RESUMO
AIM:To investigate the effects and c-Jun N-terminal kinase(JNK) expression of dexmedetomidine (DEX) on A549 cells with hypoxia/reoxygenation (H/R) injury.METHODS:A549 cells were cultivated and were randomly divided into four groups (n =10):control group (N),DEX group (D),hypoxia/reoxygenation injury group (H),hypoxia/reoxygenation injury + DEX interfere group (HD).After all models were completed,the morphological changes of A549 cells were observed under the inverted microscope.Cell activity was detected by CCK-8 and the apoptosis index (AI) was detected by in situ end labeling (TUNEL) method.The expression of GRP78,p-JNK,caspase-3 at protein levels and GRP78,JNK mRNA were detected by Western blot and RT-PCR.RESULTS:Compared with N group,the number of adherent cells in H group decreased significantly,and cell morphology changed.The expression of OD value in H group decreased obviously (P ＜ 0.01),the expression of AI value,GRP78,p-JNK,caspase-3 protein and GRP78,JNK mRNA were significantly increased (P＜ 0.01).HD group compared with H group,the cell damage alleviated,the expression of OD value was increased (P ＜ 0.01),the number of apoptosis cells and the AI value in HD group were significantly decreased (P ＜ 0.01).Dramatically decreased the expression of p-JNK,caspase-3 protein and JNK mRNA (P ＜ 0.01).CONCLUSION:DEX can effectively alleviate A549 cells damage induced by H/R injury,which may be related to inhibition of the JNK pathway.
RESUMO
[ ABSTRACT] AIM:To explore the effect of dexmedetomidine ( DEX) on the CCAAT/enhancer-binding protein-homologous protein ( CHOP) pathway during lung ischemia-reperfusion ( I/R) in mice.METHODS:C57BL/6J male mice were randomly divided into sham operation group ( sham group) , lung ischemia/reperfusion group ( I/R group) , ischemia/reperfusion +normal saline group ( I/R+NS group ) and ischemia/reperfusion+dexmedetomidine group ( I/R+DEX group) .Dexmedetomidine was infused intraperitoneally with 25 μg/kg for 30 min prior to the ischemia period in I/R+DEX group, the normal saline was administrated with the same volume of dexmedetomidine in I/R+NS group.After fini-shed the 3 h-reperfusion period , the left lung tissues were harvested to determine lung wet/dry weight ( W/D) , the total lung water content ( TLW) , and index of quantitative evaluation for alveolar damage ( IQA) .Morphological observation and terminal-deoxynucleotidyl transferase mediated nick end labeling ( TUNEL) were applied to evaluate the structure changes and the apoptosis index (AI) of the lung tissues.The expression of CHOP and glucose-regulated protein 78 (GRP78) at mRNA and protein levels in the lung tissues was detected by Western blot and RT-PCR.RESULTS:Compared with sham group, the W/D, TLW, IQA, AI, the mRNA and protein expression of CHOP and GRP78 obviously increased, and the left lung tissues structure were damaged more obviously both in I/R group and I/R+NS group.Compared with I/R group, the W/D, TLW, IQA, AI and the protein and mRNA expression of CHOP in I/R+DEX group decreased, the injury of the left lung tissue structures induced by I/R in I/R+DEX group were also alleviated .CONCLUSION:DEX alleviates the lung I/R injury, which may be related to inhibition of apoptosis mediated by CHOP pathway.
RESUMO
Objective To study the effect of ligustrazini (LGT) and propofol (PRO) on hepatocellular energy metabolism in the reperfusion injury after hepatic ischemia in rabbits and its mechanism. Methods The rabbits were randomly divided into four groups (n=10 in each), hepatic ischemia-reperfusion (HIR) group, HIR+LGT group (B), HIR+PRO group (C) and HIR+ LGT+PRO group (D). The contents of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), total adenylic acid number (TAN), energy charge (EC), malondialdehyde (MDA), superoxide dismutase (SOD) and nitric oxide products (NO2-/NO3-) in the liver tissue were measured at 45 minutes after reperfusion. Results The contents of ATP, NO and SOD activity of the liver tissue in B, C, D groups were higher than those in HIR group (P
RESUMO
AIM: To investigate the variations of heme oxygenase-1/carbon monoxide system in lung ischemia-reperfusion injury and effects of puerarin on the system.METHODS: The unilateral lung ischemia-reperfusion model was replicated in vivo.Rabbits were randomly divided into three groups(n=10 in each): control group,ischemia-reperfusion(I-R) group and puerarin group.The blood specimens collected at times before ischemia,ischemia 1 h,reperfusion 1 h,3 h and 5 h were tested for the contents of carboxyhemoglobin(COHb) and cyclic guanosine monophosphate(cGMP).The lung tissues sampled at 5 h after reperfusion were assayed for wet/dry weight ratio(W/T),the injured alveoli rate(IAR) and the activity of HO-1.The changes of ultrastructure were observed under electron microscope.The tissue slides were also stained by immunohistochemistry(IHC) and in situ hybridization(ISH) to detect the expression of HO-1.RESULTS: The plasma content of COHb and cGMP in I-R and puerarin group increased in a time-dependent manner after I-R compared with control group,but the increment in puerarin group was higher than that in I-R group(P
RESUMO
AIM:To explore the relationship between apoptosis in the lung tissues and lung ischemia/reperfusion injury,and to observe the effects of human thioredoxin (hTrx) on apoptosis in lung ischemia/reperfusion injury. METHODS:The single lung in situ ischemia/reperfusion animal model was used. Eighty four Wistar rats were randomly divided into control group (control),groups of ischemia for 1 h and reperfusion for different times (IR1h,IR3h,IR5h),and groups of IR + human thioredoxin treatment (IR1h + hTrx,IR3h + hTrx and IR5h + hTrx). Transmission electron microscope (TEM),terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) and immunocytochemistry techniques were used to observe apoptosis,apoptosis signal-regulating kinase 1 (ASK1) and expression of Bcl-2 and Bax in various phases of lung ischemia/reperfusion. RESULTS:Cell apoptosis in lung tissues was significantly high,ASK1,Bcl -2 and Bax protein were upregulated in lung tissues of lung ischemia/reperfusion injury as compared to control (all P
RESUMO
AIM:To investigate the effect of L-arginine(L-Arg) on expression of bcl-2,bax mRNA during pulmonary ischemia and reperfusion injury(PIRI) in rabbits.METHODS: Single lung ischemia and reperfusion animal model was used in vivo.The rabbits were randomly divided into three groups: sham operated group(sham,n=12),ischemia-reperfusion group(I/R,n=12) and I/R+ L-arginine group(L-Arg,n=12).Changes of several parameters,which included apoptotic index(AI),wet to dry ratio of lung tissue weight(W/D) and index of quantitative assessment of histologic lung injury(IQA),were measured at 300 min after reperfusion in lung tissue.Meanwhile the location and expression of bcl-2,bax mRNA as well as the ratio of bcl-2 mRNA/bax mRNA were observed.The lung tissue was prepared for light microscopic and electron microscopic observation at 60,180 and 300 min after reperfusion.RESULTS: As compared with I/R group,in intima and extima of small pulmonary artery,alveoli,and bronchiole epithelia,the expression of bcl-2 mRNA and the ratio of bcl-2 mRNA/bax mRNA were increased,and the expression of bax mRNA was decreased in L-Arg treatment group.The values of AI,W/D and IQA showed significantly lower than that in I/R group at 180 minutes after reperfusion in lung tissue(P