Effects of 1,25-Dihydroxyvitamin D3 on the Prevention of Chronic Obstructive Pulmonary Disease (COPD) in Rats Exposed to Air Pollutant Particles Less than 2.5 Micrometers in Diameter (PM2.5).
Effects of 1,25-Dihydroxyvitamin D3 on the Prevention of Chronic Obstructive Pulmonary Disease (COPD) in Rats Exposed to Air Pollutant Particles Less than 2.5 Micrometers in Diameter (PM2.5).
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1,25-二羟基维生素D3对暴露于直径小于2.5微米的空气污染物颗粒的大鼠预防慢性阻塞性肺疾病（COPD）的影响（PM2.5）。
DOI：
10.12659/msm.905509
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发表时间：
2018-01-18
期刊：
影响因子：
--
通讯作者：
Hu X
中科院分区：
文献类型：
--
作者：
Chen L;Yuan X;Zou L;Peng J;Hu X
本研究旨在探讨1,25-二羟基维生素D3（1,25(OH)2D3）对暴露于直径小于2.5微米的空气污染物颗粒（PM2.5）的慢性阻塞性肺病（COPD）大鼠气道变化的影响，并评估其机制。本研究包括三组：正常组、COPD模型组和COPD用1,25(OH)2D3治疗组。每组中，大鼠被分为四个亚组：对照组和不同剂量的 PM2.5（1.6、8 和 40 mg/kg 体重）。通过末端脱氧核苷酸转移酶 dUTP 缺口末端标记 (TUNEL) 检测肺组织中的细胞凋亡。通过实时聚合酶链式反应（RT-PCR）、Western blotting和免疫荧光染色检测c-Jun N端激酶1（JNK1）和粘蛋白5AC（MUC5AC）的表达。与正常组相应亚组相比，COPD组细胞凋亡率明显升高。相比之下，1,25(OH)2D3治疗组显着减少了COPD诱导的肺组织细胞凋亡。 PM2.5剂量增加后，各组细胞凋亡率也升高。与各组相应对照相比，PM2.5以剂量依赖性方式增加细胞凋亡。重要的是，1,25(OH)2D3 还可以防止暴露于 PM2.5 的 COPD 大鼠的细胞凋亡。机械方面，与正常组相应亚组相比，COPD组MUC5AC和JNK1的表达显着上调。 1,25(OH)2D3 治疗可降低 COPD 大鼠中 MUC5AC 和 JNK1 的表达。发现各组中MUC5AC和JNK1的表达随着PM2.5剂量的增加而升高。一致地，1,25(OH)2D3 也降低了暴露于 PM2.5 的 COPD 大鼠中 MUC5AC 和 JNK1 的表达。 1,25(OH)2D3 可预防接触或未接触 PM2.5 的 COPD 大鼠的肺损伤。我们的结果表明 1,25(OH)2D3 可有效减轻 COPD 造成的损伤。
This study aimed to investigate the effects of 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) on airway changes in chronic obstructive pulmonary disease (COPD) rats exposed to air pollutant particles less than 2.5 micrometers in diameter (PM2.5), and to evaluate the mechanisms. Three groups were included in this study: a normal group, a COPD model group, and a COPD with 1,25(OH)2D3 treatment group. In each group, the rats were divided into four subgroups: control and different doses of PM2.5 (1.6, 8 and 40 mg/kg body weight). Apoptosis in lung tissue was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL). The expression of c-Jun N-terminal kinase 1 (JNK1) and mucin 5AC (MUC5AC) were detected by real-time polymerase chain reaction (RT-PCR), Western blotting and immunofluorescence staining. Compared with corresponding subgroups in normal group, the apoptotic rates in COPD group were significantly increased. By contrast, 1,25(OH)2D3 treatment group significantly reduced COPD-induced apoptosis in lung tissue. Upon the dose increase of PM2.5, the apoptotic rate was also elevated in each group. Compared with the corresponding control in each group, PM2.5 increased apoptosis in a dose-dependent manner. Importantly, 1,25(OH)2D3 also prevented apoptosis in COPD rats exposed to PM2.5. Mechanically, the expression of MUC5AC and JNK1 in COPD group was significantly upregulated, compared with corresponding subgroups in the normal group. Treatment with 1,25(OH)2D3 reduced expression of MUC5AC and JNK1 in COPD rats. It was found that the expression of MUC5AC and JNK1 was elevated with the dose increase of PM2.5 in each group. Consistently, 1,25(OH)2D3 also reduced the expression of MUC5AC and JNK1 in COPD rats exposed to PM2.5. 1,25(OH)2D3 prevented lung injury in COPD rats with or without PM2.5 exposure. Our results suggest that 1,25(OH)2D3 is useful to mitigate the injury caused by COPD.
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影响因子：
3.1
作者：
Kankaanranta H;Harju T;Kilpeläinen M;Mazur W;Lehto JT;Katajisto M;Peisa T;Meinander T;Lehtimäki L
通讯作者：
Lehtimäki L
DOI：
10.1016/s0140-6736(15)60693-6
发表时间：
2015-05-02
期刊：
Lancet (London, England)
影响因子：
--
作者：
Woodruff PG;Agusti A;Roche N;Singh D;Martinez FJ
通讯作者：
Martinez FJ
影响因子：
3.7
作者：
Ghorani V;Boskabady MH;Khazdair MR;Kianmeher M
通讯作者：
Kianmeher M
PM2.5暴露对慢性阻塞性肺疾病Notch信号通路及免疫失衡的影响
影响因子：
8.9
作者：
Gu, Xing-yu;Chu, Xu;Liu, Xiao-Ju
通讯作者：
Liu, Xiao-Ju
影响因子：
10
作者：
Afzal, Shoaib;Lange, Peter;Nordestgaard, Borge G.
通讯作者：
Nordestgaard, Borge G.