Captopril attenuates lung inflammation through inhibiting the expression of CCL-2 in rats with acute radiation-induced lung injury

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<0.05), inhibited the accumulation of monocytes (CD68) in lung tissue (P<0.05), and decreased the content of CCL-2 in lung tissue (P<0.05). 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. Key words: Captopril; Rat; Acute radiation-induced lung injury; Chemoattractant cytokine ligand 2; Macrophage