Gallic acid protects against the COPD-linked lung inflammation and emphysema in mice.

Singla, E; Dharwal, V; Naura, AS

Gallic acid protects against the COPD-linked lung inflammation and emphysema in mice.

Singla, E Dharwal, V

Naura, AS

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Publisher:: SPRINGER BASEL AG
Publication Type:: Journal Article
Citation:: Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020, 69, (4), pp. 423-434
Issue Date:: 2020-04

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Field	Value	Language
dc.contributor.author	Singla, E
dc.contributor.author	Dharwal, V https://orcid.org/0000-0002-9645-3797
dc.contributor.author	Naura, AS
dc.date.accessioned	2021-02-04T02:21:34Z
dc.date.available	2020-02-26
dc.date.available	2021-02-04T02:21:34Z
dc.date.issued	2020-04
dc.identifier.citation	Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2020, 69, (4), pp. 423-434
dc.identifier.issn	1023-3830
dc.identifier.issn	1420-908X
dc.identifier.uri	http://hdl.handle.net/10453/145802
dc.description.abstract	<h4>Objective and design</h4>Gallic acid (GA) a naturally occurring phenolic compound, known to possess antioxidant/anti-inflammatory activities. The aim of the present work was to investigate the beneficial effects of GA against COPD-linked lung inflammation/emphysema by utilizing elastase (ET) and cigarette smoke (CS)-induced mice model.<h4>Materials</h4>Male BALB/c mice were treated with ET (1U/mouse) or exposed to CS (9 cigarettes/day for 4 days). GA administration was started 7 days (daily) prior to ET/CS exposure. Broncho-alveolar lavage was analyzed for inflammatory cells and pro-inflammatory cytokines. Lung homogenate was assessed for MPO activity/GSH/MDA/protein carbonyls. Further, Lung tissue was subjected to semi-quantitative RT-PCR, immunoblotting, and histological analysis.<h4>Results</h4>GA suppressed the ET-induced neutrophil infiltration, elevated MPO activity and production of pro-inflammatory cytokines (IL-6/TNF-α/IL-1β) at 24 h. Reduced inflammation was accompanied with normalization of redox balance as reflected by ROS/GSH/MDA/protein carbonyl levels. Further, GA suppressed phosphorylation of p65NF-κB and IκBα along with down-regulation of IL-1β/TNF-α/KC/MIP-2/GCSF genes. Furthermore, GA offered protection against ET-induced airspace enlargement and ameliorated MMP-2/MMP-9. Finally, GA suppressed the CS-induced influx of neutrophils and macrophages and blunted gene expression of TNF-α/MIP-2/KC.<h4>Conclusion</h4>Overall, our data show that GA effectively modulates pulmonary inflammation and emphysema associated with COPD pathogenesis in mice.
dc.format	Print-Electronic
dc.language	eng
dc.publisher	SPRINGER BASEL AG
dc.relation.ispartof	Inflammation research : official journal of the European Histamine Research Society ... [et al.]
dc.relation.isbasedon	10.1007/s00011-020-01333-1
dc.rights	info:eu-repo/semantics/restrictedAccess
dc.subject	1103 Clinical Sciences
dc.subject.classification	Immunology
dc.subject.mesh	Lung
dc.subject.mesh	Bronchoalveolar Lavage Fluid
dc.subject.mesh	Animals
dc.subject.mesh	Mice, Inbred BALB C
dc.subject.mesh	Tobacco
dc.subject.mesh	Pulmonary Disease, Chronic Obstructive
dc.subject.mesh	Emphysema
dc.subject.mesh	Gallic Acid
dc.subject.mesh	Pancreatic Elastase
dc.subject.mesh	NF-kappa B
dc.subject.mesh	Tissue Inhibitor of Metalloproteinase-1
dc.subject.mesh	Anti-Inflammatory Agents
dc.subject.mesh	Cytokines
dc.subject.mesh	Smoke
dc.subject.mesh	Male
dc.subject.mesh	Matrix Metalloproteinase 2
dc.subject.mesh	Matrix Metalloproteinase 9
dc.subject.mesh	Animals
dc.subject.mesh	Anti-Inflammatory Agents
dc.subject.mesh	Bronchoalveolar Lavage Fluid
dc.subject.mesh	Cytokines
dc.subject.mesh	Emphysema
dc.subject.mesh	Gallic Acid
dc.subject.mesh	Lung
dc.subject.mesh	Male
dc.subject.mesh	Matrix Metalloproteinase 2
dc.subject.mesh	Matrix Metalloproteinase 9
dc.subject.mesh	Mice, Inbred BALB C
dc.subject.mesh	NF-kappa B
dc.subject.mesh	Pancreatic Elastase
dc.subject.mesh	Pulmonary Disease, Chronic Obstructive
dc.subject.mesh	Smoke
dc.subject.mesh	Tissue Inhibitor of Metalloproteinase-1
dc.subject.mesh	Tobacco
dc.title	Gallic acid protects against the COPD-linked lung inflammation and emphysema in mice.
dc.type	Journal Article
utslib.citation.volume	69
utslib.location.activity	Switzerland
utslib.for	1103 Clinical Sciences
pubs.organisational-group	/University of Technology Sydney/Faculty of Science
pubs.organisational-group	/University of Technology Sydney
utslib.copyright.status	closed_access	*
dc.date.updated	2021-02-04T02:21:28Z
pubs.issue	4
pubs.publication-status	Published
pubs.volume	69
utslib.citation.issue	4

Abstract:

Objective and design

Gallic acid (GA) a naturally occurring phenolic compound, known to possess antioxidant/anti-inflammatory activities. The aim of the present work was to investigate the beneficial effects of GA against COPD-linked lung inflammation/emphysema by utilizing elastase (ET) and cigarette smoke (CS)-induced mice model.

Materials

Male BALB/c mice were treated with ET (1U/mouse) or exposed to CS (9 cigarettes/day for 4 days). GA administration was started 7 days (daily) prior to ET/CS exposure. Broncho-alveolar lavage was analyzed for inflammatory cells and pro-inflammatory cytokines. Lung homogenate was assessed for MPO activity/GSH/MDA/protein carbonyls. Further, Lung tissue was subjected to semi-quantitative RT-PCR, immunoblotting, and histological analysis.

Results

GA suppressed the ET-induced neutrophil infiltration, elevated MPO activity and production of pro-inflammatory cytokines (IL-6/TNF-α/IL-1β) at 24 h. Reduced inflammation was accompanied with normalization of redox balance as reflected by ROS/GSH/MDA/protein carbonyl levels. Further, GA suppressed phosphorylation of p65NF-κB and IκBα along with down-regulation of IL-1β/TNF-α/KC/MIP-2/GCSF genes. Furthermore, GA offered protection against ET-induced airspace enlargement and ameliorated MMP-2/MMP-9. Finally, GA suppressed the CS-induced influx of neutrophils and macrophages and blunted gene expression of TNF-α/MIP-2/KC.

Conclusion

Overall, our data show that GA effectively modulates pulmonary inflammation and emphysema associated with COPD pathogenesis in mice.

Please use this identifier to cite or link to this item:

http://hdl.handle.net/10453/145802