Introduction
Triptolide, extracted from Chinese medicinal materials Tripterygium wilfordii Hook F (TwHF), has immunosuppressive, anti-inflammatory and anti-tumour effects. The purpose of this study was to examine whether triptolide has the neuroprotective effect on cerebral ischemia-reperfusion (I/R) injury and to explore its possible mechanism.

Material and methods
The rat model of focal cerebral I/R was established by the suture-occluded method. The SD rats were randomly divided into five groups: sham operation group (Sham group), ischemia-reperfusion model group (I/R group), low concentration of triptolide group (12.5 mg/kg, TL-L group), medium concentration of triptolide group (25 mg/kg, TL-M group) and high concentration of triptolide group (50 mg/kg, TL-H group). The neurological function of the rats was scored, the degree of brain oedema was detected by the dry-wet method, and the cerebral infarction area was determined by TTC staining. Nissl staining was used to detect neuronal damage. The contents of reactive oxygen species (ROS), malondialdehyde (MDA) and superoxide dismutase (SOD) were also detected. Meanwhile, the expression level of proteins related to Wnt/-catenin signalling pathway was measured by Western blot.

Results
Compared with the I/R group, cerebral oedema, infarct volume, neurological impairment, the contents of MDA and ROS were reduced, while the SOD level was increased in the TL-L, TL-M, and TL-H groups. The results of Nissl staining showed that triptolide could reduce the nerve cell injury caused by cerebral I/R. In addition, the results of Western blot confirmed that the expression of Wnt1, -catenin, c-Myc, and Cyclin-D1 were down-regulated after triptolide intervention, that is, inhibited the activation of Wnt/-catenin signalling pathway.

Conclusions
Triptolide mediates Wnt/-catenin signalling pathway to alleviate cerebral I/R injury in rats. This study provides ideas and experimental basis for the treatment of ischemic stroke patients.



中文翻译：

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雷公藤内酯介导Wnt/β-catenin信号通路减轻大鼠脑缺血再灌注损伤

介绍
雷公藤内酯是从中药材雷公藤钩F（TwHF）中提取的，具有免疫抑制、抗炎和抗肿瘤作用。本研究旨在探讨雷公藤内酯对脑缺血再灌注（I/R）损伤是否具有神经保护作用，并探讨其可能的机制。

材料与方法
采用缝合法建立局灶性脑I/R大鼠模型。SD大鼠随机分为5组：假手术组（Sham组）、缺血再灌注模型组（I/R组）、低浓度雷公藤内酯组（12.5 mg/kg、TL-L组）、中浓度雷公藤内酯组（25 mg/kg，TL-M组）和高浓度雷公藤内酯组（50 mg/kg，TL-H组）。对大鼠进行神经功能评分，干湿法检测脑水肿程度，TTC染色确定脑梗死面积。尼氏染色用于检测神经元损伤。还检测了活性氧（ROS）、丙二醛（MDA）和超氧化物歧化酶（SOD）的含量。同时，

结果
与I/R组相比，TL-L、TL-M和TL-H组脑水肿、梗死体积、神经功能障碍、MDA和ROS含量降低，SOD水平升高。Nissl染色结果显示雷公藤内酯能减轻脑I/R引起的神经细胞损伤。此外，Western blot结果证实雷公藤内酯干预后Wnt1、-catenin、c-Myc和Cyclin-D1的表达下调，即抑制Wnt/-catenin信号通路的激活。

结论
雷公藤内酯介导Wnt/-catenin信号通路减轻大鼠脑I/R损伤。本研究为缺血性脑卒中患者的治疗提供思路和实验依据。