Agmatine Ameliorates Nicotine Induced Lung Injury in Rats through Decrease TGF-ß1 and Bax Immunoexpression and by Anti-oxidative Sress Pathway: Histological, Immunohistochemical and Biochemical Study

Attia, Ghalia M.; Nader, Manar A.; Elmansy, Rasha A.; Elsaed, Wael M.

doi:10.4172/2157-7099.1000458

J Cytol Histol

2017

DOI: 10.4172/2157-7099.1000458

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Agmatine Ameliorates Nicotine Induced Lung Injury in Rats through Decrease TGF-ß1 and Bax Immunoexpression and by Anti-oxidative Sress Pathway: Histological, Immunohistochemical and Biochemical Study

Ghalia M. Attia¹,

Manar A. Nader²,

Rasha A. Elmansy³

et al.

Abstract: Introduction: Nicotine (NIC), the chief alkaloid in tobacco, believed to be an active agent responsible for lungassociated diseases. This protocol targeted to analyze the ameliorating effect of agmatine (AG) on NIC induced lung damage.

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2024

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References 66 publications

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Alleviation of pulmonary fibrosis by the dual PPAR agonist saroglitazar and breast milk mesenchymal stem cells via modulating TGFß/SMAD pathway

Attia,

Saadawy,

El-Mahroky

et al. 2024

Naunyn-Schmiedeberg's Arch Pharmacol

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Pulmonary fibrosis (PF) is a complex disorder with high morbidity and mortality. Limited efficacies of the available drugs drive researchers to seek for new therapies. Saroglitazar (Saro), a full (PPAR α/γ) agonist, is devoid of known PPAR-mediated adverse effects. Breast milk mesenchymal stem cells (BrMSCs) are contemplated to be the ideal cell type harboring differentiation/anti-inflammatory/immunosuppressive properties. Accordingly, our aims were to investigate the potential roles of Saro and/or BrMSCs in PF and to spot their underlying protective mechanisms. In this study, PF was induced by bleomycin (BLM) via intratracheal instillation. Treatment started 14 days later. Animals were treated with oral saroglitazar (3 mg/kg daily) or intraperitoneal single BrMSCs injection (0.5 ml phosphate buffer saline (PBS) containing 2 × 107 cells) or their combination with same previous doses. At the work end, 24 h following the 6 weeks of treatment period, the levels of oxidative (MDA, SOD), inflammatory (IL-1ß, IL-10), and profibrotic markers (TGF-ß, αSMA) were assessed. The autophagy-related genes (LC3, Beclin) and the expression of PPAR-α/γ and SMAD-3/7 were evaluated. Furthermore, immunohistochemical and histological work were evaluated. Our study revealed marked lung injury influenced by BLM with severe oxidative/inflammatory/fibrotic damage, autophagy inhibition, and deteriorated lung histology. Saro and BrMSCs repaired the lung structure worsened by BLM. Treatments greatly declined the oxidative/inflammatory markers. The pro-fibrotic TGF-ß, αSMA, and SMAD-3 were decreased. Contrarily, autophagy markers were increased. SMAD-7 and PPAR α/γ were activated denoting their pivotal antifibrotic roles. Co-administration of Saro and BrMSCs revealed the top results. Our findings support the study hypothesis that Saro and BrMSCs can be proposed as potential treatments for IPF.

show abstract

Alleviation of pulmonary fibrosis by the dual PPAR agonist saroglitazar and breast milk mesenchymal stem cells via modulating TGFß/SMAD pathway

Attia,

Saadawy,

El-Mahroky

et al. 2024

Naunyn-Schmiedeberg's Arch Pharmacol

View full text Add to dashboard Cite

show abstract

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Agmatine Ameliorates Nicotine Induced Lung Injury in Rats through Decrease TGF-ß1 and Bax Immunoexpression and by Anti-oxidative Sress Pathway: Histological, Immunohistochemical and Biochemical Study

Abstract: Introduction: Nicotine (NIC), the chief alkaloid in tobacco, believed to be an active agent responsible for lungassociated diseases. This protocol targeted to analyze the ameliorating effect of agmatine (AG) on NIC induced lung damage.

Cited by 1 publication

References 66 publications

Alleviation of pulmonary fibrosis by the dual PPAR agonist saroglitazar and breast milk mesenchymal stem cells via modulating TGFß/SMAD pathway

Alleviation of pulmonary fibrosis by the dual PPAR agonist saroglitazar and breast milk mesenchymal stem cells via modulating TGFß/SMAD pathway

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