Study on the Mechanism of Butylphthalide Delaying Renal Fibrosis of Mice Model with Unilateral Ureteral Obstruction
10.3969/j.issn.1006-5725.2016.11.005
- VernacularTitle:丁苯酞延缓小鼠单侧输尿管梗阻模型纤维化的机制研究
- Author:
Yifu CAO
;
Xiufen WANG
;
Cuihong LIU
;
Lijuan NIU
;
Wenjing LI
;
Cuihong LIU
- Publication Type:Journal Article
- Keywords:
Renal Interstitial Fibrosis;
Nrf-2,γ-GCS;
Type Ⅰ collagen;
Butylphthalide
- From:
The Journal of Practical Medicine
2016;32(11):1741-1744
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study on the possible mechanism of butylphthalide delaying renal fibrosis of mice with obstructive nephropathy. Methods Totally 72 male CD-1 mice of clean grade were selected and randomly assigned into 4 groups: sham operation group (Sham), model group (UUO), control group (ACEI) and treatment group (NBP). The mice in the control group (ACEI) and the treatment group (NBP) were given benazepril and butylphthalide by gavage, and the mice in sham operation group (Sham) and model group (UUO) were given normal saline by gavage. Six mice were sacrificed at the third, 7th, 14th day, respectively. The obstructive renal tissue was selected for immunohistochemical staining and western blot. Results (1)With the longer time of ureteral obstruction, the expression of Nrf-2 was gradually strengthened in time-dependent manner;(2)Compared with the model group, the levels of Nrf-2 and γ-GCS in butylphthalide group were significantly increased, and the expression of type Ⅰ collagen was decreased significantly (P < 0.05). The expression of Nrf-2 and γ-GCS in each time points was stronger than that in the benazepril group (P < 0.05). Correlation analysis showed that: there was a positive correlation between Nrf-2 and γ-GCS (r = 0.930) and a negative correlation between Nrf-2 and the expression level of type Ⅰ collagen(r = -0.859). Conclusion Butylphthalide can relieve renal interstitial injury caused by oxidative stress and delay the progress of renal interstitial fibrosis by activation of Nrf-2 pathway and up-regulated expression ofγ-GCS.
