Salubrinal protects against cigarette smoke extract-induced HBEpC apoptosis likely via regulating the activity of PERK-eIF2α signaling pathway.

Background And Aims: Endoplasmic reticulum (ER) stress plays an important role in cigarette smoke extract (CSE)-induced apoptotic cell death, which is an important pathogenic factor of chronic obstructive pulmonary disease (COPD). The aim of this study was to explore the role of the PERK-eIF2 pathway in CSE-induced human bronchial epithelial (HBE) cell apoptosis and to evaluate the protective effects and possible mechanism of salubrinal (Sal) on CSE-induced HBE cell apoptosis.

Methods: Normal human bronchial epithelial cells (HBEpC) were cultured and then treated with CSE alone or together with Sal or preincubated with or without PERK siRNA.

[Expression of secretory leukocyte proteinase inhibitor in human bronchial epithelial cell is downregulated by transforming growth factor-beta1/Smads pathway].

Objective: To study the relationship between the downregulated expression of secretory leukocyte proteinase inhibitor (SLPI) in human bronchial epithelial cells and transforming growth factor (TGF)-beta1/Smads pathway.

Methods: Normal human bronchial epithelial cells of the line HBE were cultured and divided into 4 groups: TGF-beta1 stimulation group stimulated by TGF-beta1, interference group preincubated with Smad4 siRNA and then stimulated by TGF-beta1, interference control group preincubated with negative siRNA and then stimulated by TGF-beta1, and normal control group. Forty-eight hours later immunocytochemistry was used to observe the SLPI positive staining in the cells, and the protein and mRNA expression levels of Smad4 and SLPI were detected by Western blotting and RT-PCR respectively.

Palmitic and linoleic acids impair endothelial progenitor cells by inhibition of Akt/eNOS pathway.

Background: Endothelial progenitor cells (EPCs) are involved in adult neovasculogenesis and maintenance of vascular integrity. Scarce data have been provided for the individual effect of elevated free fatty acids (FFAs) on EPCs. This study was designed to investigate the association between Akt/eNOS signal pathway changes and the proliferation/function of EPCs in the presence of palmitic and linoleic acids.

Downregulation of secretory leukocyte proteinase inhibitor in chronic obstructive lung disease: the role of TGF-beta/Smads signaling pathways.

Background: Secretory leukocyte proteinase inhibitor (SLPI) is an important antileukoprotease in airway. The aim of the present study was to explore the expression of SLPI in the bronchi and lung tissues of chronic obstructive pulmonary disease (COPD) models and the regulative mechanism by transforming growth factor (TGF)beta(1)/Smads signal pathway in bronchial epithelial cell.

Methods: COPD rat model was established and was treated with or without TGFbeta1 monoclonal antibody.

[Expression of secretory leukocyte proteinase inhibitor in the bronchi and lung tissues of chronic obstructive pulmonary disease rat models and the regulatory mechanism by transforming growth factor beta(1)].

Objective: To study the expression of secretory leukocyte proteinase inhibitor (SLPI) in the bronchi and lung tissues of chronic obstructive pulmonary disease (COPD) rat models and the regulatory mechanism by transforming growth factor beta(1) (TGF-beta(1)).

Methods: Rat COPD models were established by intratracheal instillation of lipopolysaccharide (LPS) twice and exposure to cigarette smoke daily. The drug intervention group received TGF-beta(1) monoclonal antibody 0.