. Colchicine (COL) is an alkaloid derived from the plant Lily family Colchicum autumnale, and it is known for anti-inflammatory effects. Plant extracts containing COL have been used in the treatment of gout from ancient period. Currently, pseudogout, familial Mediterranean fever, Behçet's disease and pericarditis are also treated by COL. Furthermore, recent evidence suggests the use of COL for secondary prevention of cardiovascular disease, and the phase 3 clinical trial for it has begun. The objective of this study is to investigate whether COL could prevent the progression of aortic aneurysms. Methods In vitro: Macrophages (J774A.1 cell line) stimulated TNF-α 24 hours before and smooth muscle cell (SMC) were cultured with 10 ng/mL COL, and the gene expression of inflammatory cytokines involved in the AA formation was measured 24 hours later. In vivo: Male apolipoprotein E-deficient mice (30–35 weeks of age) were infused with angiotensin II for 28 days. COL (20 μg/kg/d) or saline (NS, as a control) was administered orally to the mice every day (COL group, n=8; NS group, n=8). Aortic diameter was measured by echography every week and all mice were sacrificed and their thoracoabdominal aorta was harvested at the last day of the administration period and elastin content, MMP activitis, and levels of inflammatory cytokines involved in the AA formation were measured. Results In vitro: The gene expression of IL-1β, TNF-α, MCP-1, NF-κB, MMP-9 in the macrophages was significantly decreased in the COL group. The gene expression of Lox, TIMP-2 in the SMC were significantly increased in COL group. In vivo: Aortic diameter measured by echography every week was significantly suppressed in the COL group (2.25 vs 2.81 mm, p<0.05). The incidence of AA was decreased in the COL group (62.5% vs 100%). COL significantly suppressed the degeneration of aortic elastin in EVG staining (p<0.05). There is no significant difference in the enzyme activities of MMP-2 and MMP-9 between COL and NS groups, but IL-1β (54.4 vs 81.4, p<0.05), TNF-α (31.0 vs 60.6, p<0.05), MCP-1 (258.2 vs 411.2, p<0.05), NLRP3 inflammasome (7.1 vs 8.6, p<0.05), NE (1.5 vs 2.4, p<0.05), MPO (44.9 vs 48.1, p<0.05) were decreased in the COL group. Discussion In AA model mice, COL seems to suppress the progression of AA by anti-infammation and preservation of the ECM structure through the inhibition of NLRP3 inflammasome. That NLRP3 inflammasome activation leads to the progression of AA in AA model mice was previously reported and this supports out results. Methods and Results (in vivo) Conclusions This results suggest that the oral administration of COL prevents the progression of AA in AA model mice and it is expected as a novel therapeutic agent for AA. Acknowledgement/Funding JSPS KAKENHI Grant

scholarly journals Cytokine-Sensitive Replication of Hepatitis B Virus in Immortalized Mouse Hepatocyte Cultures

2002 ◽  
Vol 76 (11) ◽  
pp. 5646-5653 ◽  
Author(s):  
Valérie Pasquetto ◽  
Stefan F. Wieland ◽  
Susan L. Uprichard ◽  
Marco Tripodi ◽  
Francis V. Chisari
Keyword(s):  
Gene Expression ◽  
Hepatitis B Virus ◽  
Hepatitis B ◽  
Intracellular Signaling ◽  
Growth Factor Receptor ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
B Virus ◽  
Ifn Γ

ABSTRACT We have previously shown that alpha/beta interferon (IFN-α/β) and gamma interferon (IFN-γ) inhibit hepatitis B virus (HBV) replication by eliminating pregenomic RNA containing viral capsids from the hepatocyte. We have also shown that HBV-specific cytotoxic T lymphocytes that induce IFN-γ and tumor necrosis factor alpha (TNF-α) in the liver can inhibit HBV gene expression by destabilizing preformed viral mRNA. In order to further study the antiviral activity of IFN-α/β, IFN-γ, and TNF-α at the molecular level, we sought to reproduce these observations in an in vitro system. Accordingly, hepatocytes were derived from the livers of HBV-transgenic mice that also expressed the constitutively active cytoplasmic domain of the human hepatocyte growth factor receptor (c-Met). Here, we show that the resultant well-differentiated, continuous hepatocyte cell lines (HBV-Met) replicate HBV and that viral replication in these cells is efficiently controlled by IFN-α/β or IFN-γ, which eliminate pregenomic RNA-containing capsids from the cells as they do in the liver. Furthermore, we demonstrate that IFN-γ, but not IFN-α/β, is capable of inhibiting HBV gene expression in this system, especially when it acts synergistically with TNF-α. These cells should facilitate the analysis of the intracellular signaling pathways and effector mechanisms responsible for these antiviral effects.

scholarly journals Effects of 17β-Estradiol on Monocyte/Macrophage Response to Staphylococcus aureus: An In Vitro Study

2021 ◽  
Vol 11 ◽  
Author(s):  
Clarissa Leal Silva e Souza ◽  
Camila Dutra Barbosa ◽  
Hanna I. L. N. Coelho ◽  
Manoel N. Santos Júnior ◽  
Elaine Novaes Barbosa ◽  
...  
Keyword(s):  
Gene Expression ◽  
Peripheral Blood ◽  
Bacterial Infections ◽  
Human Peripheral Blood ◽  
Blood Monocytes ◽  
Childbearing Age ◽  
Macrophage Response ◽  
Tnf Α ◽  
17Β Estradiol

To describe how 17β-estradiol (E2) influence in the monocyte/macrophage response induced by S. aureus in in vitro models of murine peritoneal macrophages (MPMs) and human peripheral blood monocytes (HPBM). MPMs (2 x 105/ml) were isolated from sham (n=3) and ovariectomized (OVX) females (n = 3) and males (n = 3) after induction by thioglycolate. The MPMs obtained from OVX females and males were treated for 24 hours with 17β-estradiol (E2) (10-7 M), and after that, inoculation with S. aureus was carried out for 6 hours. The macrophages were collected and destined to evaluate the relative gene expression of TNF-α, IL-1β, IL-6, IL-8 and TLR2. For the in vitro model of HPBMs, six men and six women of childbearing age were selected and HPBMs were isolated from samples of the volunteers’ peripheral blood. In women, blood was collected both during menstruation and in the periovulatory period. HPBMs were inoculated with S. aureus for 6 hours and the supernatant was collected for analysis of cytokines by Luminex and the HPBMs were removed for analysis of 84 genes involved in the host’s response to bacterial infections by RT-PCR array. Previous treatment with E2 decreased the gene expression and production of proinflammatory cytokines, such as TNF-α, IL-1β and IL-6 and decreased the expression of TLR2 tanto em MPMs quanto em HPBMs. The analysis of gene expression shows that E2 inhibited the NFκB pathway. It is suggested that 17β-estradiol acts as an immunoprotective in the monocyte/macrophage response induced by S. aureus.

scholarly journals Antibacterial, Immunomodulatory, and Lung Protective Effects of Boswelliadalzielii Oleoresin Ethanol Extract in Pulmonary Diseases: In Vitro and In Vivo Studies

Antibiotics ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1444
Author(s):  
Badriyah Alotaibi ◽  
Walaa A. Negm ◽  
Engy Elekhnawy ◽  
Thanaa A. El-Masry ◽  
Walaa S. Elseady ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Line ◽  
Ethanol Extract ◽  
Lung Damage ◽  
Pulmonary Diseases ◽  
Human Skin Fibroblast ◽  
Tnf Α ◽  
Cox 2

Lung diseases such as asthma, chronic obstructive pulmonary diseases, and pneumonia are causing many global health problems. The COVID-19 pandemic has directed the scientific community’s attention toward performing more research to explore novel therapeutic drugs for pulmonary diseases. Herein, gas chromatography coupled with mass spectrometry tentatively identified 44 compounds in frankincense ethanol extract (FEE). We investigated the antibacterial and antibiofilm effects of FEE against Pseudomonas aeruginosa bacteria, isolated from patients with respiratory infections. In addition, its in vitro immunomodulatory activity was explored by the detection of the gene expression of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), nitric oxide synthase (iNOS), cycloxygenase-2 (COX-2), and nuclear factor kappa-B (NF-κB) in lipopolysaccharide (LPS)-induced peripheral blood mononuclear cells (PBMC). In addition, its anticancer activity against the A549 lung cancer cell line and human skin fibroblast (HSF) normal cell line was studied. Moreover, the in vivo lung protective potential of FEE was explored histologically and immunohistochemically in mice using a benzo(a)pyrene induced lung damage model. FEE exhibited antibacterial and antibiofilm activities besides the significant inhibition of gene expression of TNFα, IL-6, and NF-κB. FEE also exerted a cytotoxic effect against A549 cell line. Histological and immunohistochemical investigations with morphometric analysis of the mean area percentage and color intensity of positive TNF-α, COX-2, and NF-κB and Bcl-2 reactions revealed the lung protective activity of FEE. This study outlined the promising therapeutic activity of oleoresin obtained from B. dalzielii in the treatment of different pulmonary diseases.

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