Pulmonary fibrosis (PF) is a fibroproliferative disease that can eventually lead to fatal lung failure. It is characterized by abnormal proliferation of fibroblasts, dysregulated fibroblast differentiation to myofibroblast, and disorganized collagen and extracellular matrix production, deposition and degradation.There is still a lack of effective treatment strategies for PF. Extracellular highmobility group box protein 1 (HMGB1) induces PF through NF-κB-mediated TGF-β1 release. Herein, we first validate the suppressive effect of HMGB1 knockdown on TGF-β1-induced α-smooth muscle actin (α-SMA) and collagen I protein expression. In PF, miRNAs exert different effects through targeting various downstream target messenger RNAs. We searched an online database for dysregulated miRNAs in PF tissues; among them, miR-627 was predicted by online tools to target HMGB1 to inhibit its expression. miR-627 overexpression could partially reverse TGF-β1-induced normal human lung fibroblast proliferation, as well as α-SMA and collagen I protein expression. miR-627 inhibition could partially reverse the suppressive effect of HMGB1 knockdown on TGF-β1-induced α-SMA and collagen I protein expression through direct binding to the 3′-untranslated region of HMGB1. Moreover, miR-627/HMGB1

Objective:The aim of the present study was to investigate the association between serum neuron-specific enolase (sNSE) levels and gender, age, body mass index (BMI) in patients with chronic obstructive pulmonary disease (COPD).Methods:This case-control study was carried out among 182 participants in Jiangxi Provincial chest hospital, Nanchang, China, in 2017. One hundred and two patients diagnosed with COPD based on the Global Initiative for Chronic Obstructive Lung Disease (GOLD) grading classification and 80 Non-COPD participants were recruited. Multivariate logistic regression analysis was employed to examine whether or not sNSE and other indicators were independently associated with COPD.Results:Serum NSE levels were not significantly different between the two groups (P=0.08). Whereas in COPD sub-groups, the levels of sNSE increased parallelly in a GOLD stage-dependent manner. There was a positive correlation between PH, PO2, pack-years, FEV1 and the presence of COPD, but there was no significant correlation between sNSE, PCO2 and the presence of COPD.Conclusions:Serum NSE gradually increased with the severity of COPD and its change reflected changes in brain cells. PH, PO2, pack-years and forced expiratory volume in one second (FEV1), were independent risk factors for COPD patients.