摘要
β-淀粉样蛋白(Aβ)、神经毒性的多肽,蓄积在阿耳茨海默氏病(AD)患者的脑部,最初引发神经炎症最终导致记忆障碍。在这里,我们证明了与假手术大鼠相比,Aβ注射的大鼠表现出认知功能障碍和神经炎症和海马区硫化氢(H2S)的水平的显着减少。有趣的是,胱硫醚β合酶(CBS)和3- mercaptopyruvate-sulfurtransferase(3MST)(负责内源性硫化氢产生的主要的酶)的表达也显著减少。但是,注射10微克Aβ1-42将导致腹膜内(IP)注射硫氢化钠(硫氢化钠,硫化氢一个供体)大大减弱了,大鼠海马认知功能障碍和神经炎症。随后,在Aβ给药后,硫氢化钠显著抑制大鼠海马的肿瘤坏死因子(TNF)-α,白细胞介素1β(IL-1β)和环氧合酶-2(COX-2)的表达。此外,硫氢化钠发挥了抑制IκB-α降解和转录因子核因子κB的随后活化(NF-κB),以及抑制细胞外信号调节激酶(ERK1 / 2)的活性和p38蛋白活性的有益效果,但C-Jun N末端激酶(JNK)的活性没有受到Aβ影响。这些结果表明,硫氢化钠是可能用于治疗神经炎症相关AD的潜在试剂。
关键词: 3- mercaptopyruvate-sulfurtransferase(3MST),阿耳茨海默氏病,β-amyloid1-42,胱硫醚β合酶(CBS),硫化氢,神经炎症。
Current Alzheimer Research
Title:Sodium Hydrosulfide Attenuates Beta-Amyloid-Induced Cognitive Deficits and Neuroinflammation via Modulation of MAPK/NF-κB Pathway in Rats
Volume: 12 Issue: 7
Author(s): Huiyu Liu, Yuanyuan Deng, Jianmei Gao, Yuangui Liu, Wenxian li, Jingshan Shi and Qihai Gong
Affiliation:
关键词: 3- mercaptopyruvate-sulfurtransferase(3MST),阿耳茨海默氏病,β-amyloid1-42,胱硫醚β合酶(CBS),硫化氢,神经炎症。
摘要: Beta-amyloid (Aβ), a neurotoxic peptide, accumulates in the brain of Alzheimer's disease (AD) subjects to initiate neuroinflammation eventually leading to memory impairment. Here, we demonstrated that Aβ-injected rats exhibited cognitive impairment and neuroinflammation with a remarkable reduction of hydrogen sulfide (H2S) levels in the hippocampus compared with that in shamoperated rats. Interestingly, the expression of cystathionine-β-synthase (CBS) and 3- mercaptopyruvate-sulfurtransferase (3MST), the major enzymes responsible for endogenous H2S generation, were also significantly decreased. However, intraperitoneal (i.p.) injection of sodium hydrosulfide (NaHS, a H2S donor) dramatically attenuated cognitive impairment and neuroinflammation induced by hippocampal injection of 10 μg of Aβ1-42 in rats. Subsequently, NaHS significantly suppressed the expression of tumor necrosis factor (TNF)-α, interleukin-1β (IL-1β) and cyclooxygenase-2 (COX-2) in rat hippocampus following Aβ administration. Furthermore, NaHS exerted a beneficial effect on inhibition of IκB-α degradation and subsequent activation of transcription factor nuclear factor κB (NF-κB), as well as inhibition of extracellular signal-regulated kinase (ERK1/2) activity and p38 MAPK activity but not c-Jun N-terminal kinase (JNK) activity induced by Aβ. These results demonstrate that NaHS might be a potential agent for treatment of neuroinflammation-related AD.
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Huiyu Liu, Yuanyuan Deng, Jianmei Gao, Yuangui Liu, Wenxian li, Jingshan Shi and Qihai Gong , Sodium Hydrosulfide Attenuates Beta-Amyloid-Induced Cognitive Deficits and Neuroinflammation via Modulation of MAPK/NF-κB Pathway in Rats, Current Alzheimer Research 2015; 12 (7) . https://dx.doi.org/10.2174/1567205012666150713102326
DOI https://dx.doi.org/10.2174/1567205012666150713102326 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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