Smoking Affects the Post-Stroke Inflammatory Response of Lipid Mediators in a Gender-Related Manner

The main goal of our study was to determine the effect of cigarette smoking on selected derivatives of arachidonic acid, linoleic acid, DHA, and EPA, which may be markers of post-stroke inflammation. The eicosanoid profile was compared in both smoking and non-smoking patients, without division and with division into gender. In the group of non-smokers, we observed higher levels of the linolenic acid derivative (LA) 9S HODE (p ≤ 0.05) than in smokers. However, after dividing the results by sex, it turned out that the level of this derivative was higher in non-smoking women compared to smoking women (p ≤ 0.01) and did not differentiate the group of men. Similarly, the level of the arachidonic acid metabolite LTX A4 (p ≤ 0.05) differed only in the group of women. In this group, we also observed a decreased level of 15S HETE in smoking women, but it was statistically insignificant (p ≤ 0.08). On the other hand, the level of this derivative was statistically significantly higher in the group of non-smoking women compared to male non-smokers. The group of men was differentiated by two compounds: TXB2 and NPD1. Male smokers had an almost two-fold elevation of TXB2 (p ≤ 0.01) compared with non-smokers, and in this group, we also observed an increased level of NPD1 compared with male non-smokers. On the other hand, when comparing female non-smokers and male non-smokers, in addition to the difference in 15S HETE levels, we also observed elevated levels of TXB2 in the group of non-smokers. We also analyzed a number of statistically significant correlations between the analyzed groups. Generally, men and women smokers showed a much smaller amount of statistically significant correlations than non-smokers. We believe that this is related to the varying degrees of inflammation associated with acute ischemic stroke and post-stroke response. On the one hand, tobacco smoke inhibits the activity of enzymes responsible for the conversion of fatty acids, but on the other hand, it can cause the failure of the inflammatory system, which is also the body’s defense mechanism. Smoking cigarettes is a factor that increases oxidative stress even before the occurrence of a stroke incident, and at the same time accelerates it and inhibits post-stroke repair mechanisms. This study highlights the effect of smoking on inflammation in both genders mediated by lipid mediators, which makes smoking cessation undeniable.