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

doi:10.3760/cma.j.issn.1004-4221.2017.10.021

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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.

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	Wang Jun
	Lu Hongda
	Lei Zhang
	Wu Hongbin
	Lu Chi

Key words： Captopril Rat Acute radiation-induced lung injury Chemoattractant cytokine ligand 2 Macrophage

Received: 03 August 2016

Cite this article:

Wang Jun,Lu Hongda,Lei Zhang et al. Captopril attenuates lung inflammation through inhibiting the expression of CCL-2 in rats with acute radiation-induced lung injury[J]. Chinese Journal of Radiation Oncology, 2017, 26(10): 1209-1213.

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http://journal12.magtechjournal.com/Jweb_fszlx/EN/10.3760/cma.j.issn.1004-4221.2017.10.021 OR http://journal12.magtechjournal.com/Jweb_fszlx/EN/Y2017/V26/I10/1209

[1] Down JD,Medhora M,Jackson IL,et al. Do variations in mast cell hyperplasia account for differences in radiation-induced lung injury among different mouse strains,rats and nonhuman primates?[J].Radiat Res,2013,180(2):216-221.DOI:10.1667/RR3245.1.
[2] Borst GR,Ishikawa M,Nijkamp J,et al. Radiation pneumonitis after hypofractionated radiotherapy:evaluation of the LQ (L) model and different dose parameters[J].Int J Radiat Oncol Biol Phys,2010,77(5):1596-1603.DOI:10.1016/j.ijrobp.2009.10.015.
[3] Asakura H,Hashimoto T,Zenda S,et al. Analysis of dose–volume histogram parameters for radiation pneumonitis after definitive concurrent chemoradiotherapy for esophageal cancer[J].Radiother Oncol,2010,95(2):240-244.DOI:10.1016/j.radonc.2010.02.006.
[4] Molthen RC,Wu QP,Fish BL,et al. Mitigation of radiation induced pulmonary vascular injury by delayed treatment with captopril[J].Respirology,2012,17(8):1261-1268.DOI:10.1111/j.1440-1843.2012.02247.x.
[5] Ghafoori P,Marks LB,Vujaskovic Z,et al. Radiation-induced lung injury:assessment,management,and prevention[J].Oncology,2008,22(1):37-47.
[6] Rubin P,Johnston CJ,Williams JP,et al. A perpetual cascade of cytokines postirradiation leads to pulmonary fibrosis[J].Int J Radiat Oncol Biol Phys,1995,33(1):99-109.DOI:10.1016/0360-3016(95)00095-G.
[7] Chen Y,Okunieff P,Ahrendt SA.Translational research in lung cancer[J].Semin Surg Oncol,2003,21(3):205-219.DOI:10.1002/ssu.10039.
[8] Jiao B,Wang YS,Cheng YN,et al. Valsartan attenuated oxidative stress,decreased MCP-1 and TGF-β₁ expression in glomerular mesangial and epithelial cells induced by high-glucose levels[J].BioSci Trends,2011,5(4):173-181.DOI:10.5582/bst.2011.v5.4.173.
[9] Molteni A,Moulder JE,Cohen EF,et al. Control of radiation-induced pneumopathy and lung fibrosis by angiotensin-converting enzyme inhibitors and an angiotensin Ⅱ type 1 receptor blocker[J].Int J Radiat Biol,2000,76(4):523-532.DOI:10.1080/095530000138538.
[10] Ghosh SN,Zhang R,Fish BL,et al. Renin-Angiotensin system suppression mitigates experimental radiation pneumonitis[J].Int J Radiat Oncol Biol Phys,2009,75(5):1528-1536.DOI:10.1016/j.ijrobp.2009.07.1743.
[11] Kma L,Gao F,Fish BL,et al. Angiotensin converting enzyme inhibitors mitigate collagen synthesis induced by a single dose of

radiation to the whole thorax[J].J Radiat Res,2012,53(1):10-17.DOI:10.1269/jrr.11035.
[12] Shenoy V,Qi YF,Katovich MJ,et al. ACE2,a promising therapeutic target for pulmonary hypertension[J].Curr Opin Pharmacol,2011,11(2):150-155.DOI:10.1016/j.coph.2010.12.002.
[13] Medhora M,Gao F,Jacobs ER,et al. Radiation damage to the lung:mitigation by angiotensin-converting enzyme (ACE) inhibitors[J].Respirology,2012,17(1):66-71.DOI:10.1111/j.1440-1843.2011.02092.x.
[14] Zhang LJ,Wang LH,Ji W,et al. Association between plasma angiotensin-converting enzyme level and radiation pneumonitis[J].Cytokine,2007,37(1):71-75.DOI:10.1016/j.cyto.2007.02.019.