Programa de Pós-graduação em Produtos Naturais e Sintéticos Bioativos, Centro de Ciências da Saúde, Universidade Federal da Paraíba, João Pessoa, PB, Brazil.
Departamento de Fisiologia e Patologia, Centro de Ciências da Saúde, Universidade Federal da Paraíba, João Pessoa, PB, Brazil.
Oxid Med Cell Longev. 2020 Jan 27;2020:5148503. doi: 10.1155/2020/5148503. eCollection 2020.
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-PGF2 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.
哮喘是一种气道慢性炎症性疾病,其特征为免疫细胞浸润、支气管高反应性和肺功能下降。因此,评估了初榨椰子油对慢性变应性肺炎症模型的可能影响。在卵白蛋白致敏的豚鼠中,气道组织和肺的形态学表现为支气管周围炎症浸润、上皮细胞增生和平滑肌增厚,而初榨椰子油补充可预防这些变化。此外,在有肺部炎症的动物中,气管在卵白蛋白给药后收缩,对乙酰胆碱(CCh)和组胺的收缩反应更大,而初榨椰子油补充可预防这些反应。NADPH 氧化酶抑制剂 apocynin 并未降低 CCh 的效力,而过氧化氢酶模拟物 tempol 仅在未致敏的动物中降低效力。过氧化氢酶降低了未致敏动物和致敏并接受椰子油治疗的动物的 CCh 效力,表明超氧化物阴离子和过氧化氢参与了超收缩,而初榨椰子油则可预防这种超收缩。在存在一氧化氮合酶(NOS)抑制剂 L-NAME 的情况下,CCh 曲线在未致敏的动物中保持不变,但在致敏的动物中效力和效力增加,表明内皮 NOS 受到抑制,但对诱导型 NOS 无效。在致敏并接受椰子油治疗的动物中,CCh 曲线未改变,表明诱导型 NOS 释放的 NO 减少。这些数据得到了 iNOS 周围支气管表达分析的证实。慢性变应性肺炎症动物的肺抗氧化能力降低,而椰子油可逆转这种降低,并通过对周围支气管 8-iso-PGF2 含量的分析得到证实。因此,初榨椰子油补充可通过氧化应激及其与 NO 途径的相互作用逆转支气管周围炎症浸润、上皮细胞增生、平滑肌增厚和高收缩性。