Abstract:

Objective To explore the effect of Microrna⁃132（mir⁃132）on rats with acute exacerbation of chronic obstructive pulmonary disease （AECOPD） induced by Streptococcus pneumoniae through the oxidase proliferator receptor γ Coactivator 1 α/Deacetylase 3（PGC⁃1）α/SIRT3 signal pathway and to provide a new direction for the clinical treatment of AECOPD caused by streptococcus pneumoniae. Methods Sixty rats were selected； 15 were included in group A（normal group），and the remaining 45 were used to construct the AECOPD model induced by Streptococcus pneumoniae. After completion，they were divided into group B，C，and D，with 15 rats in each. The miR⁃132 mimics and miR⁃132 inhibitors were constructed，and the diluted miR⁃132 mimics and miR⁃ 132 inhibitors were injected into the lungs of group D and C，respectively，and group A and B were injected with the same dose of normal saline. Lung function，peripheral blood leukocytes，neutrophil percentage counts，airway inflammation，and PGC ⁃1α/SIRT3 signaling pathway protein expression in lung tissues were compared and ana⁃ lyzed. Results Compared with that in group A，the expression of miR ⁃132 in group B and C decreased，while that in group D increased，and the difference was statistically significant（P < 0.05）. Compared with those in group A，FEV0.3/FVC，PIF，PEF，lung tissue PGC⁃1α，and SIRT3 protein expression in groups B，C，and Ddecreased；the total number of white blood cells，neutrophil percentage count，and the level of IL⁃1β，IL⁃6，and TNF ⁃ α increased，and the difference was statistically significant（P < 0.05）. Compared with those in group B， FEV0.3/FVC，PIF，PEF，lung tissue PGC⁃1α，and SIRT3 protein expression in group C were all reduced；the total number of white blood cells ，neutrophil percentage count ，and the level of IL⁃1 β ，IL⁃6 ，and TNF⁃ α increased，and the difference was statistically significant（P < 0.05）. Compared with those in group B，FEV0.3/ FVC，PIF，PEF，lung tissue PGC ⁃1α，and SIRT3 protein expression in group D increased；the total number of white blood cells，neutrophil percentage count，and the level of IL⁃1β，IL⁃6，and TNF⁃ α decreased，and the difference was statistically significant（P < 0.05）. Compared with those in group C，FEV0.3/FVC，PIF，PEF，lung tissue PGC⁃1α，and SIRT3 protein expression increased in group D；total number of white blood cells，neutrophil percentage count，and the level of IL⁃1β，IL⁃6，and TNF⁃α decreased，and the difference was statistically signifi⁃ cant（P < 0.05）. Conclusion Overexpression of mir⁃132 can improve airway inflammation and repair lung injury in AECOPD rats induced by Streptococcus pneumoniae. Its mechanism may be related to activation of PGC ⁃ 1α/ SIRT3 signaling pathway and up⁃regulation of SIRT3 expression.

Key words:

microRNA?132, peroxisome proliferator receptor γ coactivator 1α, deacetylase 3, strep? tococcus pneumoniae, chronic obstructive pulmonary disease, pulmonary function