Melissa officinalis 提取物可抑制甲状腺功能减退症诱导的大鼠在暴露于 γ 辐射下的大脑中由内质网应激诱导的细胞凋亡。

IF 3.3 3区 生物学 Q3 CELL BIOLOGY
Omayma Ar Abo-Zaid, Fatma Sm Moawed, Eman Fs Taha, Esraa S A Ahmed, Ragaa Sm Kawara
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引用次数: 0

摘要

本研究旨在证明香蜂花叶提取物(MEE)对丙基硫脲嘧啶(PTU)和/或γ-射线(IR)诱导的甲状腺机能减退引起的大鼠脑损伤具有神经保护作用。甲状腺机能减退和/或暴露于 IR 会导致血清中的 T3 和 T4 水平显著下降,同时脑组织匀浆中的脂质过氧化终产物丙二醛(MDA)和亚硝酸盐(NO)水平升高。此外,甲状腺机能减退和/或暴露于红外线通过上调蛋白激酶 RNA 样内质网激酶(PERK)、活化转录因子 6(ATF6)的基因表达,明显增强了内质网应激、脑组织匀浆中的内质网相关降解(ERAD)、CCAAT/增强子结合蛋白同源蛋白(CHOP)等基因表达上调,导致细胞凋亡,表现为 Bax、BCl2 和 caspase-12 的过度表达,最终导致脑损伤。同时,用 MEE 处理 PTU 和/或 IR 暴露的大鼠可通过 ATF6 减少氧化应激和 ERAD。此外,MEE还能阻止Bax和caspase-12基因表达的增加。对甲状腺功能减退动物的这种治疗与神经元保护有关,脑组织中微管相关蛋白 tau(MAPT)和淀粉样前体蛋白(APP)基因表达的下调表明了这一点。此外,服用 MEE 还能改善脑组织的组织学结构。总之,MEE可以预防甲状腺机能减退引起的与氧化应激和内质网应激有关的脑损伤。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Melissa officinalis extract suppresses endoplasmic reticulum stress-induced apoptosis in the brain of hypothyroidism-induced rats exposed to γ-radiation.

The purpose of this study was to demonstrate the neuroprotective effect of Melissa officinalis extract (MEE) against brain damage associated with hypothyroidism induced by propylthiouracil (PTU) and/or γ-radiation (IR) in rats. Hypothyroidism induction and/or exposure to IR resulted in a significant decrease in the serum levels of T3 and T4 associated with increased levels of lipid peroxidation end product, malondialdehyde (MDA), and nitrites (NO) in the brain tissue homogenate. Also, hypothyroidism and /or exposure to IR markedly enhance the endoplasmic reticulum stress by upregulating the gene expressions of the protein kinase RNA-like endoplasmic reticulum kinase (PERK), activated transcription factor 6 (ATF6), endoplasmic reticulum-associated degradation (ERAD), and CCAAT/enhancer-binding protein homologous protein (CHOP) in the brain tissue homogenate associated with a proapoptotic state which indicated by the overexpression of Bax, BCl2, and caspase-12 that culminates in brain damage. Meanwhile, the PTU and /or IR-exposed rats treated with MEE reduced oxidative stress and ERAD through ATF6. Also, the MEE treatment prevented the Bax and caspase-12 gene expression from increasing. This treatment in hypothyroid animals was associated with neuronal protection as indicated by the downregulation in the gene expressions of the microtubule-associated protein tau (MAPT) and amyloid precursor protein (APP) in the brain tissue. Furthermore, the administration of MEE ameliorates the histological structure of brain tissue. In conclusion, MEE might prevent hypothyroidism-induced brain damage associated with oxidative stress and endoplasmic reticulum stress.

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来源期刊
Cell Stress & Chaperones
Cell Stress & Chaperones 生物-细胞生物学
CiteScore
7.60
自引率
2.60%
发文量
59
审稿时长
6-12 weeks
期刊介绍: Cell Stress and Chaperones is an integrative journal that bridges the gap between laboratory model systems and natural populations. The journal captures the eclectic spirit of the cellular stress response field in a single, concentrated source of current information. Major emphasis is placed on the effects of climate change on individual species in the natural environment and their capacity to adapt. This emphasis expands our focus on stress biology and medicine by linking climate change effects to research on cellular stress responses of animals, micro-organisms and plants.
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