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大黄素通过 TLR3 通路在疱疹病毒感染致中枢神经损伤过程中的干预机制。

The intervention mechanism of emodin on TLR3 pathway in the process of central nervous system injury caused by herpes virus infection.

机构信息

Department of Neurology, Puren Hospital Affiliated to Wuhan University of Science and Technology, Wuhan, China.

Department of Neurology, Yantian Hospital of Southern University of Science and Technology, Shenzhen, China.

出版信息

Neurol Res. 2021 Apr;43(4):307-313. doi: 10.1080/01616412.2020.1853989. Epub 2020 Dec 4.

DOI:10.1080/01616412.2020.1853989
PMID:33274693
Abstract

: 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.: 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.: 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.: 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.

摘要

目的

研究大黄素对单纯疱疹病毒脑炎小鼠脑组织炎症反应及 TLR3 通路表达的影响。

方法

将 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化(IHC)观察 TLR3 表达的组织病理学特征和效果,通过聚合酶链反应(PCR)检测 TLR3、trif、TRADD、TRAF6、traf3、p38、Nemo 和 IRF3 的基因表达,通过 Western blot 检测 TLR3 及其下游分子的蛋白产生,通过 ELISA 检测脑内组织中 IL-6、TNF-α 和 IFN-β 的表达。

结果

与 HSV-1 组相比,HSV-1+大黄素组和 HSV-1+ACV 组的病理变化(炎症细胞浸润、坏死颞叶和大量出血)不那么明显,HSV-1 组 TLR3 染色明显增加,而 HSV-1+大黄素组减少。与 NS 组相比,HSV-1+大黄素组 TLR3、TRIF、TRADD、TRAF6、traf3、p38、NEMO 和 IRF3 的 mRNA 表达分别下降 20%60%,HSV-1+ACV 组下降 30%;HSV-1+大黄素组 IL-6、TNF-α 和 IFN-β 表达分别下降 30%50%,HSV-1+ACV 组无明显变化。

结论

大黄素可抑制单纯疱疹病毒脑炎小鼠脑内炎症反应,抑制 TLR3 表达可能在此过程中发挥重要作用。

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