Aida Abdeen Mahmoud1, Hekmat Osman Abdel-Aziz2, Mohamed Elbadr3, Hala Elbadre4. 1. Department of Medical Biochemistry, Faculty of Medicine, Sohag University, Egypt. 2. Department of Medical Histology, Sohag University, Egypt and of. 3. Department of Medical Pharmacology, Faculty of Medicine, Assiut University, Egypt. 4. Department of Medical Biochemistry, Faculty of Medicine, Assiut University, Egypt.
Abstract
BACKGROUND: Tobacco use is responsible for millions of preventable deaths due to cancer. Nicotine, an alkaloid chemical found in tobacco was proved to cause chronic inflammation and oxidative stress. The transcription factor STAT1 induces the expression of many proinflammatory genes and has been suggested to be a target for anti-inflammatory therapeutics. The following study investigated the effect of Nicotine on STAT1 pathway and oxidative stress in rat lung tissue. METHODS: Thirty rats were divided into 3 groups; group I considered as control, group II; its rats were daily injected with Nicotine at a dose of 0.4 mg/100 gm body for 8 successive weeks and group III; its rats were daily injected with Nicotine as group II, but the injection was stopped for another 4 weeks. STAT1α protein was assessed by immunohistochemistry, COX-2 and iNOS genes expression were evaluated by real time PCR and thiobarbituric acid reactive substances (TBARS) and total thiols were measured using spectrophotometric methods in the lung tissues of the rats. RESULTS: The results of the study revealed that group II rats had the highest expression of STAT1α protein and COX-2 and iNOS genes and oxidative stress in their lung tissues. Nicotine cessation for 4 weeks caused a marked reduction in the expression of STAT1α protein, COX-2 and iNOS genes and oxidative stress. CONCLUSION: Induction of STAT1 pathway and the increase in oxidative stress may be the mechanisms through which Nicotine may induce its harmful effects.
BACKGROUND: Tobacco use is responsible for millions of preventable deaths due to cancer. Nicotine, an alkaloid chemical found in tobacco was proved to cause chronic inflammation and oxidative stress. The transcription factor STAT1 induces the expression of many proinflammatory genes and has been suggested to be a target for anti-inflammatory therapeutics. The following study investigated the effect of Nicotine on STAT1 pathway and oxidative stress in rat lung tissue. METHODS: Thirty rats were divided into 3 groups; group I considered as control, group II; its rats were daily injected with Nicotine at a dose of 0.4 mg/100 gm body for 8 successive weeks and group III; its rats were daily injected with Nicotine as group II, but the injection was stopped for another 4 weeks. STAT1α protein was assessed by immunohistochemistry, COX-2 and iNOS genes expression were evaluated by real time PCR and thiobarbituric acid reactive substances (TBARS) and total thiols were measured using spectrophotometric methods in the lung tissues of the rats. RESULTS: The results of the study revealed that group II rats had the highest expression of STAT1α protein and COX-2 and iNOS genes and oxidative stress in their lung tissues. Nicotine cessation for 4 weeks caused a marked reduction in the expression of STAT1α protein, COX-2 and iNOS genes and oxidative stress. CONCLUSION: Induction of STAT1 pathway and the increase in oxidative stress may be the mechanisms through which Nicotine may induce its harmful effects.
Authors: Rekha Chaudhuri; Eric Livingston; Alex D McMahon; Jane Lafferty; Iona Fraser; Mark Spears; Charles P McSharry; Neil C Thomson Journal: Am J Respir Crit Care Med Date: 2006-04-27 Impact factor: 21.405
Authors: Talat Islam; Carrie Breton; Muhammad T Salam; Rob McConnell; Made Wenten; W James Gauderman; David Conti; David Van Den Berg; John M Peters; Frank D Gilliland Journal: Thorax Date: 2009-12-08 Impact factor: 9.139