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首页> 外文期刊>Frontiers in Neuropharmacology >α-Asarone Attenuates Cognitive Deficit in a Pilocarpine-Induced Status Epilepticus Rat Model via a Decrease in the Nuclear Factor-κB Activation and Reduction in Microglia Neuroinflammation
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α-Asarone Attenuates Cognitive Deficit in a Pilocarpine-Induced Status Epilepticus Rat Model via a Decrease in the Nuclear Factor-κB Activation and Reduction in Microglia Neuroinflammation

机译：α-Asarone通过减少核因子-κB的激活和减少小胶质细胞神经炎症来减轻毛果芸香碱诱导的癫痫持续状态大鼠模型的认知缺陷。

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Background: Temporal lobe epilepsy (TLE) is one of the most drug-resistant types of epilepsy with about 80% of TLE patients falling into this category. Increasing evidence suggests that neuroinflammation, which has a critical role in the epileptogenesis of TLE, is associated with microglial activation. Therefore, agents that act towards the alleviation in microglial activation and the attenuation of neuroinflammation are promising candidates to treat TLE. α-Asarone is a major active ingredient of the Acori Graminei Rhizoma used in Traditional Chinese Medicine, which has been used to improve various disease conditions including stroke and convulsions. In addition, an increasing number of studies suggested that α-asarone can attenuate microglia-mediated neuroinflammation. Thus, we hypothesized that α-asarone is a promising neuroprotective agent for the treatment of the TLE. Methods: The present study evaluated the therapeutic effects of α-asarone on microglia-mediated neuroinflammation and neuroprotection in vitro and in vivo, using an untreated control group, a SE-induced group, and an SE-induced α-asarone pre-treated group. A pilocarpine-induced rat model of TLE was established to investigate the neuroprotective effects of α-asarone in vivo. For the in vitro study, lipopolysaccharide (LPS)-stimulated primary cultured microglial cells were used. Results: The results indicated that the brain microglial activation in the rats of the status epilepticus rat model led to important learning and memory deficit. Preventive treatment with α-asarone restrained microglial activation and reduced learning and memory deficit. In the in vitro studies, α-asarone significantly suppressed pro-inflammatory cytokine production in primary cultured microglial cells and attenuated the LPS-stimulated neuroinflammatory responses. Our mechanistic study revealed that α-asarone inhibited inflammatory processes by regulation the transcription levels of kappa-B, by blocking the degradation pathway of kappa B-alpha (IκB-α)and kappa B-beta (IκB-β) kinase in both the status epilepticus rats and in primary cultured microglial cells. Conclusions: Taken together, these data demonstrate that α-asarone is a promising neuroprotective agent for the prevention and treatment of microglia-mediated neuroinflammatory conditions including TLE, for which further assessment studies are pertinent.
机译：背景：颞叶癫痫（TLE）是最耐药的癫痫类型之一，约80％的TLE患者属于此类。越来越多的证据表明，在TLE的癫痫发生中起关键作用的神经炎症与小胶质细胞活化有关。因此，在减轻小胶质细胞活化和减轻神经炎症方面起作用的药物有望成为治疗TLE的候选药物。 α-Asarone是中药Acori Graminei Rhizoma的主要活性成分，已被用于改善各种疾病，包括中风和惊厥。此外，越来越多的研究表明α-细辛可以减轻小胶质细胞介导的神经炎症。因此，我们假设α-细辛酮是用于治疗TLE的有前途的神经保护剂。方法：本研究使用未经治疗的对照组，SE诱导组和SE诱导的α-细辛酮预处理组，评估了α-细辛酮对小胶质细胞介导的神经炎症和神经保护作用的体内外治疗作用。 。建立了毛果芸香碱诱导的TLE大鼠模型，以研究α-细辛醚在体内的神经保护作用。对于体外研究，使用脂多糖（LPS）刺激的原代培养小胶质细胞。结果：结果表明，癫痫持续状态大鼠模型的脑小胶质细胞活化导致重要的学习和记忆缺陷。 α-细辛醚的预防性治疗可抑制小胶质细胞活化，并减少学习和记忆障碍。在体外研究中，α-细辛醚显着抑制了原代培养的小胶质细胞中促炎性细胞因子的产生，并减弱了LPS刺激的神经炎症反应。我们的机理研究表明，α-细辛可以通过调节kappa-B的转录水平，阻断kappaB-α（IκB-α）和kappa B-beta（IκB-β）激酶的降解途径来抑制炎症过程。状态癫痫大鼠和原代培养的小胶质细胞。结论：综上所述，这些数据表明，α-细辛醚是预防和治疗小胶质细胞介导的神经炎性疾病（包括TLE）的有前途的神经保护剂，对此进行进一步的评估研究。

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