Li N, Ouyang B S, Liu L, Lin C S, Xing D D, Liu J
Bratisl Lek Listy. 2016;117(9):539-542. doi: 10.4149/bll_2016_106.
To study the mechanism of protection provided by dexmedetomidine against COPD-induced lung injury.
COPD rat model was determined by measuring lung function, and comparing HE staining between two different groups. We got the lung tissue and cells from the control and COPD groups. The cells were divided into three groups: control group, and blank and drug groups that were from the COPD rats. Cell apoptosis, relative gene expression and TNF-α and IL-1β from nutrient solution were measured.
The TV, PEF, EF50, FEV0.3 and FEV0.3/FVC in COPD group were significantly lower than in control group (1.26±0.17 vs 2.65±0.21; 17.61±0.35 vs 38.55±0.24; 1.20±0.14 vs 1.81±0.06; 2.52±0.28 vs 4.44±0.26; 63.39±0.22 vs 88.45±0.34, p < 0.05, respectively). Cell apoptosis was significantly different in blank and drug groups (21.65±0.86 vs 10.74±0.15; p < 0.05, respectively). The gene expressions of miRNA-146a, p53 and Bcl-2 were significantly downregulated compared with blank group.
Dexmedetomidine protected COPD-induced lung injury by inhibiting miRNA-146a expression to reduce cell apoptosis (Tab. 1, Fig. 3, Ref. 25).
研究右美托咪定对慢性阻塞性肺疾病（COPD）所致肺损伤的保护机制。
通过测量肺功能确定COPD大鼠模型，并比较两组之间的苏木精-伊红（HE）染色。我们从对照组和COPD组获取肺组织和细胞。将细胞分为三组：对照组，以及来自COPD大鼠的空白组和药物组。检测细胞凋亡、相关基因表达以及营养液中的肿瘤坏死因子-α（TNF-α）和白细胞介素-1β（IL-1β）。
COPD组的潮气量（TV）、呼气峰流速（PEF）、50%用力呼气流量（EF50）、0.3秒用力呼气容积（FEV0.3）和FEV0.3/用力肺活量（FVC）显著低于对照组（分别为1.26±0.17 vs 2.65±0.21；17.61±0.35 vs 38.55±0.24；1.20±0.14 vs 1.81±0.06；2.52±0.28 vs 4.44±0.26；63.39±0.22 vs 88.45±0.34，p均<0.05）。空白组和药物组的细胞凋亡存在显著差异（分别为21.65±0.86 vs 10.74±0.15；p<0.05）。与空白组相比，微小RNA-146a（miRNA-146a）、p53和Bcl-2的基因表达显著下调。
右美托咪定通过抑制miRNA-146a表达以减少细胞凋亡，从而保护COPD所致的肺损伤（表1，图3，参考文献25）。
