Captopril attenuates lung inflammation through inhibiting the expression of CCL-2 in rats with acute radiation-induced lung injury
10.3760/cma.j.issn.1004-4221.2017.10.021
- VernacularTitle:卡托普利通过抑制CCL-2表达缓解大鼠急性放射性肺损伤的机制研究
- Author:
Jun WANG
1
;
Hongda LU
;
Zhang LEI
;
Hongbin WU
;
Chi LU
Author Information
1. 湖北省肿瘤医院肿瘤内科
- Keywords:
Captopril;
Rat;
Acute radiation-induced lung injury;
Chemoattractant cytokine ligand 2;
Macrophage
- From:
Chinese Journal of Radiation Oncology
2017;26(10):1209-1213
- CountryChina
- Language:Chinese
-
Abstract:
Objective To explore the inhibitory effect of captopril on acute radiation-induced lung injury in rats and the possible mechanism. Methods Sixty-four female Wistar rats were randomly divided into control group, irradiation group, irradiation+low-dose captopril group, and irradiation+high-dose captopril group. A single dose of 20 Gy was given to the right lung of all rats except those in the control group to establish a rat model of acute radiation-induced lung injury. These rats were sacrificed at 1, 2, 4, and 8 weeks. HE staining was used to observe the pathological changes in lung tissue;RT-PCR and Western blot were used to measure the mRNA and protein expression of CCL-2 in lung tissue;immunohistochemical assay was used to determine the number of monocytes ( CD68 ) in lung tissue. A one-way analysis of variance was performed. Results Captopril significantly reduced lung inflammation in rats with acute radiation-induced lung injury (P<005), inhibited the accumulation of monocytes (CD68) in lung tissue (P<005), and decreased the content of CCL-2 in lung tissue ( P<005 ) . Conclusions For rats with acute radiation-induced lung injury, captopril can reduce the expression of CCL-2 to inhibit the accumulation of monocytes in lung tissue and thus attenuate lung inflammation.