Aim To explore the effect and mechanism of annexin A1 mimic peptide Ac2-26 on ferroptosis in hu-man umbilical vein endothelial cells(HUVEC).Methods Induction of HUVEC ferroptosis was achieved by the clas-sical ferroptosis agonist RSL3,with subsequent intervention by the annexin A1 mimtic peptide Ac2-26.The cell number and viability were detected by CCK-8 kit,the levels of malondialdehyde(MDA)and glutathione(GSH)were detected by ELISA,the expression of ferroptosis-related molecules and adhesion molecules was detected by Western blot,the lipid re-active oxygen species(ROS)levels were detected by C11-BODIPY fluorescent probe,and the mitochondrial reactive oxy-gen species(mtROS)levels were detected by MitoSOX probe.FeRhoNOX-1 fluorescent probe was used to detect intra-cellular Fe2+content,perspective microscopy was used to observe mitochondrial morphology,JC-1 fluorescent probe was used to detect mitochondrial membrane potential,kit was used to detect ATP levels,the Scratch assay was used to detect cell migration ability,and nitrate reductase assay was used to detect nitric oxide(NO)level.Results Ac2-26 inhibi-ted RSL3-induced decrease in HUVEC viability,up-regulated the expression of suppressor of ferroptosis proteolytic carrier family 7 member 11(SLC7A11),GPX4,and ferritin heavy chain 1(FTH1),increased the GSH content,decreased the MDA content,reduced the generation of intracellular lipid ROS,and decreased the intracellular Fe2+aggregation(P＜0.05 or P＜0.01);Ac2-26 inhibited RSL3-induced damage to HUVEC mitochondrial morphology and function,up-regulated ATP content(P＜0.05)and mitochondrial membrane potential(P＜0.001);Ac2-26 inhibited RSL3-induced decrease in HUVEC migratory ability,up-regulated NO levels,inhibited intercellular adhesion molecule-1(ICAM-1)and interleukin-1β(IL-1β)protein expression(P＜0.05 or P＜0.01).Conclusion Ac2-26 inhibits RSL3-induced ferroptosis in HUVEC and maintains mitochondrial morphology and function,as well as HUVEC function.

Aim To explore the effect and mechanism of annexin A1 mimic peptide Ac2-26 on ferroptosis in hu-man umbilical vein endothelial cells(HUVEC).Methods Induction of HUVEC ferroptosis was achieved by the clas-sical ferroptosis agonist RSL3,with subsequent intervention by the annexin A1 mimtic peptide Ac2-26.The cell number and viability were detected by CCK-8 kit,the levels of malondialdehyde(MDA)and glutathione(GSH)were detected by ELISA,the expression of ferroptosis-related molecules and adhesion molecules was detected by Western blot,the lipid re-active oxygen species(ROS)levels were detected by C11-BODIPY fluorescent probe,and the mitochondrial reactive oxy-gen species(mtROS)levels were detected by MitoSOX probe.FeRhoNOX-1 fluorescent probe was used to detect intra-cellular Fe2+content,perspective microscopy was used to observe mitochondrial morphology,JC-1 fluorescent probe was used to detect mitochondrial membrane potential,kit was used to detect ATP levels,the Scratch assay was used to detect cell migration ability,and nitrate reductase assay was used to detect nitric oxide(NO)level.Results Ac2-26 inhibi-ted RSL3-induced decrease in HUVEC viability,up-regulated the expression of suppressor of ferroptosis proteolytic carrier family 7 member 11(SLC7A11),GPX4,and ferritin heavy chain 1(FTH1),increased the GSH content,decreased the MDA content,reduced the generation of intracellular lipid ROS,and decreased the intracellular Fe2+aggregation(P＜0.05 or P＜0.01);Ac2-26 inhibited RSL3-induced damage to HUVEC mitochondrial morphology and function,up-regulated ATP content(P＜0.05)and mitochondrial membrane potential(P＜0.001);Ac2-26 inhibited RSL3-induced decrease in HUVEC migratory ability,up-regulated NO levels,inhibited intercellular adhesion molecule-1(ICAM-1)and interleukin-1β(IL-1β)protein expression(P＜0.05 or P＜0.01).Conclusion Ac2-26 inhibits RSL3-induced ferroptosis in HUVEC and maintains mitochondrial morphology and function,as well as HUVEC function.

Biliary fibrosis (BF) is the result of pathological repair of bile tract injury, characterized by thickening and sclerosis of the bile duct wall and progressive stricture of the lumen, which may ultimately lead to serious adverse outcomes such as biliary obstruction, biliary cirrhosis, liver failure, and hepatobiliary malignancies. Current research describes BF as a pathological feature of certain bile tract diseases, lacking a systematic summary of its etiology, pathophysiology, molecular mechanisms, and treatment. BF is a common but easily neglected disease state in biliary system, which may promote the development and progression of hepatobiliary diseases through abnormal repair mechanism after pathological biliary tract injury. Based on the latest research progress from both domestic and international perspectives, the authors review the concept, clinical manifestation, etiology, pathogenesis, and therapeutic strategies of BF to provide a reference for clinical physicians.

ObjectiveTo study the effects of placental transfusion of umbilical cord milking on very low birth weight (VLBW) infants. Methods Fifty-seven VLBW infants born from September 2011 to May 2014 who had umbilical cord milking at birth were selected as experimental group. Sixty-one VLBW infants born from January 2008 to August 2011 who had normal cord clamping at birth were selected as control group. The complications of VLBW infants, blood transfusion, frequency of using pulmonary surfactant (PS), the duration of mechanical ventilation, the duration of oxygen and mortality were compared between two groups.Results The incidence of severe asphyxia, IVH and anemia was signiifcantly lower in experimental group than in control group (P< 0.05). The blood transfusion and transfusion volume, duration of mechanical ventilation, and duration of oxy-gen were signiifcantly lower in experimental group than in control group (P< 0.05).Conclusions Umbilical cord milking can reduce the incidence of severe asphyxia, IVH and anemia. It also can reduce the blood transfusion, the duration of mechanical ventilation, and the duration of oxygen in VLBW infants.