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The intervention mechanism of emodin on TLR3 pathway in the process of central nervous system injury caused by herpes virus infection
Neurological Research ( IF 1.7 ) Pub Date : 2020-12-04 , DOI: 10.1080/01616412.2020.1853989
Yongqian Huang 1 , Xing Li 1 , Chunlian Pan 1 , Wei Cheng 1 , Xijia Wang 1 , Zhigang Yang 1 , Lifang Zheng 2
Affiliation  

ABSTRACT

Background and purpose: To investigate the effect of Emodin on the inflammatory response of brain tissue and the expression of the TLR3 pathway in mice with herpes virus encephalitis.

Method: Twenty male BALB/c mice were randomly divided into the NS group, HSV-1 group, HSV-1 + Emodin group and HSV-1 + ACV group. The histopathological features and the effect of TLR3 expression were observed by staining and immunohistochemistry (IHC) respectively. The gene expression of TLR3, trif, TRADD, TRAF6, traf3, p38, Nemo and IRF3 was detected by polymerase chain reaction (PCR). The protein production of TLR3 and its downstream molecules was detected by Western blot. The expression of IL-6, TNF-α and IFN-β in the brain tissues was detected by ELISA.

Result: Compared to the HSV-1 group, the pathological changes (inflammatory cell infiltration, necrotic temporal lobe and massive hemorrhage) were not as obvious as those in the HSV-1+emodin and HSV-1+ACV groups. The TLR3 staining increased significantly in the HSV-1 groups and decreased in the HSV-1 + emodin group. Compared with the NS group, the mRNA expression of TLR3, TRIF, TRADD, TRAF6, traf3, p38, NEMO and IRF3 decreased by 20%–60% in the HSV-1 + emodin group and 30% in the HSV-1 + ACV group, respectively. The expression of IL-6, TNF-α and IFN-β decreased by 30%-50% in the HSV-1 + emodin group and showed no significant change in the HSV-1 + ACV group, respectively.

Conclusion: Emodin could inhibit the inflammatory response in the brain of mice with herpes virus encephalitis. The inhibition of TLR3 expression may play an important role in this process.



中文翻译:

大黄素在疱疹病毒感染中枢神经系统损伤过程中对TLR3通路的干预机制

摘要

背景与目的:研究大黄素对疱疹病毒性脑炎小鼠脑组织炎症反应及TLR3通路表达的影响。

方法:20只雄性BALB/c小鼠随机分为NS组、HSV-1组、HSV-1+大黄素组和HSV-1+ACV组。分别通过染色和免疫组织化学(IHC)观察组织病理学特征和TLR3表达的影响。聚合酶链反应(PCR)检测TLR3、trif、TRADD、TRAF6、traf3、p38、Nemo和IRF3的基因表达。通过蛋白质印迹检测TLR3及其下游分子的蛋白质产生。ELISA检测脑组织中IL-6、TNF-α和IFN-β的表达。

结果:与HSV-1组相比,病理改变(炎症细胞浸润、颞叶坏死、大出血)不如HSV-1+大黄素组和HSV-1+ACV组明显。TLR3 染色在 HSV-1 组中显着增加,在 HSV-1 + 大黄素组中减少。与NS组相比,HSV-1+大黄素组TLR3、TRIF、TRADD、TRAF6、traf3、p38、NEMO和IRF3的mRNA表达下降20%~60%,HSV-1+ACV下降30%组,分别。HSV-1+大黄素组IL-6、TNF-α和IFN-β表达降低30%-50%,HSV-1+ACV组无明显变化。

结论:大黄素能抑制疱疹病毒性脑炎小鼠脑部炎症反应。TLR3表达的抑制可能在这一过程中起重要作用。

更新日期:2020-12-04
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