Objective:To explore the causes of immune dysfunction in neonatal rats with hyperbilirubinemia.Methods:A total of 60 newborn SD rats were equally randomized into normal saline(NS) group,LPS control group,bilirubin con...Objective:To explore the causes of immune dysfunction in neonatal rats with hyperbilirubinemia.Methods:A total of 60 newborn SD rats were equally randomized into normal saline(NS) group,LPS control group,bilirubin control group,low-dose group and high-dose group.After anesthesia,0.1 mL NS was given to the NS and LPS control group and different doses of bilirubin for the other groups;1 h later,the NS and bilirubin control group received the intraperitoneal injection of 0.05 mL NS and 1mg/kg LPS for the other groups.After 5 or 24 hours of model establishment,spleens were collected for detecting the expression levels of MyD88 and p-TAK1 protein and the spleen cells apoptosis by immunohistochemmistry and TUNEL method.After 24 hours of model establishment,scrum inflammatory factors levels and T cell subsets distribution were determined by ELISA and flow cytometry.Results:In contrast to low-dose bilirubin,high-dose bilirubin could induce spleen cells apoptosis in coordination with LPS.After 5 hours of model establishment,compared with NS group.MyD88 expression level in low-dose group elevated while p-TAK1 level in high-dose group reduced(P<0.05).In high-dose group,inflammotory factors levels and CD8^+T cells percentage were all higher than LPS control and NS group(P<0.05),while CD4^+ T cells percentage was lower than NS group(P<0.05).Conclusions:High-concentration plasma bilirubin in coordination with LPS could inhibit NF- κB signal pathways activation and aggravate inflammatory reaction,thus caused immunosuppression with inflammation cascade,which resulted in the immune dysfunction.展开更多
文摘Objective:To explore the causes of immune dysfunction in neonatal rats with hyperbilirubinemia.Methods:A total of 60 newborn SD rats were equally randomized into normal saline(NS) group,LPS control group,bilirubin control group,low-dose group and high-dose group.After anesthesia,0.1 mL NS was given to the NS and LPS control group and different doses of bilirubin for the other groups;1 h later,the NS and bilirubin control group received the intraperitoneal injection of 0.05 mL NS and 1mg/kg LPS for the other groups.After 5 or 24 hours of model establishment,spleens were collected for detecting the expression levels of MyD88 and p-TAK1 protein and the spleen cells apoptosis by immunohistochemmistry and TUNEL method.After 24 hours of model establishment,scrum inflammatory factors levels and T cell subsets distribution were determined by ELISA and flow cytometry.Results:In contrast to low-dose bilirubin,high-dose bilirubin could induce spleen cells apoptosis in coordination with LPS.After 5 hours of model establishment,compared with NS group.MyD88 expression level in low-dose group elevated while p-TAK1 level in high-dose group reduced(P<0.05).In high-dose group,inflammotory factors levels and CD8^+T cells percentage were all higher than LPS control and NS group(P<0.05),while CD4^+ T cells percentage was lower than NS group(P<0.05).Conclusions:High-concentration plasma bilirubin in coordination with LPS could inhibit NF- κB signal pathways activation and aggravate inflammatory reaction,thus caused immunosuppression with inflammation cascade,which resulted in the immune dysfunction.
