This study sought to investigate whether Ganoderma lucidum polysaccharide(GLP)has a protective effect on lipopolysaccharide(LPS)-induced inflammatory injury to mammary epithelial HC-11 cells and to characterize the me...This study sought to investigate whether Ganoderma lucidum polysaccharide(GLP)has a protective effect on lipopolysaccharide(LPS)-induced inflammatory injury to mammary epithelial HC-11 cells and to characterize the mechanism involved.Cell viability was assessed using the cell counting kit 8(CCK-8)method,tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and IL-1βlevels were measured by enzyme linked immunosorbent assay(ELISA),and IκBa,p65 NF-κB and STAT3 mRNA were determined using quantitative reverse transcription PCR(qRT-PCR),p65 and STAT3 protein expression were determined using Western blotting,respectively.GLP was shown to inhibit LPS-induced TNF-α,IL-6,and IL-1βproduction(P<0.01 or P<0.05),GLP was also shown to increase IκBαmRNA expression(P<0.01),decrease p65 and STAT3 mRNA expression(P<0.01 or P<0.05),and decrease p-p65,p65,p-STAT3,and STAT3 protein expression in breast epithelial cells(P<0.01 or P<0.05).The findings suggest that GLP inhibits nuclear factor kappa-B(NF-κB)and signal transducers and activators of transcription(STAT)signaling by preventing IκBαdegradation and p65 and STAT3 phosphorylation.This results in lower LPS-induced TNF-α,IL-6,and IL-1βproduction and prevents inflammatory cell injury.展开更多
基金This study was financially supported by the Henan Major Public Welfare Projects(201300110200).
文摘This study sought to investigate whether Ganoderma lucidum polysaccharide(GLP)has a protective effect on lipopolysaccharide(LPS)-induced inflammatory injury to mammary epithelial HC-11 cells and to characterize the mechanism involved.Cell viability was assessed using the cell counting kit 8(CCK-8)method,tumor necrosis factor-α(TNF-α),interleukin-6(IL-6)and IL-1βlevels were measured by enzyme linked immunosorbent assay(ELISA),and IκBa,p65 NF-κB and STAT3 mRNA were determined using quantitative reverse transcription PCR(qRT-PCR),p65 and STAT3 protein expression were determined using Western blotting,respectively.GLP was shown to inhibit LPS-induced TNF-α,IL-6,and IL-1βproduction(P<0.01 or P<0.05),GLP was also shown to increase IκBαmRNA expression(P<0.01),decrease p65 and STAT3 mRNA expression(P<0.01 or P<0.05),and decrease p-p65,p65,p-STAT3,and STAT3 protein expression in breast epithelial cells(P<0.01 or P<0.05).The findings suggest that GLP inhibits nuclear factor kappa-B(NF-κB)and signal transducers and activators of transcription(STAT)signaling by preventing IκBαdegradation and p65 and STAT3 phosphorylation.This results in lower LPS-induced TNF-α,IL-6,and IL-1βproduction and prevents inflammatory cell injury.
