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. 2018 Jan 18:24:356-362.
doi: 10.12659/msm.905509.

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)

Lerong Chen  1 , Xiaolan Yuan  2 , Luru Zou  3 , Jianping Peng  4 , Xinchun Hu  5
Affiliations

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)

Lerong Chen et al. Med Sci Monit. .

Abstract

BACKGROUND 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. MATERIAL AND METHODS 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. RESULTS 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. CONCLUSIONS 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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Figures

Figure 1
Figure 1
1,25(OH)2D3 attenuates COPD-induced apoptosis in lung tissue. (A) Representative images from each group; (B) Quantification data of the apoptotic rate. * p<0.05 compared to corresponding control; # p<0.05 compared to corresponding subgroups in the normal group; & p<0.05 compared to corresponding subgroups in COPD group.
Figure 2
Figure 2
1,25(OH)2D3 attenuates COPD-induced MUC5AC and JNK1 mRNA expression. (A) MUC5AC expression; (B) JNK1 expression. * p<0.05 compared to corresponding control; # p<0.05 compared to corresponding subgroups in the normal group; & p<0.05 compared to corresponding subgroups in COPD group.
Figure 3
Figure 3
1,25(OH)2D3 attenuates COPD-induced MUC5AC and JNK1 protein expression. (A) Representative blots for MUC5AC and JNK1; (B) Quantification data of MUC5AC; (C) Quantification data of JNK1 expression. *p<0.05 compared to corresponding control; #p<0.05 compared to corresponding subgroups in the normal group; & p<0.05 compared to corresponding subgroups in COPD group.
Figure 4
Figure 4
1,25(OH)2D3 attenuates COPD-induced MUC5AC expression detected by immunohistochemistry (200×).
Figure 5
Figure 5
1,25(OH)2D3 attenuates COPD-induced JNK1 expression detected by immunohistochemistry (200×).
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