Virgin Coconut Oil Supplementation Prevents Airway Hyperreactivity of Guinea Pigs with Chronic Allergic Lung Inflammation by Antioxidant Mechanism.

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.

Effects of Redox Disturbances on Intestinal Contractile Reactivity in Rats Fed with a Hypercaloric Diet.

Few studies have associated the effects of changes in caloric intake and redox disturbances in the gastrointestinal tract. Therefore, the present study aimed at evaluating the hypercaloric diet consumption influence on the contractile reactivity of intestinal smooth muscle, morphology, and oxidative stress of rat ileum. Wistar rats were randomly divided into groups that received a standard diet and fed with a hypercaloric diet for 8 weeks. Animals were euthanized, and the ileum was isolated to isotonic contraction monitoring. Morphology was evaluated by histological staining and oxidative stress by quantification of malondialdehyde levels and total antioxidant activity. Cumulative concentration-response curves to KCl and carbachol were attenuated in rats fed with a hypercaloric diet compared to those that received a standard diet. In addition, an increase in caloric intake promotes a rise in the thickness of the longitudinal smooth muscle layer of rat ileum and tissue malondialdehyde levels, characterizing lipid peroxidation, as well as a decrease in the antioxidant activity. Thus, it was concluded that the consumption of a hypercaloric diet impairs rat intestinal contractility due to mechanisms involving modifications in the intestinal smooth muscle architecture triggered by redox disturbances.

Hypercaloric Diet Establishes Erectile Dysfunction in Rat: Mechanisms Underlying the Endothelial Damage.

Obesity is characterized by an excessive increase in body mass, leading to endothelial damage that may favor the development of erectile dysfunction (ED). ED is defined as the inability to achieve or maintain a penile erection long enough to have a sexual intercourse. In this context, different ED models were developed, however the high price of special animals or the long period to establish the disease has limited studies in this field. Therefore, this study proposed to establish and characterize a novel model of ED in rats associated to a hypercaloric diet consumption. Animals were randomly divided into control group (CG), which received a standard diet, and obese group (OG), fed with a hypercaloric diet during 8 weeks. Rat's erectile function was evaluated in vivo and in vitro. Food and caloric intake of OG were reduced compared to CG, due to an increased diet energy efficiency. However, OG presented an increased body mass, inguinal, retroperitoneal and epididymal adipose tissues, as well as body adiposity index at the end of experimental protocol. In erectile function analysis, there was a decrease in the number and the latency of penile erections in OG. Additionally, the contractile reactivity of corpus cavernosum was increased in OG, favoring penile detumescence and related to a reduced nitric oxide bioavailability and an increased in contractile prostaglandins levels as a consequence of endothelial damage. Moreover, the endothelium-relaxation reactivity of corpus cavernosum was attenuated in OG associated to the oxidative stress. Thus, it was provided a model for advances in sexual dysfunction field and drug discovery for ED treatment.

Acute Aerobic Swimming Exercise Induces Distinct Effects in the Contractile Reactivity of Rat Ileum to KCl and Carbachol.

Aerobic exercise promotes short-term physiological changes in the intestinal smooth muscle associated to the ischemia-reperfusion process; however, few studies have demonstrated its effect on the intestinal contractile function. Thus, this work describes our observations regarding the influence of acute aerobic swimming exercise in the contractile reactivity, oxidative stress, and morphology of rat ileum. Wistar rats were divided into sedentary (SED) and acutely exercised (EX-AC) groups. Animals were acclimated by 10, 10, and 30 min of swimming exercise in intercalated days 1 week before exercise. Then they were submitted to forced swimming for 1 h with a metal of 3% of their body weight attached to their body. Animals were euthanized immediately after the exercise section and the ileum was suspended in organ baths for monitoring isotonic contractions. The analysis of lipid peroxidation was performed in order to determinate the malondialdehyde (MDA) levels as a marker of oxidative stress, and intestinal smooth muscle morphology by histological staining. Cumulative concentration-response curves to KCl were altered in the EX-AC with an increase in both its efficacy and potency (E max = 153.2 ± 2.8%, EC 50 = 1.3 ± 0.1 × 10(-2) M) compared to the SED group (E max = 100%, EC 50 = 1.8 ± 0.1 × 10(-2) M). Interestingly, carbachol had its efficacy and potency reduced in the EX-AC (E max = 67.1 ± 1.4%, EC 50 = 9.8 ± 1.4 × 10(-7) M) compared to the SED group (E max = 100%, EC 50 = 2.0 ± 0.2 × 10(-7) M). The exercise did not alter the MDA levels in the ileum (5.4 ± 0.6 µ mol/mL) in the EX-AC compared to the SED group (8.4 ± 1.7 µ mol/mL). Moreover, neither the circular nor the longitudinal smooth muscle layers thickness were modified by the exercise (66.2 ± 6.0 and 40.2 ± 2.6 µm, respectively), compared to the SED group (61.6 ± 6.4 and 34.8 ± 3.7 µm, respectively). Therefore, the ileum sensitivity to contractile agents is differentially altered by the acute aerobic swimming exercise, without affecting the oxidative stress and the morphology of ileum smooth muscle.