Реферат
Pulmonary atresia with intact ventricular septum (PA/IVS) is a rare,critical and complicated cyanotic congenital heart disease,the natural mortality rate is high,if not treated,50% of newborns died within 2 weeks after birth,about 85% of newborns will die within six months.In recent years,with cardiac surgery procedures,catheter intervention and other treatment levels improved,the survival rate of newborns after surgery has improved.Over the past decade,the disease 5-year survival rate increased by 75% or more.In this paper,PA/IVS cardiac surgery procedures,catheter intervention and hybrid treatment were reviewed,aimed at providing a reference for clinical treatment.
Реферат
Objective:To explore the effect of taxifolin on H2O2-induced pyroptosis in H9C2 cells and the possible mechanisms.Methods:The H9C2 cells was divided into 3 groups:a control group,a hydrogen peroxide (H2O2) group and a taxifolin group.The morphology of H9C2 cells was observed by inverted phase contrast microscope.The mitochondrial membrane potential was measured by JC-1 staining and flow cytometry.The alteration of the level of reactive oxygen species (ROS) was detected by specific mitochondrial probe.The protein levels of cysteinyl aspartate specific proteinase-1 (caspase-1) was determined by Western blot.The mRNA levels of interleukin-18 (IL-18),interleukin-1a (IL-1a),interleukin-1b (IL-1b),absent in melanoma 2 (AIM2),apoptosis-associated apeck-like protein (ASC),nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3)and nucleotide-binding oligomerization domain-like receptor family caspase recruitment domaincontaining protein 4 (NLRC4) were determined by reverse transcription-polymerase chain reaction (RT-PCR).Results:Compared with the control group,the morphology of H9C2 cells obviously changed in the H2O2-treated group,which was guadually improved in the presence of taxifolin.Compared with the control group,the mitochondrial membrane potential was markedly decreased in the H2O2-treated cells,accompanied by the increase of ROS (both P<0.05).Compared with the H2O2 group,the mitochondrial membrane potential changes in the taxifolin group was increased while the ROS was decreased,with significant difference (both P<0.05).Compared with the control group,the protein level of caspase-1 and the mRNA levels of IL-18,IL-1a,IL-1b,AIM2,ASC,NLRP3 and NLRC4 in the H2O2-treated group were significantly increased (all P<0.05),which were attenuated in the presence of taxifolin (all P<0.05).Conclusion:Taxifolin can protect H9C2 cells from oxidative injury,and it is able to suppress the H2O2-induced H9C2 cell pyroptosis through inhibition of AIM2,NLRP3 and NLRC4 in flammasome.
Реферат
To observe the effect of high-mobility group box 1 (HMGB1) on autophagy and chemotherapy resistance in human leukemiacell line (K562) cells, and to explore the underlying mechanisms. Methods: The K562 cells were cultured in vitro and divided into 6 groups: a chemotherapeutic group, a chemotherapeutic control group, a HMGB1 preconditioning group, a HMGB1 preconditioning control group, a HMGB1 siRNA group and a siRNA control group. The chemotherapeutic group was further divided into a vincristine (VCR) group, an etoposide (VP-16) group, a cytosine arabinoside (Ara-C) group, a adriamycin (ADM) group and a arsenic trioxide (As2O3) group. The cell activity was evaluated by cell counting kit-8. The protein levels of HMGB1, microtubule-associate protein1light chain3 (LC3), AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (m-TOR) were determined by Western blotting. The level of serum HMGB1 was evaluated by enzyme-linked immunosorbent assay (ELISA). The autophagy was examined by monodansylcadaverine staining and observed under transmission electron microscopy. Results: Compared with the control group, the cell activity was significantly decreased and the level of serum HMGB1 was significantly increased in the chemotherapeutic (VCR, VP-16, Ara-C, ADM and As2O3) groups (all P<0.05). Compared with the control group, the cell activity and the level of serum HMGB1 were significantly increased in the HMGB1 preconditioning group (both P<0.05). Compared with the siRNA control group, the cell activity and the level of serum HMGB1 were significantly decreased in the HMGB1 siRNA group (both P<0.05). Compared with the control group, the expression of LC3-II and the formation of autophagic bodies were increased in the HMGB1 preconditioning group (both P<0.05), the p-AMPK expression was increased and p-mTOR expression was decreased (both P<0.05). Conclusion: HMGB1 can increase the autophagy and promote chemotherapy resistance through the pathway of AMPK/m-TOR in K562 cells.