Abstract
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. 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. 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. Induction of STAT1 pathway and the increase in oxidative stress may be the mechanisms through which Nicotine may induce its harmful effects.
Highlights
Tobacco leaves used for smoking contain an abundant amount of the alkaloid chemical, Nicotine [1]
This study evaluated the effect of Nicotine injection and its cessation on the expression of STAT1α protein, the gene expression of COX2 and iNO synthase, lipid peroxides and –SH group in the lung tissues of rats
The gene expression of Cyclooxygenase 2 (COX-2) and iNO synthase As indicated in Table 2; the expression of COX-2 and iNOS genes increased in lung tissues of group II (Nicotine Treated Group) compared to group I (p< 0.0001)
Summary
Tobacco leaves used for smoking contain an abundant amount of the alkaloid chemical, Nicotine [1]. STAT1 expression increases in response to oxidative stress and inflammatory stimuli [7]. The following study investigated the effect of Nicotine on STAT1 pathway and oxidative stress in rat lung tissue. 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. Conclusions: Induction of STAT1 pathway and the increase in oxidative stress may be the mechanisms through which Nicotine may induce its harmful effects
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