2013•Zhonghua zhongyiyao zazhiRequires access

Protective effect of icariin on cigarette smoke extract induced inflammation in alveolar epithelial cells

Jingcheng Dong

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Abstract

Objective: To investigate the effect of icariin on cigarette smoke extract(CSE) induced inflammation in alveolar epithelial(AT II) cells.Methods: Cell model was established by stimulating AT II of neonatal SD rats by CSE.The cells were divided into six groups: control group,CSE group,PDTC group,40μg/mL,80μg/mL and 160μg/mL icariin group.AT II cells were identified by modified papanicolaou staining and electron microscopy;cell proliferation was detected by CCK-8 assay;cytokines in cell supernatants was measured by ELISA assay;expressions of IκB-α and p65 phosphorylation were identified by western blot;NF-κB DNA binding activity was detected by electrophoretic mobility shift assay(EMSA).Results: Isolated and cultured cells were positive by papanicolaou stain;icariin groups did not show cytotoxicity,while CSE showed a time and concentration-dependent inhibition on AT II cells;compared with control group,IL-8,IL-6 and TNF-α in cell supernatant in CSE group significantly increased,with IL-10 decreased,while as the dose increased,IL-8,IL-6,TNF-α expression icariin groups decreased,with IL-10 increased.After CSE stimulation,P-p65 expression increased and IκB-α decreased;P-p65 expression decreased and IκB-α increased in icariin groups.NF-κB DNA binding activity was weak in control group,and was enhanced significantly in CSE group.After icariin intervention,it was weakened.Conclusion: The Icariin attenuated CSE-induced expression of IL-8,IL-6,TNF-α and NF-κB activation,and increased IL-10 expression in AT II cells.

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Objective: To investigate the effect of icariin on cigarette smoke extract(CSE) induced inflammation in alveolar epithelial(AT II) cells.Methods: Cell model was established by stimulating AT II of neonatal SD rats by CSE.The cells were divided into six groups: control group,CSE group,PDTC group,40μg/mL,80μg/mL and 160μg/mL icariin group.AT II cells were identified by modified papanicolaou staining and electron microscopy;cell proliferation was detected by CCK-8 assay;cytokines in cell supernatants was measured by ELISA assay;expressions of IκB-α and p65 phosphorylation were identified by western blot;NF-κB DNA binding activity was detected by electrophoretic mobility shift assay(EMSA).Results: Isolated and cultured cells were positive by papanicolaou stain;icariin groups did not show cytotoxicity,while CSE showed a time and concentration-dependent inhibition on AT II cells;compared with control group,IL-8,IL-6 and TNF-α in cell supernatant in CSE group significantly increased,with IL-10 decreased,while as the dose increased,IL-8,IL-6,TNF-α expression icariin groups decreased,with IL-10 increased.After CSE stimulation,P-p65 expression increased and IκB-α decreased;P-p65 expression decreased and IκB-α increased in icariin groups.NF-κB DNA binding activity was weak in control group,and was enhanced significantly in CSE group.After icariin intervention,it was weakened.Conclusion: The Icariin attenuated CSE-induced expression of IL-8,IL-6,TNF-α and NF-κB activation,and increased IL-10 expression in AT II cells.

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Available abstract

Objective: To investigate the effect of icariin on cigarette smoke extract(CSE) induced inflammation in alveolar epithelial(AT II) cells.Methods: Cell model was established by stimulating AT II of neonatal SD rats by CSE.The cells were divided into six groups: control group,CSE group,PDTC group,40μg/mL,80μg/mL and 160μg/mL icariin group.AT II cells were identified by modified papanicolaou staining and electron microscopy;cell proliferation was detected by CCK-8 assay;cytokines in cell supernatants was measured by ELISA assay;expressions of IκB-α and p65 phosphorylation were identified by western blot;NF-κB DNA binding activity was detected by electrophoretic mobility shift assay(EMSA).Results: Isolated and cultured cells were positive by papanicolaou stain;icariin groups did not show cytotoxicity,while CSE showed a time and concentration-dependent inhibition on AT II cells;compared with control group,IL-8,IL-6 and TNF-α in cell supernatant in CSE group significantly increased,with IL-10 decreased,while as the dose increased,IL-8,IL-6,TNF-α expression icariin groups decreased,with IL-10 increased.After CSE stimulation,P-p65 expression increased and IκB-α decreased;P-p65 expression decreased and IκB-α increased in icariin groups.NF-κB DNA binding activity was weak in control group,and was enhanced significantly in CSE group.After icariin intervention,it was weakened.Conclusion: The Icariin attenuated CSE-induced expression of IL-8,IL-6,TNF-α and NF-κB activation,and increased IL-10 expression in AT II cells.

Key concepts: Icariin, Chemistry, Molecular biology, Inflammation, Apoptosis, Western blot, Tumor necrosis factor alpha, Andrology

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