Therapeutic Effects of Arctiin on Alzheimer's Disease-like Model in Rats by Reducing Oxidative Stress, Inflammasomes and Fibrosis.

Mohamed T Almeaqli, Yazeed Alaidaa, Faisal M Alnajjar, Abdullah S Al Shararh, Danah S Alharbi, Yazeed I Almslmani, Yousef A Alotibi, Hani S Alrashidi, Wael A Alshehri, Hanan M Hassan, Mohammed M H Al-Gayyar
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Abstract

Background: Alzheimer's disease (AD) affects approximately 50 million people globally and is expected to triple by 2050. Arctiin is a lignan found in the Arctium lappa L. plant. Arctiin possesses anti-proliferative, antioxidative and anti-adipogenic.

Objectives: We aimed to explore the potential therapeutic effects of Arctiin on rats with AD by evaluating the expression of TLR4, NLRP3, STAT3, TGF-β, cyclin D1, and CDK2.

Methods: AD was induced in rats by administering 70 mg/kg of aluminum chloride through intraperitoneal injection daily for six weeks. After inducing AD, some rats were treated with 25 mg/kg of Arctiin daily for three weeks through oral gavage. Furthermore, to examine the brain tissue structure, hippocampal sections were stained with hematoxylin/eosin and anti-TLR4 antibodies. The collected samples were analyzed for gene expression and protein levels of TLR4, NLRP3, STAT3, TGF-β, cyclin D1, and CDK2.

Results: In behavioral tests, rats showed a significant improvement in their behavior when treated with Arctiin. Microimages stained with hematoxylin/eosin showed that Arctiin helped to improve the structure and cohesion of the hippocampus, which was previously impaired by AD. Furthermore, Arctiin reduced the expression of TLR4, NLRP3, STAT3, TGF-β, cyclin D1, and CDK2.

Conclusion: Arctiin can enhance rats' behavior and structure of the hippocampus in AD rats. This is achieved through its ability to reduce the expression of both TLR4 and NLRP3, hence inhibiting the inflammasome pathway. Furthermore, Arctiin can improve tissue fibrosis by regulating STAT3 and TGF-β. Lastly, it can block the cell cycle proteins cyclin D1 and CDK2.

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通过降低氧化应激、炎症体和纤维化,八角苷对阿尔茨海默病样模型大鼠的治疗作用
背景:阿尔茨海默病(AD)影响着全球约 5000 万人,预计到 2050 年将增加两倍。Arctiin 是一种木质素,存在于牛蒡(Arctium lappa L.)植物中。辛夷苷具有抗增殖、抗氧化和抗脂肪生成的作用:我们旨在通过评估 TLR4、NLRP3、STAT3、TGF-β、细胞周期蛋白 D1 和 CDK2 的表达,探讨牛蒡苷对 AD 大鼠的潜在治疗效果:每天腹腔注射 70 毫克/千克氯化铝诱导大鼠 AD,连续注射六周。诱导 AD 后,部分大鼠通过口服每天 25 毫克/千克的 Arctiin,持续三周。此外,为了检查脑组织结构,海马切片用苏木精/伊红和抗TLR4抗体染色。对采集的样本进行基因表达分析,并检测 TLR4、NLRP3、STAT3、TGF-β、细胞周期蛋白 D1 和 CDK2 的蛋白水平:在行为测试中,接受 Arctiin 治疗的大鼠行为明显改善。用苏木精/伊红染色的显微图像显示,Arctiin 有助于改善海马体的结构和凝聚力。此外,阿胶还能减少TLR4、NLRP3、STAT3、TGF-β、细胞周期蛋白D1和CDK2的表达:结论:牛蒡子素能改善AD大鼠的行为和海马结构,这是通过降低TLR4、NLRP3、STAT3、TGF-β、cyclin D1和CDK2的表达来实现的。结论:苦杏仁苷能改善 AD 大鼠的行为和海马结构,这是因为它能减少 TLR4 和 NLRP3 的表达,从而抑制炎性体通路。此外,阿克替因还能通过调节 STAT3 和 TGF-β 改善组织纤维化。最后,它还能阻断细胞周期蛋白 cyclin D1 和 CDK2。
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