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[金荞麦对肺炎克雷伯菌肺炎大鼠肺损伤的保护作用及机制]

[Protection and mechanism of Fagopyrum cymosum on lung injury in rats with Klebsiella pneumonia].

作者信息

Dong Liu-Yi, Wang Chun-Yan, Wu Chang-Qing, Jiang Qin, Zhang Zhi-Fen

机构信息

Department of Pharmacology, Key Laboratory of Anti-inflammatory and Immunopharmacology, Ministry of Education, Anhui Medical University, Hefei 230032, China.

出版信息

Zhong Yao Cai. 2012 Apr;35(4):603-7.

PMID:23019909
Abstract

OBJECTIVE

To study the mechanism of protective effect of Fagopyrum cymosum on lung injury induced by Klebsiella pneumonia in rats.

METHODS

The model of rats with Klebsiella pneumonia was established. The male SD rats were randomly divided into control group, model group, Fagopyrum cymosum (6, 3, 1.5 g/kg) three groups, levofloxacin (25 mg/kg) group. The pathological change of lung was observed. The content of IL-1beta, IL-6, IL-8, TNF-alpha, ICAM-1, INF-gamma in serum were measured by radioimmunoassay and Elisa. TNF-alpha, ICAM-1, NF-kappaB p65 protein expressions were measured by immunohistochemistry. MIP-2mRNA expression was detected by in situ hybridization.

RESULTS

The rats of model group had obvious lung injury, but those of Fagopyrum cymosum and levofloxacin groups had less injury. The contents of IL-1beta, IL-6, IL-,8, TNF-alpha, ICAM-1 and INF-gamma in serum and the expressions of TNF-a, ICAM-1, NF-kappaB p65 and MIP--2mRNA of model group were significantly higher than those of the control group (P < 0.05 or P < 0.01), while the indexes of Fagopyrum cymosum and levofloxacin groups were significantly lower than those of model group (P < 0.05 or P < 0.01).

CONCLUSION

The lung injury induced by Klebsiella pneumonia is related to TNF-alpha, ICAM-1, NF-kappaB p65 and MIP-2mRNA. To decrease the excessive expression of TNF-alpha, ICAM-1, NF-kappaB p65 and MIP-2mRNA might be the main mechanism of protective effect of Fagopyrum cymosum on lung injury.

摘要

目的

研究金荞麦对大鼠肺炎克雷伯菌所致肺损伤的保护作用机制。

方法

建立肺炎克雷伯菌大鼠模型。将雄性SD大鼠随机分为对照组、模型组、金荞麦(6、3、1.5 g/kg)三组、左氧氟沙星(25 mg/kg)组。观察肺组织病理变化。采用放射免疫法和酶联免疫吸附测定法检测血清中白细胞介素-1β、白细胞介素-6、白细胞介素-8、肿瘤坏死因子-α、细胞间黏附分子-1、干扰素-γ的含量。采用免疫组织化学法检测肿瘤坏死因子-α、细胞间黏附分子-1、核因子-κB p65蛋白表达。采用原位杂交法检测巨噬细胞炎性蛋白-2mRNA表达。

结果

模型组大鼠肺损伤明显,而金荞麦组和左氧氟沙星组大鼠肺损伤较轻。模型组血清中白细胞介素-1β、白细胞介素-6、白细胞介素-8、肿瘤坏死因子-α、细胞间黏附分子-1和干扰素-γ的含量以及肿瘤坏死因子-α、细胞间黏附分子-1、核因子-κB p65和巨噬细胞炎性蛋白-2mRNA的表达均显著高于对照组(P < 0.05或P < 0.01),而金荞麦组和左氧氟沙星组的指标显著低于模型组(P < 0.05或P < 0.01)。

结论

肺炎克雷伯菌所致肺损伤与肿瘤坏死因子-α、细胞间黏附分子-1、核因子-κB p65和巨噬细胞炎性蛋白-2mRNA有关。降低肿瘤坏死因子-α、细胞间黏附分子-1、核因子-κB p65和巨噬细胞炎性蛋白-2mRNA的过度表达可能是金荞麦对肺损伤保护作用的主要机制。

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