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L-carnitine and Co Q10 ameliorate potassium dichromate -induced acute brain injury in rats targeting AMPK/AKT/NF-κβ
International Immunopharmacology ( IF 5.6 ) Pub Date : 2021-09-04 , DOI: 10.1016/j.intimp.2021.107867
Abeer Salama 1 , Rania Elgohary 2
Affiliation  

Adenosine monophosphate-activated protein kinase (AMPK) has a crucial role in neuroprotection. It phosphorylates serine/threonine kinase (Akt) Substrate inhibiting the inflammatory responses induced by the nuclear factor-κB (NF-κB). Exposure to chromium VI dust among workers has been reported and induced brain injury, as the absorption of chromium through the nasal membrane has been found to deliver it directly to the brain. The study aimed to investigate the influence of administration of L-carnitine or/and Co Q10 as theraputic agents against potassium dichromate (PD)-induced brain injury via AMPK/AKT/NF-κβ signaling pathway. Brain injury was induced by PD intranasally as a single dose of 2 mg/kg, 24 h latter rats received L-carnitine (100 mg/kg; orally), Co Q10 (50 mg/kg; orally) and L-carnitine (50 mg/kg; orally) + Co Q10 (25 mg/kg; orally) respectively for 3 days. Locomotor activity was assessed before and at the end of the experiment, then, biochemical and histopathological investigations were assessed in brain homogenate. The exposure of rats to PD promoted oxidative stress and inflammation via an increase in MDA and a decrease in GSH serum contents with an increase in brain contents of TNF-α, IL-6, and NF-kβ and reduced AMPK and AKT brain contents as compared to the control group. Treatment with L-carnitine + Co Q10 ameliorated cognitive impairment and oxidative stress, decreased the brain contents of inflammatory mediators; TNF-α, IL-6, and NF-κβ elevated AMPK and AKT, as compared to each drug. Also, L-carnitine + Co Q10 administration restored morphological changes as degenerated neurons and necrosis. L-carnitine + Co Q10 play important role in AMPK/AKT/NF-κβ pathway that responsible for their antioxidant and anti-inflammatory effects against PD-induced brain injury in rats.



中文翻译:

左旋肉碱和辅酶 Q10 改善重铬酸钾诱导的大鼠急性脑损伤,靶向 AMPK/AKT/NF-κβ

腺苷一磷酸活化蛋白激酶 (AMPK) 在神经保护中具有至关重要的作用。它磷酸化丝氨酸/苏氨酸激酶 (Akt) 底物,抑制由核因子-κB (NF-κB) 诱导的炎症反应。据报道,工人接触六价铬粉尘会导致脑损伤,因为已发现通过鼻膜吸收铬会直接将铬输送到大脑。本研究旨在通过 AMPK/AKT/NF-κβ 信号通路研究左旋肉碱或/和 Co Q10 作为治疗剂对重铬酸钾 (PD) 诱导的脑损伤的影响。PD 鼻内单剂量 2 mg/kg 诱导脑损伤,24 小时后大鼠接受左旋肉碱(100 mg/kg;口服)、Co Q10(50 mg/kg;口服)和左旋肉碱(50 mg/kg;口服)+ Co Q10(25 mg/kg;口服)分别为 3 天。在实验之前和结束时评估运动活动,然后在脑匀浆中评估生化和组织病理学研究。大鼠暴露于 PD 通过增加 MDA 和降低 GSH 血清含量来促进氧化应激和炎症,同时脑内 TNF-α、IL-6 和 NF-kβ 含量增加,并降低 AMPK 和 AKT 脑含量与对照组相比。左旋肉碱 + 辅酶 Q10 治疗可改善认知障碍和氧化应激,降低炎症介质的脑含量;与每种药物相比,TNF-α、IL-6 和 NF-κβ 升高了 AMPK 和 AKT。此外,左旋肉碱 + 辅酶 Q10 给药恢复了退化神经元和坏死的形态变化。

更新日期:2021-09-04
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