Effect of Mangiferin on Morphology of Relevant Vessels and MCP-1/CCR-2 Pathway in Spontaneously Hypertensive Rats

Cheng-pu LIAO; Xue-wen ZENG; Tian-tian XIN; Yu-mei MENG; Da-li HUANG; Xiao-qin HU

doi:10.13422/j.cnki.syfjx.20192039

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Effect of Mangiferin on Morphology of Relevant Vessels and MCP-1/CCR-2 Pathway in Spontaneously Hypertensive Rats

Pharmacology | 更新时间：2021-02-09

- Effect of Mangiferin on Morphology of Relevant Vessels and MCP-1/CCR-2 Pathway in Spontaneously Hypertensive Rats
- Chinese Journal of Experimental Traditional Medical Formulae Vol. 25, Issue 19, Pages: 39-45(2019)
- 作者机构：
  
  1.广西中医药大学，广西中药药效研究重点实验室，南宁　 530001；
  2.广西崇左市食品药品检验所，广西　崇左　 532200
- 作者简介：
- 基金信息：
- DOI：10.13422/j.cnki.syfjx.20192039
  CLC： R2-0; R285.5; R289
- Received：02 April 2019，
  
  Published Online：05 July 2019，
  
  Published：05 October 2019
- 稿件说明：
移动端阅览
Cheng-pu LIAO, Xue-wen ZENG, Tian-tian XIN, et al. Effect of Mangiferin on Morphology of Relevant Vessels and MCP-1/CCR-2 Pathway in Spontaneously Hypertensive Rats[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(19): 39-45.
DOI：

Cheng-pu LIAO, Xue-wen ZENG, Tian-tian XIN, et al. Effect of Mangiferin on Morphology of Relevant Vessels and MCP-1/CCR-2 Pathway in Spontaneously Hypertensive Rats[J]. Chinese journal of experimental traditional medical formulae, 2019, 25(19): 39-45. DOI： 10.13422/j.cnki.syfjx.20192039.

摘要

目的：

观察自发性高血压大鼠(SHR)颈动脉、胸主动脉、肠系膜上动脉形态学变化，进一步深入研究芒果苷对SHR相关血管炎性因子表达及单核细胞趋化蛋白-1(MCP-1)/趋化因子受体-2(CCR-2)通路的影响。

方法：

SHR 40只，随机分为模型组，苯那普利组(10 mg·kg

－1

)与芒果苷低、中、高剂量组(25，50，100 mg·kg

－1

)，另选同周龄8只雄性Wistar-Kyoto (WKY)大鼠为正常组。连续灌胃8周后，每两周观察各组大鼠收缩压情况，苏木素-伊红(HE)染色观察颈动脉、胸主动脉、肠系膜上动脉形态学，免疫组化(IHC)和蛋白免疫印迹法(Western blot)检测胸主动脉MCP-1，CCR-2的蛋白表达水平，实时荧光定量PCR(Real-time PCR)检测胸主动脉MCP-1，CCR-2 mRNA的表达。

结果：

与正常组比较，模型组炎症细胞明显增多，收缩压显著高于WKY组血压(

0.01)，胸主动脉中MCP-1，CCR-2蛋白和mRNA表达显著升高(

0.01)；与模型组比较，苯那普利以及芒果苷高剂量组炎症细胞明显减少，内皮边缘有改善、纤维组织浸润明显好转，收缩压显著降低(

0.01)，苯那普利及芒果苷低、中、高剂量组胸主动脉中MCP-1，CCR-2蛋白和mRNA表达水平显著降低(

0.01)。

结论：

自发性高血压大鼠颈动脉、胸主动脉、肠系膜上动脉存在一定的炎症损伤。其机制可能是芒果苷通过抑制SHR血管中MCP-1/CCR-2通路表达，从而对血管产生抗炎作用。

Abstract

Objective:

To observe the morphological changes of carotid artery

thoracic aorta and superior mesenteric artery in spontaneously hypertensive rats(SHR)

in order to further study the effect of Mangiferin on the expressions of inflammatory factors and monocyte chemoattract protein-1 (MCP-1)/c-chemokine receptor type 2 (CCR-2) pathway in SHR.

Method:

Forty spontaneously hypertensive rats were randomly divided into model group

benazepril group (10 mg·kg

-1

·d

-1

) and low

medium and high-dose mangiferin groups (25

100 mg·kg

-1

·d

-1

). Eight male WKY rats of the same age were selected as normal control group. Systolic blood pressure was observed every two weeks after eight weeks of administration. Morphology of carotid artery

thoracic aorta and superior mesenteric artery was observed by hematoxylin-eosin (HE) staining. Immunohistochemical assay (IHC) and Western blot were used to detect MCP-1 and CCR-2 protein expressions in thoracic aorta. MCP-1 and CCR-2 mRNA expression levels in thoracic aorta were detected by Real-time quantitative fluorescence PCR (Real-time PCR).

Result:

Compared with the normal group

the inflammatory cells in the model group increased significantly

the systolic blood pressure was significantly higher than that in the WKY group (

0.01)

and MCP-1

CCR-2 protein and mRNA expressions in thoracic aorta were increased obviously (

0.01). Compared with model group

in high-dose benazepril and mangiferin groups

inflammatory cells were decreased significantly

endothelial margin and fibrous tissue infiltration were improved significantly

and systolic blood pressure was decreased significantly (

0.01). MCP-1

CCR-2 protein and mRNA expression in thoracic aorta of benazepril and mangiferin groups decreased significantly (

0.01).

Conclusion:

There are inflammation damages in carotid artery

thoracic aorta and superior mesenteric artery of spontaneously hypertensive rats. Mangiferin has an anti-inflammatory effect by possibly inhibiting the expressions of MCP-1/CCR-2 pathway in SHR vessels.

关键词

Keywords

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