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  • It is known that cigarette smoke increases

    2021-04-27

    It is known that cigarette smoke increases the oxidative burden in the lungs of mice with emphysema, which leads to oxidative stress [[34], [35], [36]]. However, in addition to cigarette smoke, studies have shown that endogenous oxidative stress is associated with proteolytic buy ink receptor in several mouse models [[37], [38], [39]]. In our study, we observed increased activity of the SOD enzyme in the PPE 64d group compared with the control group. However, we did not observe an increase in the CAT enzyme, which disrupts hydrogen peroxide, leading to an imbalance between the production of the generated reactive species with a detrimental effect on the production and activity of antioxidant enzymes. Escribano et al. [40] studied the parameters of oxidative stress and the activity of the main antioxidant enzymes in children diagnosed with α1-antitrypsin deficiency. They observed reduced levels of glutathione and decreased catalase activity leading to an accumulation of hydrogen peroxide, justifying the increased levels of oxidative stress biomarkers. We observed a significant reduction in SOD activity at all doses of atorvastatin administered compared with the PPE 64d group, and the 20 mg dose produced the best results. Alnaeb et al. [41] demonstrated that post-treatment with atorvastatin (10–20 mg/day) reduced platelet superoxide anion production in patients with hypercholesterolemia compared with placebo. Another finding demonstrated reduced expression of Rac GTPase in the platelet cell membrane, leading to a reduction of the ability of NADPH oxidase to form superoxide anion since Rac is an integral part of the NADPH oxidase system. As a result, conformational changes necessary for the release of superoxide occurred. Regarding the activity of the CAT enzyme, we did not observe any difference in the A1mg and A5mg groups compared with the PPE 64d group, except for the A20 mg group, which attained levels similar to the control group. Chen et al. [42] analyzed the influence of atorvastatin (10 mg/kg) on vascular endothelial cell growth factor (VEGF) expression in non-small cell lung cancer, both in vitro and in vivo, and evaluated the role of reactive oxygen species (ROS) and derivatives of the Rac1/NADPH oxidase pathway in the regulation of VEGF. They concluded that atorvastatin inhibited the generation of ROS by partially suppressing Rac1/NADPH oxidase activity, which significantly upregulated GPx and CAT activity, contributing to the inhibition of VEGF expression. In addition to altering antioxidant enzyme levels, our study model demonstrated that PPE caused significant oxidative damage, as shown by the increase in MDA levels and nitrite as well as the reduced GSH/GSSG ratio used to estimate the oxidation-reduction state in biological systems compared with the control group. Kumar et al. [43] developed an experimental model of Parkinson’s disease using 6-hydroxydopamine (6-OHDG) in Wister rats. Treatment with 10 mg and 20 mg doses of atorvastatin and 15 mg and 30 mg doses of simvastatin was administered for 14 days to observe the neuroprotective effects of these statins. The authors observed a significant reduction in oxidative damage, as demonstrated by decreased MDA and nitrite levels and by the restoration of GSH levels to control group levels, and these results were dose-dependent. The authors attributed the neuroprotection to the anti-inflammatory response to statins. The main oxidative stress factor in COPD is related to the reduction in endogenous concentrations of antioxidants, and many of the genes that encode these antioxidants are regulated by the transcription factor Nrf2 [4,34,44]. In this way, exposure to oxidants upregulates endogenous antioxidants in an attempt to contain the onset of oxidative stress and thus restore the balance between oxidants-antioxidants. The expression of Nrf2 is known to be reduced in the lung periphery of patients with COPD and is associated with the decrease in antioxidant genes regulated by this pathway [45]. We did not observe a decrease in Nrf2 expression in this emphysema induction model. In contrast, we discovered an increase in the expression of this transcription factor in the PPE 64d group, and treatment with all doses of atorvastatin reduced this expression to levels of the control group. It is worth buy ink receptor remembering that emphysema was established on the 32nd day and analyses were performed 32 days after this establishment (day 64). By following this model, it is unknown how soon the expression of Nrf2 began after the onset of emphysema. We suggest that this elevated expression 32 days later may be an attempt by the organism to modulate the oxidative stress generated by elastase since morphological changes such as an increase in Lm, alveolar septa Vv, and collagen and elastic fibers in the tissue were observed in both the PPE 32d and PPE 64d groups.