Abstract：
BACKGROUND: Sleep and stress interact bidirectionally by acting on brain circuits that affect metabolism. Sleep and its alterations have impact on blood leptin levels, metabolic hormone that regulates appetite. Brain expresses the receptors for the peptide hormone leptin produced from adipocytes. The hypothalamic orexin neurons are low during sleep and active when awake, influenced by a complex interaction with leptin. Thymoquinone was found to be the major bioactive component of Nigella sativa. The aim of this study was to study the role of thymoquinone on sleep restriction and its mitigating effect on leptin-mediated signaling pathway in rat brain.
RESULTS: 30 adult male Wistar rats were divided into 5 groups with 6 animals in each group: Control; Thymoquinone (TQ); Corn oil; Chronic Sleep restriction (CSR); and CSR + TQ. After 30 days, behavioral analysis, antioxidant, lipid profile, glucose level, liver and kidney function test, neurotransmitters, neuropeptides, and mRNA expression in in vivo studies were also assessed and pharmacokinetic and docking were done for thymoquinone. Thymoquinone has also shown good binding affinity to the target proteins. CSR has induced oxidative stress in the discrete brain regions and plasma. Current study has shown many evidences that sleep restriction has altered the neurobehavioral, antioxidant status, lipid profile, neurotransmitters, neuropeptide levels, and feeding behavior which damage the Orexin-leptin system which regulates the sleep and feeding that leads to metabolic dysfunction.
CONCLUSIONS: The potentiality of Thymoquinone was revealed in in silico studies, and its action in in vivo studies has proved its effectiveness. The study concludes that Thymoquinone has exhibited its effect by diminishing the metabolic dysfunction by its neuroprotective, antioxidant, and hypolipidemic properties.
RESULTS: 30 adult male Wistar rats were divided into 5 groups with 6 animals in each group: Control; Thymoquinone (TQ); Corn oil; Chronic Sleep restriction (CSR); and CSR + TQ. After 30 days, behavioral analysis, antioxidant, lipid profile, glucose level, liver and kidney function test, neurotransmitters, neuropeptides, and mRNA expression in in vivo studies were also assessed and pharmacokinetic and docking were done for thymoquinone. Thymoquinone has also shown good binding affinity to the target proteins. CSR has induced oxidative stress in the discrete brain regions and plasma. Current study has shown many evidences that sleep restriction has altered the neurobehavioral, antioxidant status, lipid profile, neurotransmitters, neuropeptide levels, and feeding behavior which damage the Orexin-leptin system which regulates the sleep and feeding that leads to metabolic dysfunction.
CONCLUSIONS: The potentiality of Thymoquinone was revealed in in silico studies, and its action in in vivo studies has proved its effectiveness. The study concludes that Thymoquinone has exhibited its effect by diminishing the metabolic dysfunction by its neuroprotective, antioxidant, and hypolipidemic properties.
摘要：
背景：睡眠和压力通过作用于影响新陈代谢的大脑回路而双向相互作用。睡眠及其改变对血液瘦素水平有影响，调节食欲的代谢激素。大脑表达由脂肪细胞产生的肽激素瘦素的受体。下丘脑食欲素神经元在睡眠时很低，清醒时很活跃，受与瘦素复杂相互作用的影响。发现胸腺醌是紫花苜蓿的主要生物活性成分。本研究的目的是研究百里香醌对睡眠限制的作用及其对大鼠脑内瘦素介导的信号通路的缓解作用。
结果:将30只成年雄性Wistar大鼠分为5组,每组6只动物:对照组;胸醌(TQ);玉米油;慢性睡眠限制(CSR);和CSR+TQ。30天后,行为分析,抗氧化剂，血脂谱,葡萄糖水平，肝肾功能检查,神经递质,神经肽，还评估了体内研究中的mRNA表达，并对百里香醌进行了药代动力学和对接。胸醌还显示了对靶蛋白的良好结合亲和力。CSR在离散的大脑区域和血浆中诱导了氧化应激。目前的研究表明，许多证据表明睡眠限制改变了神经行为，抗氧化状态，血脂谱,神经递质,神经肽水平，和摄食行为，破坏调节睡眠和摄食的食欲素-瘦素系统，导致代谢功能障碍。
结论：在计算机研究中揭示了胸腺醌的潜力，其在体内的作用研究已经证明了其有效性。该研究得出结论，胸腺醌通过其神经保护作用减少代谢功能障碍，抗氧化剂，和降血脂特性。
结果:将30只成年雄性Wistar大鼠分为5组,每组6只动物:对照组;胸醌(TQ);玉米油;慢性睡眠限制(CSR);和CSR+TQ。30天后,行为分析,抗氧化剂，血脂谱,葡萄糖水平，肝肾功能检查,神经递质,神经肽，还评估了体内研究中的mRNA表达，并对百里香醌进行了药代动力学和对接。胸醌还显示了对靶蛋白的良好结合亲和力。CSR在离散的大脑区域和血浆中诱导了氧化应激。目前的研究表明，许多证据表明睡眠限制改变了神经行为，抗氧化状态，血脂谱,神经递质,神经肽水平，和摄食行为，破坏调节睡眠和摄食的食欲素-瘦素系统，导致代谢功能障碍。
结论：在计算机研究中揭示了胸腺醌的潜力，其在体内的作用研究已经证明了其有效性。该研究得出结论，胸腺醌通过其神经保护作用减少代谢功能障碍，抗氧化剂，和降血脂特性。
