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胡黄连苷II对小鼠脑损伤的神经保护作用。

Neuroprotective effect of picroside II in brain injury in mice.

作者信息

Wang Yida, Fang Wei, Wu Liang, Yao Xueya, Wu Suzhen, Wang Jie, Xu Zhen, Tian Fubo, He Zhenzhou, Dong Bin

机构信息

Department of Neurosurgery, The First Affiliated Hospital of Dalian Medical University Dalian, China.

Department of Medicine, Hebei North University Zhangjiakou, Hebei, China.

出版信息

Am J Transl Res. 2016 Dec 15;8(12):5532-5544. eCollection 2016.

Abstract

Various types of brain injury which led to the damage of brain tissue structure and neurological dysfunction continues to be the major causes of disability and mortality. Picroside II (PII) possesses a wide range of pharmacological effects and has been proved to ameliorate ischemia and reperfusion injury of kidney and brain. However, critical questions remain about other brain injuries. We investigated the protective effect of PII in four well-characterized murine models of brain injury. Models showed a subsequent regional inflammatory response and oxidative stress in common, which might be improved by the administration of PII (20 mg/kg). Meanwhile, a series of morphological and histological analyses for reinforcement was performed. In traumatic, ischemic and infectious induced injuries, it was observed that the survival rate, apoptosis related proteins, Caspase-3, and the expression of acute inflammatory cytokines (IL-1β, IL-6 and TNF-α) were significantly alleviated after PII injection, but PII treatment alone showed no effect on them as well. The western blot results indicated that TLR4 and NF-κB were clearly downregulated with PII administration. In conclusion, our results suggested that PII with a recommended concentration of 20 mg/kg could provide neuroprotective effects against multi-cerebral injuries in mice by suppressing the over-reactive inflammatory responses and oxidative stress and attenuating the damage of brain tissue for further neurological recovery.

摘要

各类导致脑组织结构损伤和神经功能障碍的脑损伤仍是致残和致死的主要原因。胡黄连苷II(PII)具有广泛的药理作用,已被证明可改善肾脏和脑的缺血再灌注损伤。然而,关于其他脑损伤仍存在关键问题。我们研究了PII在四种特征明确的小鼠脑损伤模型中的保护作用。这些模型均表现出随后的局部炎症反应和氧化应激,而给予PII(20 mg/kg)可能会改善这些情况。同时,进行了一系列强化的形态学和组织学分析。在创伤性、缺血性和感染性诱导损伤中,观察到注射PII后存活率、凋亡相关蛋白、半胱天冬酶-3以及急性炎症细胞因子(IL-1β、IL-6和TNF-α)的表达均显著减轻,但单独使用PII治疗对它们也无影响。蛋白质印迹结果表明,给予PII后TLR4和NF-κB明显下调。总之,我们的结果表明,推荐浓度为20 mg/kg的PII可通过抑制过度活跃的炎症反应和氧化应激以及减轻脑组织损伤以促进进一步的神经功能恢复,从而对小鼠的多种脑损伤提供神经保护作用。

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