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首页> 外文期刊>Annals of anatomy =: Anatomischer Anzeiger : official organ of the Anatomische Gesellschaft >Neuroprotective effects of food restriction on autonomic innervation of the lacrimal gland in. the rat
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Neuroprotective effects of food restriction on autonomic innervation of the lacrimal gland in. the rat

机译：食品限制对泪腺自主密验的神经保护作用。大鼠

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Inflammatory mechanisms and oxidative stress play important roles in age-related lacrimal gland (LG) degeneration as well as neural degeneration. Research suggests that caloric restriction can prevent age related LG dysfunction and increase the life span of neurons. In the present study, we hypothesized that caloric restriction prevents age-related LG dysfunction by ameliorating the influence of inflammatory/oxidative stress on autonomic neurons controlling lacrimal function. We evaluated the effects of food restriction (FR) on inflammatory/oxidative status and on autonomic neural/neuroglial cell populations in LGs from aging rats. A total of 45 female albino rats were divided into young adult, aged, and aged-FR groups. The FR group was subjected to a 50% reduction in food from 14 to 20 months of age. LG samples were collected for each group and subjected to biochemical, histological, and immunohistochemical studies. LGs from aged-FR rats, rather than those from aged rats, showed preservation of their cellular structures, organelles, and Schwan cell units. LG preservation was associated with a marked decrease in inflammatory markers, an increase in cellular antioxidants, and the up-regulation of choline acetyltransverase, tyrosine hydroxylase, neuron-specific enolase and S100. These findings strongly suggest that in aged rats, both oxidative and inflammatory stressors directly contribute to LG dysfunction by mediating the degeneration of autonomic neurons, and that FR can protect against these effects. (C) 2017 Elsevier GmbH. All rights reserved.
机译：炎症机制和氧化应激在年龄相关的泪腺（LG）变性以及神经变性中起重要作用。研究表明，热量限制可以预防年龄相关的LG功能障碍并增加神经元的寿命。在本研究中，我们假设热量限制通过改善炎症/氧化应激对控制泪腺功能的自主神经元的影响来防止年龄相关的LG功能障碍。我们评估了食品限制（FR）对炎症/氧化地位的影响以及老鼠血液炎症状态的LGS中的自主神经性/神经性高兴细胞群。共有45只雌性白化大鼠分为年轻人，年龄和龄和龄群。 FR组在14至20个月的14岁以下的食物减少50％。为每组收集LG样品，并进行生化，组织学和免疫组织化学研究。来自aged-FR大鼠的LGS，而不是来自老年大鼠的大鼠，表明它们的细胞结构，细胞器和Schwan细胞单元的保存。 LG保存与炎症标记的显着降低相关，细胞抗氧化剂的增加，以及胆碱乙酰转移酶，酪氨酸羟化酶，神经元特异性烯醇酶和S100的上调。这些发现强烈表明，在老年的大鼠中，通过介导自主神经元的退化，氧化和炎症液均直接导致LG功能障碍，并且FR可以防止这些效果。 （c）2017 Elsevier GmbH。版权所有。

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