Home Bratislava Medical Journal 2016 Bratislava Medical Journal Vol.117, No.9, p.539-542, 2016

Journal info


Published Monthly, in English
Founded: 1919
ISSN 0006-9248
(E)ISSN 1336-0345

Impact factor 1.564


Aims and Scope
Editorial Info
Submission Guidelines

Select Journal

Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Bratislava Medical Journal Vol.117, No.9, p.539-542, 2016

Title: Dexmedetomidine protected COPD-induced lung injury by regulating miRNA-146a
Author: N. Li, B. S. Ouyang, L. Liu, C. S. Lin, D. D. Xing, J. Liu


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).

Keywords: miRNA-146a expression, COPD, IL-1β, TNF-α
Published online: 21-Sep-2016
Year: 2016, Volume: 117, Issue: 9 Page From: 539, Page To: 542

download file

© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.