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首页> 外文期刊>Oxidative Medicine and Cellular Longevity >Virgin Coconut Oil Supplementation Prevents Airway Hyperreactivity of Guinea Pigs with Chronic Allergic Lung Inflammation by Antioxidant Mechanism
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Virgin Coconut Oil Supplementation Prevents Airway Hyperreactivity of Guinea Pigs with Chronic Allergic Lung Inflammation by Antioxidant Mechanism

机译:维珍椰子油补充防止豚鼠的气道过度反应性通过抗氧化机理进行慢性过敏性肺炎

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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.
机译:哮喘是气道的慢性炎症疾病,其特征在于免疫细胞浸润,支气管高反应性和肺功能下降。因此,评估了处女椰子油对慢性过敏性肺炎症模型的可能影响。肺和呼吸道组织的形态表现出血浆加湿浸润,上皮增生和在提交给卵巢溶解的豚鼠中平滑肌增厚,由处女椰子油补充预防。另外,在具有肺炎的动物中,响应于卵蛋白给药的气管挛缩,表现出对卡巴山(CCH)和组胺的更大的收缩响应,并通过原始椰子油补充来防止这些反应。 NADPH氧化酶抑制剂的APOCYNIN并未降低CCH的效力,而TEMPOL,超氧化物歧化酶模拟,仅在非致密的动物中降低效力。过氧化氢酶降低了非致密的动物和动物的CCH效力,用椰子油敏化并治疗,表明超氧化物阴离子和过氧化氢在近距离的参与,由原始椰子油预防。在L-NAME的存在下,一氧化氮合酶(NOS)抑制剂,CCH曲线在非致密的动物中保持不变,但在敏化动物中具有增加的疗效和效力,表明抑制诱导诱导型NOS的内皮NO,但无效。在用椰子油致敏和处理的动物中,没有改变CCH曲线,表明诱导NOS的释放减少。通过INOS的血脂Chiolar表达分析证实了这些数据。抗氧化能力在慢性过敏性肺炎症的动物肺中减少,由椰子油反转,并通过分析Peribronchiolar 8-ISO-PGF2α含量来证实。因此,维珍椰子油补充反转过血管加速炎性浸润,上皮增生,平滑肌增厚,通过氧化应激及其与NO途径的相互作用。

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