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[非促有丝分裂人酸性成纤维细胞生长因子对N-甲基-N-亚硝基脲诱导的Sprague-Dawley大鼠视网膜损伤的保护作用]

[Protective effect of non-mitogenic haFGF on retinal injury induced by N-methyl-N-nitrosourea in Sprague-Dawley rats].

作者信息

Xu Hua, Yang Jin-nan, Zheng Qing, Yao Cheng-can, Wang Yan-ping, Xiang Ji-zhou, Li Xiao-kun

机构信息

Pharmacy College of Jinan University, Guangzhou 510632, China.

出版信息

Yao Xue Xue Bao. 2005 Apr;40(4):306-10.

Abstract

AIM

To study the effect of non-mitogenic human acidic fibroblast growth factor (nm-haFGF) on retinal injury induced by N-methyl-N-nitrosourea (MNU) in Sprague-Dawley rats and its mechanism.

METHODS

Female rats of 50-days-old were injected with MNU (60 mg x kg(-1)) intraperitoneally, and three doses of nm-haFGF (1.25 microg, 2.5 microg and 5 microg in one eye of each rat) were injected, separately, into vitreous body of one eye of each rat twice a day at 0 and 12 h after MNU treatment. 24 h later, apoptotic index of photoreceptor cells was detected by TUNEL labeling and the expressions of Bcl-2 and Bax were analyzed by Western blotting. At the 7th day, retinal injury was evaluated based on retinal thickness.

RESULTS

Compared with model group, apoptotic index of photoreceptor cells was significantly reduced in nm-haFGF groups at the dose of 1.25 microg and 2.5 microg in one eye of each rat at 24 h, and the total retinal thickness as well as the outer retinal thickness markedly increased 7 days after MNU, respectively. The expressions of Bcl-2 increased and that of Bax decreased adversely after being injected with different doses of nm-haFGF.

CONCLUSION

nm-haFGF partially suppressed retinal injury induced by MNU in Sprague-Dawley rats. The mechanism could be related to up-regulation of Bcl-2 and down-regulation of Bax.

摘要

目的

研究非促有丝分裂人酸性成纤维细胞生长因子(nm-haFGF)对N-甲基-N-亚硝基脲(MNU)诱导的Sprague-Dawley大鼠视网膜损伤的影响及其机制。

方法

50日龄雌性大鼠腹腔注射MNU(60 mg·kg⁻¹),在MNU处理后0小时和12小时,每天两次分别向每只大鼠的一只眼玻璃体内注射三剂nm-haFGF(每只大鼠一只眼分别为1.25μg、2.5μg和5μg)。24小时后,通过TUNEL标记检测光感受器细胞的凋亡指数,并通过蛋白质免疫印迹法分析Bcl-2和Bax的表达。在第7天,根据视网膜厚度评估视网膜损伤情况。

结果

与模型组相比,在24小时时,每只大鼠一只眼给予1.25μg和2.5μg剂量nm-haFGF组的光感受器细胞凋亡指数显著降低,MNU处理7天后,视网膜总厚度以及视网膜外层厚度分别显著增加。注射不同剂量nm-haFGF后,Bcl-2表达增加,Bax表达呈相反降低。

结论

nm-haFGF部分抑制了Sprague-Dawley大鼠由MNU诱导的视网膜损伤。其机制可能与上调Bcl-2和下调Bax有关。

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