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 StudyGhalia M Attia1,2, Manar Ahmed Nader3,4, Rasha A Elmansy5,6 and Wael M Elsaed1,7*
- *Corresponding Author:
- Elased MW
Department of Anatomy, Faculty of Medicine
Taibah University, Al Madina Al Monawarrah
Kingdom of Saudi Arabia
E-mail: [email protected]
Received Date: May 18, 2017; Accepted Date: June 20, 2017; Published Date: June 29, 2017
Citation: Attia GM, Nader MA, Elmansy RA, Elsaed WM (2017) 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. J Cytol Histol 8: 458. doi: 10.4172/2157-7099.1000458
Copyright: © 2017 Attia GM, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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. Mateiral and methods: Forty-five adult male rats were divided into: Control group received intraperitoneal (IP) injection of distilled water, 2) NIC group recieved NIC (10 mg/kg/day) IP and 3) (NIC+AG) group treated by AG (10 mg/kg/day) orally+NIC (10 mg/kg/day) by IP injection for 9 weeks. Total serum protein, triglycerides (TGs), total cholesterol (TC), high density lipoprotein (HDL), Low density lipoprotein cholesterol (LDL-C), malondialdehyde (MDA), superoxide dismutase (SOD), reduced glutathione (GSH) and vascular cell adhesion molecule 1 (VCAM- 1) were estimated. Lung specimens were prepared and stained with H&E, Masson trichrome and immunehistochemical stains for assessment of transforming growth factor beta 1 (TGF-β1) and Bax. Morphometric study followed by statistical analysis were done. Results: NIC group showed elevation in serum levels of total protein, TC, LDL-C, TGs, MDA and VCAM-1 with evident diminishing in the serum levels of HDL-C, SOD, and GSH. Apoptosis and damage of alveolar epithelium and bronchiolar cells, marked fibrosis, inflammatory cell infiltrate and congestion of blood vessels were observed. Marked increase in the mean alveolar wall thickness, mean area% of collagen fibers deposition, mean area% of TGFβ1 immuno-expression and mean number of Bax immune positive cells while a decrease in the mean linear intercept were detected. AG co-administered with nicotine ameliorated these biochemical, histopathological and morphometric changes. Conclusion: AG ameliorates NIC induced lung damage in rats through improving the biochemical parameters and by decreasing TGF-ß1 and Bax immunoexpression.