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银杏叶提取物通过抑制COX-2和NF-κB途径减轻脂多糖诱导的急性肺损伤炎症反应。

Ginkgo biloba extracts attenuate lipopolysaccharide-induced inflammatory responses in acute lung injury by inhibiting the COX-2 and NF-κB pathways.

作者信息

Yao Xin, Chen Nan, Ma Chun-Hua, Tao Jing, Bao Jian-An, Zong-Qi Cheng, Chen Zu-Tao, Miao Li-Yan

机构信息

Department of Pharmacy, First Affiliated Hospital of Soochow University, Suzhou 215006, China.

Medical College of Soochow University, Suzhou 215000, China.

出版信息

Chin J Nat Med. 2015 Jan;13(1):52-8. doi: 10.1016/S1875-5364(15)60006-1.

DOI:10.1016/S1875-5364(15)60006-1
PMID:25660288
Abstract

In the present study, we analyzed the role of Ginkgo biloba extract in lipopolysaccharide(LPS)-induced acute lung injury (ALI). ALI was induced in mice by intratracheal instillation of LPS. G. biloba extract (12 and 24 mg·kg(-1)) and dexamethasone (2 mg·kg(-1)), as a positive control, were given by i.p. injection. The cells in the bronchoalveolar lavage fluid (BALF) were counted. The degree of animal lung edema was evaluated by measuring the wet/dry weight ratio. The superoxidase dismutase (SOD) and myeloperoxidase (MPO) activities were assayed by SOD and MPO kits, respectively. The levels of inflammatory mediators, tumor necrosis factor-a, interleukin-1b, and interleukin-6, were assayed by enzyme-linked immunosorbent assay. Pathological changes of lung tissues were observed by H&E staining. The levels of NF-κB p65 and COX-2 expression were detected by Western blotting. Compared to the LPS group, the treatment with the G. biloba extract at 12 and 24 mg·kg(-1) markedly attenuated the inflammatory cell numbers in the BALF, decreased NF-κB p65 and COX-2 expression, and improved SOD activity, and inhibited MPO activity. The histological changes of the lungs were also significantly improved. The results indicated that G. biloba extract has a protective effect on LPS-induced acute lung injury in mice. The protective mechanism of G. biloba extract may be partly attributed to the inhibition of NF-κB p65 and COX-2 activation.

摘要

在本研究中,我们分析了银杏叶提取物在脂多糖(LPS)诱导的急性肺损伤(ALI)中的作用。通过气管内滴注LPS诱导小鼠发生ALI。腹腔注射给予银杏叶提取物(12和24 mg·kg⁻¹)和作为阳性对照的地塞米松(2 mg·kg⁻¹)。对支气管肺泡灌洗液(BALF)中的细胞进行计数。通过测量湿/干重比评估动物肺水肿程度。分别使用超氧化物歧化酶(SOD)和髓过氧化物酶(MPO)试剂盒测定SOD和MPO活性。采用酶联免疫吸附测定法检测炎症介质肿瘤坏死因子-α、白细胞介素-1β和白细胞介素-6的水平。通过苏木精-伊红(H&E)染色观察肺组织的病理变化。通过蛋白质免疫印迹法检测NF-κB p65和环氧化酶-2(COX-2)的表达水平。与LPS组相比,12和24 mg·kg⁻¹的银杏叶提取物治疗显著减少了BALF中的炎症细胞数量,降低了NF-κB p65和COX-2的表达,并提高了SOD活性,抑制了MPO活性。肺组织的组织学变化也得到显著改善。结果表明,银杏叶提取物对LPS诱导的小鼠急性肺损伤具有保护作用。银杏叶提取物的保护机制可能部分归因于对NF-κB p65和COX-2激活的抑制。

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