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蜜蜂花提取物通过调节γ射线照射大鼠的Nrf-2/Keap-1基因表达,减轻与甲状腺功能亢进诱导的肝损伤相关的氧化还原失衡和炎症。

Melissa officinalis extract palliates redox imbalance and inflammation associated with hyperthyroidism-induced liver damage by regulating Nrf-2/ Keap-1 gene expression in γ-irradiated rats.

作者信息

Kawara Ragaa Sm, Moawed Fatma Sm, Elsenosi Yakout, Elmaksoud Hussein Abd, Ahmed Esraa S A, Abo-Zaid Omayma Ar

机构信息

Biochemistry and Molecular Biology Department, Faculty of Vet. Med, Benha University, Banha, Egypt.

Health radiation research, National Center for Radiation Research and Technology, Egyptian Atomic Energy Authority, Nasr City, 11787, Cairo, Egypt.

出版信息

BMC Complement Med Ther. 2024 Feb 1;24(1):71. doi: 10.1186/s12906-024-04370-z.

DOI:10.1186/s12906-024-04370-z
PMID:38303002
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10832092/
Abstract

BACKGROUND

Melissa officinalis (MO) is a well-known medicinal plant species used in the treatment of several diseases; it is widely used as a vegetable, adding flavour to dishes. This study was designed to evaluate the therapeutic effect of MO Extract against hyperthyroidism induced by Eltroxin and γ-radiation.

METHODS

Hyperthyroidism was induced by injecting rats with Eltroxin (100 µg/kg/ day) for 14 days and exposure to γ-radiation (IR) (5 Gy single dose). The hyperthyroid rats were orally treated with MO extract (75 mg/kg/day) at the beginning of the second week of the Eltroxin injection and continued for another week. The levels of thyroid hormones, liver enzymes and proteins besides the impaired hepatic redox status and antioxidant parameters were measured using commercial kits. The hepatic gene expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and its inhibitor Kelch-like ECH-associated protein-1(Keap-1) in addition to hepatic inflammatory mediators including tumor necrosis factor-α (TNF- α), Monocyte chemoattractant protein-1 (MCP-1) and fibrogenic markers such as transforming growth factor-beta1 (TGF-β1) were determined.

RESULTS

MO Extract reversed the effect of Eltroxin + IR on rats and attenuated the thyroid hormones. Moreover, it alleviated hyperthyroidism-induced hepatic damage by inhibiting the hepatic enzymes' activities as well as enhancing the production of proteins concomitant with improving cellular redox homeostasis by attenuating the deranged redox balance and modulating the Nrf2/Keap-1 pathway. Additionally, MO Extract alleviated the inflammatory response by suppressing the TNF- α and MCP-1 and prevented hepatic fibrosis via Nrf2-mediated inhibition of the TGF-β1/Smad pathway.

CONCLUSION

Accordingly, these results might strengthen the hepatoprotective effect of MO Extract in a rat model of hyperthyroidism by regulating the Nrf-2/ Keap-1 pathway.

摘要

背景

蜜蜂花(MO)是一种著名的药用植物,可用于治疗多种疾病;它还被广泛用作蔬菜,为菜肴增添风味。本研究旨在评估MO提取物对左甲状腺素和γ射线辐射诱导的甲状腺功能亢进的治疗效果。

方法

通过给大鼠注射左甲状腺素(100μg/kg/天)14天并暴露于γ射线辐射(IR)(单次剂量5Gy)来诱导甲状腺功能亢进。在注射左甲状腺素的第二周开始,对甲状腺功能亢进的大鼠口服MO提取物(75mg/kg/天),并持续一周。使用商业试剂盒测量甲状腺激素、肝酶和蛋白质水平,以及受损的肝脏氧化还原状态和抗氧化参数。此外,还测定了肝脏中核因子红细胞2相关因子2(Nrf2)及其抑制剂 Kelch样ECH相关蛋白1(Keap-1)的基因表达,以及包括肿瘤坏死因子-α(TNF-α)、单核细胞趋化蛋白-1(MCP-1)等肝脏炎症介质和诸如转化生长因子-β1(TGF-β1)等纤维化标志物。

结果

MO提取物逆转了左甲状腺素+IR对大鼠的影响,并减弱了甲状腺激素的作用。此外,它通过抑制肝酶活性减轻了甲状腺功能亢进引起的肝损伤,同时通过减弱紊乱的氧化还原平衡和调节Nrf2/Keap-1途径来增强蛋白质的产生,从而改善细胞氧化还原稳态。此外,MO提取物通过抑制TNF-α和MCP-1减轻了炎症反应,并通过Nrf2介导的对TGF-β1/Smad途径的抑制预防了肝纤维化。

结论

因此,这些结果可能通过调节Nrf-2/Keap-1途径增强MO提取物在甲状腺功能亢进大鼠模型中的肝保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/7488da2be468/12906_2024_4370_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/bc39e0033592/12906_2024_4370_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/fc162060d775/12906_2024_4370_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/c59cef78eebf/12906_2024_4370_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/df7ac68a4e49/12906_2024_4370_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/c12f3a051bf8/12906_2024_4370_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/b09b61d2a1f0/12906_2024_4370_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/070bc8d74992/12906_2024_4370_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/7488da2be468/12906_2024_4370_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/bc39e0033592/12906_2024_4370_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/fc162060d775/12906_2024_4370_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/c59cef78eebf/12906_2024_4370_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/df7ac68a4e49/12906_2024_4370_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/c12f3a051bf8/12906_2024_4370_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/b09b61d2a1f0/12906_2024_4370_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/070bc8d74992/12906_2024_4370_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c700/10832092/7488da2be468/12906_2024_4370_Fig8_HTML.jpg

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