Many studies have shown that sleep deprivation can affect a wide range of tissues and organs, and most of these effects are related to oxidative stress. Oxidative stress can cause functional and morphological changes in cells, which are closely related to autophagy and apoptosis. In this study, we examined changes in thyroid morphology and function, oxidative stress, autophagy, and apoptosis in rats after sleep deprivation. Thyroid hormones, thyroid-stimulating hormone, functional substances required for the synthesis of thyroid hormones, and thyroid morphological observations were used to evaluate the changes and impairment of thyroid function. Methane dicarboxylic aldehyde and total antioxidant capacity were measured to assess oxidative stress in the thyroid. To evaluate the balance of autophagy and apoptosis, the expression of autophagy- and apoptosis-related proteins was examined by western blotting, and apoptotic cells were labeled with TUNEL staining. The body weight of rats in the sleep deprivation group decreased, but the relative weight of the thyroid gland increased. Sleep deprivation led to morphological changes in the thyroid. The levels of thyroid hormones and thyroid-stimulating hormone increased after sleep deprivation. Total antioxidant capacity decreased, and methane dicarboxylic aldehyde levels increased in the thyroid in the sleep deprivation group. Analysis of autophagy- and apoptosis-related proteins indicated that the microtubule-associated protein 1 light chain 3 beta- (LC3B-) and LC3A-II/I ratio and Beclin 1 levels significantly decreased in the sleep deprivation group and P62 levels significantly increased. The number of apoptotic cells in the thyroid gland of sleep-deprived rats increased significantly. Taken together, these results indicate that sleep deprivation can lead to oxidative stress in the thyroid and ultimately cause thyroid damage, which may be related to the imbalance of autophagy and apoptosis.

中文翻译：

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氧化应激诱导的自噬和细胞凋亡失衡可能与大鼠睡眠剥夺引起的甲状腺损伤有关

许多研究表明，睡眠不足会影响广泛的组织和器官，而这些影响大多与氧化应激有关。氧化应激可引起细胞的功能和形态变化，这些变化与自噬和细胞凋亡密切相关。在这项研究中，我们检查了睡眠剥夺后大鼠甲状腺形态和功能、氧化应激、自噬和细胞凋亡的变化。采用甲状腺激素、促甲状腺激素、合成甲状腺激素所需的功能性物质、甲状腺形态学观察来评价甲状腺功能的变化和损害。测量甲烷二羧酸醛和总抗氧化能力以评估甲状腺中的氧化应激。为了评估自噬和细胞凋亡的平衡，Western blotting检测自噬和凋亡相关蛋白的表达，TUNEL染色标记凋亡细胞。睡眠剥夺组大鼠体重下降，但甲状腺相对重量增加。睡眠剥夺导致甲状腺的形态变化。睡眠剥夺后甲状腺激素和促甲状腺激素水平升高。睡眠剥夺组的总抗氧化能力下降，甲状腺中的甲烷二羧酸醛水平升高。自噬和凋亡相关蛋白的分析表明，睡眠剥夺组的微管相关蛋白 1 轻链 3β-（LC3B-）和 LC3A-II/I 比值和 Beclin 1 水平显着降低，P62 水平显着升高。睡眠剥夺大鼠甲状腺中凋亡细胞的数量显着增加。综上所述，这些结果表明，睡眠剥夺会导致甲状腺发生氧化应激，最终导致甲状腺损伤，这可能与自噬和细胞凋亡的失衡有关。