绿原酸调控NLRP3炎性小体对新生儿败血症发挥保护作用

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【中图分类号】R722.19 【文献标志码】A

【AbstractObective：Toexaminetheeffectsofchlorogenicacid（CGA）onccalserousflud（CSI）-inducedsepsisandlipopolysac charide（LPS）-inducedbonemarowmacrophage（BMM）-mediatedinflammationinneonatalmice，andtoelucidatetheregulatory roleofCGAinNLRP3inflammasomeactivation.Methods：Forty7-day-oldC57BL6mice wererandomlydividedintothecontrolgroup （Ctrl group），sepsis group（CSI group），sepsis + 10 mg/kg CGA group（CS + CGA-10 group），and sepsis +20mg/kg CGA group（CSI + CGA-20 group），with10 mice per group.Neonatal mouse BMMs weredivided into thecontrol group（Ctrl group），LPSgroup，LPS + （204 2 μmol/L CGA group[LPS+CGA（2 μmol/L） group]，and LPS + 20 μmol/L CGA group[LPS + CGA（20 μmol/L）group]. Pathological injuryoflungtisseswasexamindbyHEstaning，ndNRP3andcaspase-expressionandistributionweremeasuredbyuno histochemistry（IHC） staining.Protein expression levels of GSDMD，NLRP3，ASC，caspase-1 and caspase- -1 （P20） in lung tissue were quantified by Western blot.IL-18 and IL-1β levels in the supernatant were measured by ELISA，and TNF- α and IL-6 levels as well asreactiveoxygenspecies（ROS）fluorescenceintensityinthesupeatantweredeterminedbyflowcytometryResults：Animalexperiments showed attenuated lung injury and downregulated GSDMD，NLRP3，ASC，caspase -1 ，and caspase -1 （P20）protein expression in the CSI+CGA-10 groupandCS+CGA-20 groupcomparedwith theCSI group.Inadition，cellexperimentsrevealedthatIL-18，IL1β，TNF- α ，and IL-6 levels and ROS fluorescence intensity were lower in the LPS + CGA（2 μmol/L） group and LPS+CGA（ 20 μmol/L） groupthan in theLPS group.Conclusion：CGA alleviates sepsisinduced lung injury，suppresses inflammatory cytokine release from BMMs，and reduces oxidative stress in neonatal mice，potentially through the inhibition of NLRP3 inflammasome activation.

【Keywords】chlorogenic acid;sepsis;NLR family，pyrin domain containingprotein3;neonates;inflammasome

新生儿败血症是新生儿死亡的主要原因之一，病死率高达 16%[1] 。（剩余10166字）