OBJECTIVE: To study the mechanism of protection provided by dexmedetomidine against COPD-induced lung injury. METHODS: 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. RESULTS: 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. CONCLUSION: Dexmedetomidine protected COPD-induced lung injury by inhibiting miRNA-146a expression to reduce cell apoptosis (Tab. 1, Fig. 3, Ref. 25).
OBJECTIVE: To study the mechanism of protection provided by dexmedetomidine against COPD-induced lung injury. METHODS: 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. RESULTS: 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. CONCLUSION:Dexmedetomidine protected COPD-induced lung injury by inhibiting miRNA-146a expression to reduce cell apoptosis (Tab. 1, Fig. 3, Ref. 25).