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首页> 外文期刊>Journal of cellular physiology. >Melatonin attenuates reactive astrogliosis and glial scar formation following cerebral ischemia and reperfusion injury mediated by GSK‐3β and RIP1K
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Melatonin attenuates reactive astrogliosis and glial scar formation following cerebral ischemia and reperfusion injury mediated by GSK‐3β and RIP1K

机译：褪黑激素变弱反应astrogliosis和脑缺血后神经胶质疤痕形成和再灌注损伤由葛兰素史克3β

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Abstract Even though astrocytes have been widely reported to support several brain functions, studies have emerged that they exert deleterious effects on the brain after ischemia and reperfusion (I/R) injury. The present study investigated the neuroprotective effects of melatonin on the processes of reactive astrogliosis and glial scar formation, as well as axonal regeneration after transient middle cerebral artery occlusion. Male Wistar rats were randomly divided into four groups: sham‐operated, I/R, I/R treated with melatonin, and I/R treated with edaravone. All drugs were administered via intraperitoneal injection at the onset of reperfusion and were continued until the rats were sacrificed on Day 7 or 14 after the surgery. Melatonin presented long‐term benefits on cerebral damage after I/R injury, as demonstrated by a decreased infarct volume, histopathological changes, and reduced neuronal cell death. We also found that melatonin attenuated reactive astrogliosis and glial scar formation and, consequently, enhanced axonal regeneration and promoted neurobehavioral recovery. Furthermore, glycogen synthase kinase‐3 beta (GSK‐3β) and receptor‐interacting serine/threonine‐protein 1 kinase (RIP1K), which had previously been revealed as proteins involved in astrocyte responses, were significantly reduced after melatonin administration. Taken together, melatonin effectively counteracted the deleterious effects due to astrocyte responses and improved axonal regeneration to promote functional recovery during the chronic phase of cerebral I/R injury by inhibiting GSK‐3β and RIP1K activities.
机译：摘要尽管星形胶质细胞广泛据报道,支持一些大脑功能,研究发现他们施加有害对脑缺血后的影响再灌注(I / R)损伤。调查的神经保护作用褪黑激素反应的过程astrogliosis和胶质瘢痕的形成,以及轴突再生后短暂的中间脑动脉闭塞。随机分为四组:虚假的高操作I / R, I / R褪黑激素处理,和I / R治疗药物不良反应。腹腔内注射的发作再灌注,并一直持续到老鼠是牺牲了手术后7天或14。褪黑激素了长期利益脑损伤后的I / R损伤,作为证明通过减少梗塞体积,组织病理学变化,减少神经细胞死亡。发现褪黑激素减毒活性astrogliosis和胶质疤痕形成,因此,轴突再生和提高促进神经行为复苏。糖原合成酶激酶3β(GSK 3β)应承担的和受体相互作用应承担的丝氨酸/苏氨酸蛋白质1以前的激酶(RIP1K)发现是蛋白质参与星形胶质细胞反应,后被显著降低褪黑激素。褪黑激素有效抵消由于有害影响星形胶质细胞反应和改善促进轴突再生在慢性阶段的功能恢复脑I / R损伤,抑制葛兰素史克的3βRIP1K活动。

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