Abstract
Here we investigate the effects of the green tea extract in an animal model of acute inflammation, carrageenan-induced pleurisy. We report here that green tea extract (given at 25 mg/kg i.p. bolus 1 h prior to carrageenan), exerts potent anti-inflammatory effects in an animal model of acute inflammation in vivo.Injection of carrageenan (2%) into the pleural cavity of mice elicited an acute inflammatory response characterized by fluid accumulation in the pleural cavity that contained many neutrophils (PMNs), an infiltration of PMNs in lung tissues and increased production of nitrite/nitrate, tumour necrosis factor alpha. All parameters of inflammation were attenuated by green tea extract treatment. Furthermore, carrageenan induced an up-regulation of the adhesion molecule ICAM-1, as well as nitrotyrosine and poly (ADP-ribose) synthetase (PARS) formation, as determined by immunohistochemical analysis of lung tissues. Staining for the ICAM-1, nitrotyrosine, and PARS was reduced by green tea extract.Our results clearly demonstrate that treatment with green tea extract exerts a protective effect and offers a novel therapeutic approach for the management of lung injury.
Highlights
The role of oxyradical formation in various forms of inflammation is well established [1] Reactive oxygen species (ROS) are associated with the inflammatory response and frequently they contribute to the tissue damaging effects of inflammatory reactions [2,3,4]
We have investigated the effect of the green tea on: pleural cavity that contained many neutrophils (PMNs) infiltration [myeloperoxidase (MPO) activity]; Signal transducers and activators of transcription (STAT)-1 activity, up-regulation of ICAM-1; the nitration of tyrosine residues and lung damage
When compared with lung sections taken from saline-treated animals (Fig. 1A), histological examination of lung sections of mice treated with carrageenan showed oedema, tissue injury (Fig 1B), and infiltration of the tissue with neutrophils (PMNs) (Fig. 1B1)
Summary
The role of oxyradical formation in various forms of inflammation is well established [1] Reactive oxygen species (ROS) are associated with the inflammatory response and frequently they contribute to the tissue damaging effects of inflammatory reactions [2,3,4]. Certain levels of ROS are required for normal cell functions, but if in surplus, they will cause oxidative stress [5,6,7]. Peroxynitrite, a cytotoxic oxidant species formed from the reaction of NO and superoxide [13], may mediate part of the oxidative injury associated with simultaneous production of NO and oxyradicals. It has been established that antioxidants such as glutathione, ascorbic acid, and alpha-tocopherol are scavengers of peroxynitrite and inhibitors of its oxidant capacity [17,18]
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