Protective effects of mangiferin on inflammatory injury of cerebral tissue in spontaneously hypertensive rats
10.3969/j.issn.1001-1528.2017.06.004
- VernacularTitle:芒果苷对自发性高血压大鼠脑组织炎症损伤的保护作用
- Author:
Xiaoqin HU
;
Jiagang DENG
;
Zhengcai DU
;
Erwei HAO
;
Wenhui QIN
- Keywords:
mangiferin;
spontaneously hypertensive rat;
cerebral tissue;
inflammatory reaction;
MCP/CCR2 signaling pathway
- From:
Chinese Traditional Patent Medicine
2017;39(6):1126-1133
- CountryChina
- Language:Chinese
-
Abstract:
AIM To observe the protective effects of mangiferin on the inflammatory injury and expression of the inflammatory factor in the cerebral tissue of spontaneously hypertensive rats and on MCP-1/CCR2 signal pathway.METHODS Forty spontaneously hypertensive rats were randomly divided into model,benazepril [10 mg/(kg · d)] and mangiferin high,middle and low dose [40,20,10 mg/(kg · d)] groups and other eight rats of same week age served as control group.After consecutive intragastric administration for eight weeks,morphology of the rats' cerebral tissue was observed;their levels of ICAM-1,IL-6 and TNF-α in cerebral tissue were determined by ELISA;their expressions of MCP-1 and CCR2 protein in brain tissue of rats were detected by immunohistochemistry and Western blot and the detection of mRNA expressions of MCP-1 and CCR2 in cerebral tissue of rats were carried out by RT-PCR.RESULTS Compared with the model group,the blood pressure of mangiferin in each dosage group decreased slightly,but there was no significant statistical difference.In the control group and the model group,there was no obvious morphological change in the cerebral tissue.The morphology of rats in the benazepril group,each dose of mangiferin group were all normal.The contents of IL-6,TNF-α,ICAM-1 and MCP1,CCR2 protein and mRNA expression were significantly decreased in the cerebral tissues of spontaneously hypertensive rats.CONCLUSION Mangiferin has obvious anti-inflammatory effects on inflammatory reaction in spontaneously hypertensive rats,its mechanism may be related to inhibiting the expression of MCP/CCR2 signaling pathway.
