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抗碱性成纤维细胞生长因子对博莱霉素诱导的大鼠肺纤维化模型的干预作用

[The interventional effect of anti-basic fibroblast growth factor on the model of bleomycin-induced pulmonary fibrosis in rats].

作者信息

Mu Jian-qin, Wei Lu-qing

机构信息

Affiliated Hospital of Medical College of Chinese People Armed Police Force, Tianjin 300162, China.

出版信息

Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2010 May;26(2):222-6.

Abstract

OBJECTIVE

To study the effect of anti-basic jibroblast grouth factor (bFGF) on bleomycin-induced pulmonary fibrosis in rats and its possible mechanism.

METHODS

Pulmonary fibrosis was induced in Wistar rats by intratracheal instillation of bleomycin (model group, group M). Then the rats received anti-bFGF on 1, 2, 3, 8, 12, 19, 25 days intracavitary injection (group K), normal saline(group C) orally. Normal controls received normal saline both intratracheally and orally. Five rats in each group were sacrificed on 1.4 week after intratracheal instillation. Histological changes of the lungs were evaluated by HE stain and Massons trichrome stain. Lung expression of bFGF proteins was assessed by immunohistochemistry and the level of bFGF protein in serum and BALF was further measured by ELISA.

RESULTS

Pulmonary fibrosis of group M was higher than that of group C. bFGF in group M was higher than that in group C in lung, serum and BALF on 1.4 week. Pulmonary fibrosis of group K was lower than that of group M. bFGF in group K was lower than that in group M in lung, serum and BALF on 1.4 week.

CONCLUSION

Anti-bFGF alleviates bleomycin-induced pulmonary fibrosis in rats. Inhibiting the expressions of bFGF in lung tissues may be one of the mechanisms.

摘要

目的

研究抗碱性成纤维细胞生长因子(bFGF)对博来霉素诱导的大鼠肺纤维化的影响及其可能机制。

方法

通过气管内滴注博来霉素诱导Wistar大鼠发生肺纤维化(模型组,M组)。然后在第1、2、3、8、12、19、25天对大鼠进行抗bFGF腔内注射(K组),口服生理盐水(C组)。正常对照组气管内和口服均给予生理盐水。气管内滴注后第1、4周每组处死5只大鼠。通过HE染色和Masson三色染色评估肺组织学变化。通过免疫组织化学评估肺组织中bFGF蛋白的表达,并通过ELISA进一步检测血清和支气管肺泡灌洗液(BALF)中bFGF蛋白的水平。

结果

M组肺纤维化程度高于C组。第1、4周时,M组肺组织、血清和BALF中的bFGF高于C组。K组肺纤维化程度低于M组。第1、4周时,K组肺组织、血清和BALF中的bFGF低于M组。

结论

抗bFGF可减轻博来霉素诱导的大鼠肺纤维化。抑制肺组织中bFGF的表达可能是其机制之一。

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