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七氟醚后处理通过 TLR4/NF-κB 通路对大鼠脑缺血再灌注损伤的影响。

Effects of sevoflurane post-conditioning in cerebral ischemia-reperfusion injury via TLR4/NF-κB pathway in rats.

机构信息

Department of Anesthesiology, School of Medicine, Shandong University, Jinan, Shandong, China.

出版信息

Eur Rev Med Pharmacol Sci. 2018 Mar;22(6):1770-1775. doi: 10.26355/eurrev_201803_14595.

Abstract

OBJECTIVE

The aim of the study was to investigate the anti-inflammatory effect of sevoflurane post-conditioning on cerebral ischemia-reperfusion injury in rats.

MATERIALS AND METHODS

Thirty Sprague Dawley (SD) rats were randomly divided into 3 groups: sham operation group (Sham), ischemia/reperfusion injury (I/R) group and sevoflurane post-conditioning group (Se). Hematoxylin-eosin (HE) staining was used to observe the inflammatory response in the brain tissue. The levels of TNF-α, IL-1β, IL-6 in serum were measured by ELISA. The mRNA and protein expression of TLR4 and NF-κB p65 were detected by RT-PCR and Western blot in the brain tissue.

RESULTS

The post-conditioning of sevoflurane decreased the level of inflammatory reaction in ischemic-reperfusion rat cerebral infarction area and reduced the levels of pro-inflammatory cytokines such as TNF-α, IL-1β, IL-6 in rats with ischemia-reperfusion injury. In addition, after treatment with sevoflurane, the mRNA and protein expression of TLR4 and NF-κBp65 in TLR4/NF-κB pathway was inhibited.

CONCLUSIONS

Sevoflurane post-conditioning can decrease the inflammatory reaction in cerebral infarct area induced by cerebral ischemia-reperfusion injury in rats. The neuroprotective effect mechanism of sevoflurane may be related to TLR4/NF-κB signaling pathway.

摘要

目的

本研究旨在探讨七氟醚后处理对大鼠脑缺血再灌注损伤的抗炎作用。

材料与方法

30 只 Sprague Dawley(SD)大鼠随机分为 3 组:假手术组(Sham)、缺血再灌注损伤组(I/R)和七氟醚后处理组(Se)。苏木精-伊红(HE)染色观察脑组织的炎症反应。酶联免疫吸附试验(ELISA)检测血清中 TNF-α、IL-1β、IL-6 的水平。采用 RT-PCR 和 Western blot 检测脑组织中 TLR4 和 NF-κB p65 的 mRNA 和蛋白表达。

结果

七氟醚后处理降低了缺血再灌注大鼠脑梗死区炎症反应水平,降低了缺血再灌注损伤大鼠 TNF-α、IL-1β、IL-6 等促炎细胞因子的水平。此外,七氟醚处理后,TLR4/NF-κB 通路中 TLR4 和 NF-κBp65 的 mRNA 和蛋白表达受到抑制。

结论

七氟醚后处理可减轻大鼠脑缺血再灌注损伤所致脑梗死区的炎症反应。七氟醚的神经保护作用机制可能与 TLR4/NF-κB 信号通路有关。

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