1. Introduction

In the last decades, it has been a widespread use of an increasing number of chemical compounds with analgesic, antipyretic, and anti-inflammatory properties. In order to remark their differences with other group of medicines which presents known bad side effects, they were labeled as nonsteroidal anti-inflammatory drugs with the acronym NSAIDs [1–3].

© 2017 The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

© The Author(s). Licensee InTech. This chapter is distributed under the terms of the Creative Commons

Attribution License (http://creativecommons.org/licenses/by/3.0), which permits unrestricted use, distribution, and eproduction in any medium, provided the original work is properly cited.

At the same time, many neuroinflammatory mediators, including oxidative agents such as reactive oxygen species (ROS), were found to be upregulated in neurodegenerative disorders (ND) that affect human brain areas [4, 5]. This fact immediately allows the proposal of some kind of cause-effect link between the presence of ROS, oxidation processes, neuroinflammation, and ND pathogenesis [4, 5].

Oxidative stress is a process that occurs in early stages of ND and is considered an identifier mark for their detection as could be evaluated by DNA, RNA, lipids, and protein oxidation levels [6–8]. Simultaneously, several studies have observed an inverse correspondence between prolonged NSAID administration and the development of some ND in humans, (for review, see Ref. [9]). So, it is now accepted that NSAIDs could play a protective role on many ND and one of the reasons of the great interest for getting more insight into the elucidation of the pathways and mechanisms of the oxidative processes in which several NSAIDs and different ROS take part.

The present chapter will analyze the results presented in two relatively recent papers that have been dedicated to evaluate the possible action of some NSAIDs as protectors against ROSmediated oxidation/deterioration of biological targets [10, 11]. Those research works are focused on NSAIDs from different chemical structure classes, one salicylic acid derivative, diflunisal (DFN), an indolic acid derivative, indomethacin (IMT) (Figure 1) and the enolic acid derivatives, oxicams, represented by meloxicam (MEL), tenoxicam (TEN) and piroxicam (PIR) (Figure 2).

Figure 1. Chemical structures of a: 2′,4′-difluoro-4-hydroxyphenyl-3-carboxylic acid, diflunisal (DFN) and b: 2-{1′-[(4 chlorophenyl)carbonyl]-5-methoxy-2-methyl-1H-indol-3-yl} acetic acid, indomethacin (IMT).

Figure 2. Chemical structures of a: [4-hydroxy-2-methyl-N-(5-methyl-2-thiazolyl)-2H-1,2-benzothiazine-3-carboxamide 1,1 dioxide], meloxicam (MEL), b: [4-hydroxy-2-methyl-N-(pyridin-2-yl)-2H-thieno(2,3-e)-1,2 thiazine-3-carboxamide 1,1 dioxide], tenoxicam (TEN) and c: [4-hydroxy-2-methyl-N-(pyridin-2-yl)-2H-1,2-benzothiazine-3-carboxamide 1,1-dioxide], piroxicam (PIR).
