Asthma is a chronic inflammatory disease of the airways related to epithelial damage, bronchial hyperresponsiveness to contractile agents, tissue remodeling, and luminal narrowing. Currently, there are many data about the pathophysiology of asthma; however, a new aspect has emerged related to the influence of reactive oxygen and nitrogen species (ROS and RNS) on the origin of this disease. Several studies have shown that an imbalance between the production of ROS and RNS and the antioxidant enzymatic and nonenzymatic systems plays an important role in the pathogenesis of this disease. Considering this aspect, this study is aimed at gathering data from the scientific literature on the role of oxidative distress in the development of inflammatory airway and lung diseases, especially bronchial asthma. For that, articles related to these themes were selected from scientific databases, including human and animal studies. The main findings of this work showed that the respiratory system works as a highly propitious place for the formation of ROS and RNS, especially superoxide anion, hydrogen peroxide, and peroxynitrite, and the epithelial damage is reflected in an important loss of antioxidant defenses that, in turn, culminates in an imbalance and formation of inflammatory and contractile mediators, such as isoprostanes, changes in the activity of protein kinases, and activation of cell proliferation signalling pathways, such as the MAP kinase pathway. Thus, the oxidative imbalance appears as a promising path for future investigations as a therapeutic target for the treatment of asthmatic patients, especially those resistant to currently available therapies.

Asthma is a chronic inflammatory disease of the airways characterized by immune cell infiltrates, bronchial hyperresponsiveness, and declining lung function. Thus, the possible effects of virgin coconut oil on a chronic allergic lung inflammation model were evaluated. Morphology of lung and airway tissue exhibited peribronchial inflammatory infiltrate, epithelial hyperplasia, and smooth muscle thickening in guinea pigs submitted to ovalbumin sensitization, which were prevented by virgin coconut oil supplementation. Additionally, in animals with lung inflammation, trachea contracted in response to ovalbumin administration, showed a greater contractile response to carbachol (CCh) and histamine, and these responses were prevented by the virgin coconut oil supplementation. Apocynin, a NADPH oxidase inhibitor, did not reduce the potency of CCh, whereas tempol, a superoxide dismutase mimetic, reduced potency only in nonsensitized animals. Catalase reduced the CCh potency in nonsensitized animals and animals sensitized and treated with coconut oil, indicating the participation of superoxide anion and hydrogen peroxide in the hypercontractility, which was prevented by virgin coconut oil. In the presence of L-NAME, a nitric oxide synthase (NOS) inhibitor, the CCh curve remained unchanged in nonsensitized animals but had increased efficacy and potency in sensitized animals, indicating an inhibition of endothelial NOS but ineffective in inhibiting inducible NOS. In animals sensitized and treated with coconut oil, the CCh curve was not altered, indicating a reduction in the release of NO by inducible NOS. These data were confirmed by peribronchiolar expression analysis of iNOS. The antioxidant capacity was reduced in the lungs of animals with chronic allergic lung inflammation, which was reversed by the coconut oil, and confirmed by analysis of peribronchiolar 8-iso-PGF2α content. Therefore, the virgin coconut oil supplementation reverses peribronchial inflammatory infiltrate, epithelial hyperplasia, smooth muscle thickening, and hypercontractility through oxidative stress and its interactions with the NO pathway.

The blue alga Spirulina platensis has presented several pharmacological activities, highlighting its actions as an anti-inflammatory and antioxidant. In addition, there are few studies with the influence of strength training on physiological parameters, as intestinal contractility and oxidative cell damage. We evaluated the influence of S. platensis supplementation, strength training, and its association on contractile reactivity of rat ileum, as well as the balance of oxidative stress/antioxidant defenses. Methods: Male Wistar rats were divided into; sedentary (S); S + supplemented with algae at 50 (S50), 150 (S150), and 500 mg/kg (S500); trained (T); and T + supplemented (T50, T150, and T500). Contractile reactivity was analyzed by kymographs; oxidative stress on ileum by the malondialdehyde (MDA) formation; and the antioxidant capacity by 2,2-diphenyl-1-picrylhydrazyl (DPPH) method. S. platensis supplementation reduced the reactivity of rat ileum to carbachol (CCh) and KCl, while training reduced only the CCh efficacy. In addition, association potentiated the reduction on contractile reactivity. Supplementation reduced the oxidative stress and increased oxidation inhibition; training alone did not alter this parameter, however association potentiated this beneficial effect. Therefore, this study demonstrated that both supplementation and its association with strength training promote beneficial effects regarding intestinal contractile reactivity and oxidative stress, providing new insights for intestinal disorders management.

Piptadenia stipulacea (Benth) Ducke is a tree of the Caatinga, in Northeast Brazil, popularly known as “Jurema-branca”, “Jurema malícia-da-serra”, “Carcará” and “Calumbi”. In folk medicine, a decoction or tincture of its bark and leaves are used to treat wounds and as healing agents. Galetin 3,6-dimethyl ether (FGAL) is a flavonoid isolated from the aerial components of Piptadenia stipulacea (Benth) Ducke. We decided to investigate a possible FGAL spasmolytic effect on preparations of both the guinea pig ileum and trachea, the rat uterus and the male rat aorta. FGAL inhibited oxytocin (IC50 = 2.2 ± 0.4 × 10–5 M) and carbachol (CCh)-induced (IC50 = 7.7 ± 1.3 × 10–5 M) phasic contractions in the rat uterus, but was more effective in the inhibition of the oxytocin-induced contractions. In the guinea pig ileum, FGAL equipotently inhibited CCh (IC50 = 2.8 ± 0.4 × 10–5 M) and histamine-induced (IC50 = 2.3 ± 0.5 × 10–5 M) phasic contractions. FGAL equipotently and concentration-dependently relaxed guinea pig trachea preparations pre-contracted with CCh, both in the absence (EC50 = 0.8 ± 0.1 × 10–5 M) and presence (EC50 = 1.0 ± 0.1 × 10–5 M) of a functional epithelium. FGAL also relaxed preparations of the rat aorta pre-contracted with phenylephrine in both the absence (EC50 = 5.0 ± 1.1 × 10–6 M) and presence (EC50 = 5.4 ± 1.2 × 10–6 M) of a functional endothelium. FGAL shows a non-selective spasmolytic effect on each of the smooth muscle preparations we have tested, but with a greater effect on those from the rat aorta. The relaxant effect on preparations of both the guinea pig trachea and the rat aorta seems to not involve the epithelium or endothelium-derived relaxing factors.

Xylopia frutescens Aubl. (embira, semente-de-embira or embira-vermelha), is used in folk medicine as antidiarrheal. The essential oil from its leaves (XF-EO) has been found to cause smooth muscle relaxation. Thus, the aim of this study was to investigate the spasmolytic action by which XF-EO acts on guinea pig ileum. The components of the XF-EO were identified by gas chromatography-mass spectrometry. Segments of guinea pig ileum were suspended in organ bath containing modified Krebs solution at 37 °C, bubbled with carbogen mixture under a resting tension of 1 g. Isotonic contractions were registered using kymographs and isometric contractions using force transducer coupled to an amplifier and computer. Fluorescence measurements were obtained with a microplate reader using Fluo-4. Forty-three constituents were identified in XF-EO, mostly mono- and sesquiterpenes. XF-EO has been found to cause relaxation on guinea pig ileum. The essential oil inhibited in a concentration-dependent manner both CCh- and histamine-induced phasic contractions, being more potent on histamine-induced contractions as well as antagonized histamine-induced cumulative contractions in a non-competitive antagonism profile. XF-EO relaxed in a concentration-dependent manner the ileum pre-contracted with KCl and histamine. Since the potency was smaller in organ pre-contracted with KCl, it was hypothesized that XF-OE would be acting as a K+ channel positive modulator. In the presence of CsCl (non-selective K+ channel blocker), the relaxant potency of XF-OE was not altered, indicating a non-participation of these channels. Moreover, XF-EO inhibited CaCl2-induced cumulative contractions in a depolarizing medium nominally without Ca2+ and relaxed the ileum pre-contracted with S-(-)-Bay K8644 in a concentration-dependent manner, thus, was confirmed the inhibition of Ca2+ influx through Cav1 by XF-EO. In cellular experiments, the viability of longitudinal layer myocytes from guinea pig ileum was not altered in the presence of XF-OE and the Fluo-4-associated fluorescence intensity in these intestinal myocytes stimulated by histamine was reduced by the essential oil, indicating a [Ca2+]c reduction. Spasmolytic action mechanism of XF-EO on guinea pig ileum can involve histaminergic receptor antagonism and Ca2+ influx blockade, which results in [Ca2+]c reduction leading to smooth muscle relaxation.