Protective Effect and Mechanism of Sodium Ferulate on Cerebral  Ischemia-reperfusion Inflammatory Injury in Rats

Wan GONG; Xiao-ling CHEN; Li ZHOU; Ke-na ZHANG

doi:10.13422/j.cnki.syfjx.20190341

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Protective Effect and Mechanism of Sodium Ferulate on Cerebral Ischemia-reperfusion Inflammatory Injury in Rats

Pharmacology | 更新时间：2021-02-09

- Protective Effect and Mechanism of Sodium Ferulate on Cerebral Ischemia-reperfusion Inflammatory Injury in Rats
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 3, Pages: 94-99(2019)
- 作者机构：
  
  1.浙江中医药大学　基础医学院，杭州　 310053
  2.浙江中医药大学　附属第一医院，杭州　 310006
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20190341
  CLC： R285;R285.5;R743.31
- Received：06 September 2018，
  
  Published Online：16 November 2018，
  
  Published：05 February 2019
- 稿件说明：
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Wan GONG, Xiao-ling CHEN, Li ZHOU, et al. Protective Effect and Mechanism of Sodium Ferulate on Cerebral Ischemia-reperfusion Inflammatory Injury in Rats[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(3): 94-99.
DOI：

Wan GONG, Xiao-ling CHEN, Li ZHOU, et al. Protective Effect and Mechanism of Sodium Ferulate on Cerebral Ischemia-reperfusion Inflammatory Injury in Rats[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(3): 94-99. DOI： 10.13422/j.cnki.syfjx.20190341.

摘要

目的:

观察阿魏酸钠对大鼠脑缺血再灌注炎症损伤的保护作用，并探讨其作用机制。

方法:

取SD雄性大鼠，建立大脑中动脉阻塞(MCAO)致脑缺血／再灌注损伤模型，造模成功的36只随机分成模型组，阿魏酸钠低、中、高剂量组(25，50，100 mg·kg

-1

)，并另取9只作为假手术组。采用神经功能评分法观察大鼠神经功能情况；苏木精-伊红(HE)染色观察大鼠脑组织病理学形态变化；酶联免疫吸附测定(ELISA)检测大鼠血清和脑组织中肿瘤坏死因子-

(TNF-

)，白细胞介素-1

(IL-1

)，白细胞介素-6(IL-6)含量变化；蛋白免疫印迹法(Western blot)检测缺血周边区核转录因子-кB p65(NF-

B p65)蛋白表达。

结果:

与假手术组比较，模型组大鼠神经行为学评分升高，神经元坏死，大量炎症细胞产生，血清和脑组织中TNF-

，IL-1

，IL-6水平显著升高(

0.01)，细胞核／细胞浆NF-

B p65蛋白表达比例显著升高(

0.01)；与模型组比较，阿魏酸钠可明显降低脑损伤大鼠神经行为学评分(

0.05，

0.01)，抑制神经元坏死，减少炎症细胞产生，并可明显降低血清和脑组织中TNF-

，IL-1

，IL-6水平(

0.05，

0.01)，抑制NF-

B p65由细胞质向细胞核转位(

0.05，

0.01)，最终减轻缺血再灌注造成的神经细胞炎症损伤。

结论:

阿魏酸钠可通过抑制NF-

B p65核转位减轻缺血再灌注大鼠脑神经细胞炎症反应，维持脑部正常形态，这可能是其发挥脑保护作用的机制之一。

Abstract

Objective:

To investigate the protective effect of sodium ferulate on cerebral ischemia-reperfusion injury in rats and to explore its possible mechanism.

Method:

The cerebral ischemia reperfusion injury model was established by middle cerebral artery occlusion (MCAO) in SD male rats. 36 modeled rats with neurologic damage were randomly divided into 4 groups: model group

low

medium

high-dose sodium ferulate groups (25

100 mg·kg

-1

). Another nine rats were selected as a sham operation group.Neurological function was assessed by neurological scoring system in rats.Hematoxylin-eosin (HE) staining was performed to observe the pathological changes of the rats' brain. The levels of tumor necrosis factor

(TNF-

)

interleukin-1

(IL-1

) and interleukin-6 (IL-6) in serum and brain tissues were detected by enzyme-linked immunosorbent assay (ELISA). Western blot was used to detect the protein expression of nucleus and cytoplasm nuclear factor-kappa B p65 (NF-

B p65) in brain tissues.

Result:

As compared with normal group

neurological deficit score was increased; the neuronal necrosis and inflammatory cell number were present; the serum and brain tissue levels of TNF-

IL-1

and IL-6 were increased; nucleus/cytoplasm NF-

B p65 protein expression ratio was increased significantly in model group (

0.01). As compared with model group

sodium ferulate distinctly decreased the neurological deficit score(

0.05

0.01)

inhibited neuronal necrosis

reduce inflammatory cell number

significantly reduce the serum and brain tissue levels of TNF-

IL-1

and IL-6(

0.05

0.01). Western blot showed that sodium ferulate could inhibit the nuclear translocation of NF-

B p65 protein(

0.05

0.01)

and finally

it can alleviate the inflammatory injury caused by ischemia reperfusion.

Conclusion:

Sodium ferulate protects the brain against focal cerebral ischemia reperfusion injury

and the mechanism may be related to inhibiting nuclear translocation of NF-

B p65 protein to alleviate inflammatory response.

关键词

Keywords

references

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