In order to provide us new clues to induce some endogenous protective molecular mechanisms, the changes in gene expression profile induced by ischemia-reperfusion in pulmonary tissues of rats were investigated and the...In order to provide us new clues to induce some endogenous protective molecular mechanisms, the changes in gene expression profile induced by ischemia-reperfusion in pulmonary tissues of rats were investigated and the dynamic mechanism of pulmonary ischemia-reperfusion injury was elucidated. Thirty male Wistar rats were randomly divided into 6 groups： 5 ischemia-reperfusion （I/R） groups （I/R 0-h, I/R 1-h, I/R 3-h, I/R 6-h, I/R 24-h） and control group （n=5 in each）. An in situ ischemia-reperfusion lung injury rat model was established by occluded hilus of lung. The RatRef-12 Expression Beadchip （22 226 gene probes per array） was used to analyze the pattern of gene expression in all groups. The results showed that 648, 340, 711, 1279 and 641 genes were differentially expressed in I/R 0-, 1-, 3-, 6- and 24-h groups respectively. The differentially expressed genes were classified as following 7 functional categories： cytokine, adhesion molecule, growth factor and apoptosis-related factor, oxidation and antioxidation molecule, metabolic enzyme, ion channel and aquaporin, signal transduction molecule. It was suggested that gene chip technology was an effective and quick method for screening differentially expressed genes. Many differentially expressed genes with different functions interacted each other to result in pulmonary ischemia-reperfusion injury.展开更多
Objective:To investigate the effect of sevoflurane on tissue permeability of lung ischemiareperfusion injury(LIRI)in rats.Methods:A total of 45 wistar rats were randomly divided into3 groupsⅠ,Ⅱ,Ⅲ.Modified Eppinger ...Objective:To investigate the effect of sevoflurane on tissue permeability of lung ischemiareperfusion injury(LIRI)in rats.Methods:A total of 45 wistar rats were randomly divided into3 groupsⅠ,Ⅱ,Ⅲ.Modified Eppinger method was adopted to establish the rat lung ischemiareperfusion injury model.GroupⅠserved as the control group,groupⅡas ischemia reperfusion group,groupⅢas sevoflurane ischemia-reperfusion group.Blood gas index,lung permeability index(LPI)change,lung tissue pathology change and lung water content were observed and compared between groups of rats at different time points.Results:During ischemia reperfusion,all rats kept balance of the MAP during different time points,SPO_2 of groupⅡandⅢdecreased significantly thanⅠgroup(P<0.05);after reperfusion lung permeability index in GroupⅡandⅢwas higher than the control group significantly(P<0.05),120 min after reperfusion LPI change and iujury of groupⅢwas significantly lower thanⅡgroup(P<0.05);interstitial and alveolar cavity effusion in of groupⅢwere lower than that of groupⅡ.Conclusions:Sevoflurane pretreatment can reduce the lung tissue permeability,and LIRI plays a protective role in LIRI.展开更多
Objective：To observe the protective effects of safflor Injection（SI） and extract of Ginkgo biloba（EGB） on lung ischemia-reperfusion injury（LIRI） and investigate its mechanism.Methods：In vivo rabbit model of LI...Objective：To observe the protective effects of safflor Injection（SI） and extract of Ginkgo biloba（EGB） on lung ischemia-reperfusion injury（LIRI） and investigate its mechanism.Methods：In vivo rabbit model of LIRI was reconstructed.Forty rabbits were randomly and equally divided into four groups：sham-operation group（sham group）,ischemia-reperfusion group（model group）,ischemia-reperfusion plus SI group（safflor group） and ischemia-reperfusion plus EGB injection group（EGB group）.Malondialdehyde（MDA） content,superoxide dismutase（SOD） and xanthine oxidase（XO） activity in serum were measured.The wet/dry weight ratio（W/D） of the lung tissue and activity of myeloperoxidase（MPO） were also tested.Ultrastructure change of the lung tissue was observed by the electron microscope.The expression of intercellular adhesion molecule-1（ICAM-1） was measured by immunohistochemistry（IHC）.Results：In the model group,MDA and XO increased and SOD decreased in serum compared with the sham group（P〈0.01）.The values of W/D,MPO and ICAM-1 of the model group were higher than those of the sham group（P〈0.01）,but those of the safflor group and EGB group were significantly lower than those of the model group（P〈0.01）.The IHC demonstrated that ICAM-1 expression in lung tissue of the model group was significantly higher than those of the safflor group（P〈0.01）.Compared with safflor group,in the EGB group MDA,XO,MPO decreased,SOD and ICAM-1expression increased（P〈0.05）,but the change of W/D was not statistically significant（P〉0.05）.Conclusions：SI and EGB may attenuate LIRI through antioxidation,inhibition of neutrophil aggregation and down-regulation of ICAM-1expression.But EGB had more effect on the antioxidation,while SI did better on regulating ICAM-1 expression.展开更多
BACKGROUND: Toll-like receptor 2 and 4 (TLR2/4) may play important roles in ischemia-reperfusion (I/R) injury, and N-acetylcysteine (NAC) can prevent the generation of reactive oxygen species (ROS) induced by I/R inju...BACKGROUND: Toll-like receptor 2 and 4 (TLR2/4) may play important roles in ischemia-reperfusion (I/R) injury, and N-acetylcysteine (NAC) can prevent the generation of reactive oxygen species (ROS) induced by I/R injury. This study aimed to investigate the changes in TLR2/4 gene expression in the liver and lung after I/R injury with or without NAC pretreatment. METHODS: BALB/c mice were used in a model of partial hepatic I/R injury and randomly assigned to a sham-operated control group (SH), a hepatic ischemia/reperfusion group (I/R) or a NAC pretreated, hepatic I/R group (I/R-NAC). The levels of TNF-alpha in the portal vein and plasma alanine aminotransferase (ALT) were measured at 1 and 3 hours after reperfusion. The lung wet-to-dry ratio was measured, and the expression of TLR2/4 mRNA and protein in the liver and lung were assessed with RT-PCR and Western blotting at the same time points. RESULTS: Compared with the I/R group, the expression of TLR2/4 mRNA and protein in the liver and lung in the I/R-NAC group was decreased at the same time point (P<0.05). The levels of portal vein TNF-a and plasma ALT increased continuously in the l/R group at I and 3 hours of reperfusion compared with the SH group; however, they declined significantly in the group pretreated with NAC (P<0.05). The extent of lung edema was relieved in the I/R-NAC group compared with the I/R group (P<0.05). CONCLUSIONS: TLR2/4 was activated in the liver and lung in the process of partial hepatic I/R injury. NAC inhibited the activation of TLR2/4 and the induction of TNF-alpha resulting from I/R injury via modulating the redox state, thus it may mitigate liver and lung injury following partial hepatic I/R in mice.展开更多
Objective To study the effects of isoflurane on ischemia-reperfusion(IR)-induced injury in isolated rat lungs.Methods This study was performed on an isolated buffer-perfused rat lung model.There were four groups:CON g...Objective To study the effects of isoflurane on ischemia-reperfusion(IR)-induced injury in isolated rat lungs.Methods This study was performed on an isolated buffer-perfused rat lung model.There were four groups:CON group(n=6):perfusion for60min without ischemia;IR group(n=6):after perfusion for30min,then interruption of perfusion and ventilation for45min followed by reperfu-sion for30min;ISO1group(n=6):1.38%isoflurane was administered for30min before45min ischemia,then followed by30min reper-fusion;ISO2group(n=6):1.38%isoflurane was administered during the period of reperfusion.The Myeloperoxidase(MPO)activity of lung,neutrophils counts,tumor necrosis factor-α(TNF-α),superoxide dismutase(SOD)activity,malondialdehyde(MDA)in perfusate,and the Wet-to-Dry lung weight ratios were measured.Results IR caused significant increases in the wet-to-dry lung weight ratios,the activity of lung MPO,the contents of MDA and TNF-αin perfusate,but decreasess in the SOD activity and neutrophils counts.Administration of isoflu-rane(both ISO1and ISO2groups)significantly protected against IR-induced injury the via inhibiting increases of MPO activity and contents of MDA and TNF-αin perfusate.Isoflurane significantly increased the SOD activity and neutrophils counts in perfusate.No difference was found between ISO1and ISO2groups.Conclusion Our results suggest that isoflurane protects the lungs against IR-induced injury in isolated rat lung model.展开更多
Objective To investigate the expression of bradykinin as a substrate of CD26 /DPP IV in rats with ischemia/reperfusion injury following lung transplantation ( LTx) . Methods Thirty - six syngeneic male SD rats were ra...Objective To investigate the expression of bradykinin as a substrate of CD26 /DPP IV in rats with ischemia/reperfusion injury following lung transplantation ( LTx) . Methods Thirty - six syngeneic male SD rats were randomly allocated into control group and experimental group ( n = 18 each) ,and 36 rats served as do-展开更多
目的探讨长链非编码RNA(long non-coding RNA,lncRNA)肺腺癌转录子1(MALAT1)以及下游调控蛋白高迁移率族蛋白B1(High-mobility group protein box-1,HMGB1)在缺血后处理降低大鼠心肌缺血-再灌注损伤(ischemia/reperfusion injury,IRI)...目的探讨长链非编码RNA(long non-coding RNA,lncRNA)肺腺癌转录子1(MALAT1)以及下游调控蛋白高迁移率族蛋白B1(High-mobility group protein box-1,HMGB1)在缺血后处理降低大鼠心肌缺血-再灌注损伤(ischemia/reperfusion injury,IRI)中的作用。方法将24只大鼠饲养7天后,随机分成3组:假手术(Sham)组、缺血再灌注(ischemia/reperfusion,IR)组、缺血后处理(ischemic post-conditioning,IPO)组。模型构建完毕24 h进行检测大鼠血清中心肌肌钙蛋白I(cTnI)和白介素6(IL-6)表达水平,取材检测大鼠心肌梗死面积,检测大鼠心肌组织中MALAT1转录表达水平的差异,HMGB1、Toll样受体4(Toll-like receptor4,TLR4)蛋白含量差异。结果与Sham组比较,IR、IPO组血清中cTnI、IL-6水平明显升高,心肌梗死面积明显增加,心肌组织中MALAT1表达水平显著上调,HMGB1、TLR4水平明显升高(P<0.05)。与IR组比较,IPO组cTnI浓度显著降低,心肌梗死面积显著减小,心肌组织中lncRNA-MALAT1相对表达量降低,HMGB1、TLR4蛋白含量降低(P<0.05)。结论及时的缺血后处理可有效减缓大鼠心肌缺血-再灌注的损伤程度,其相关机制可能与抑制MALAT1调节控制HMGB1、TLR4表达水平之间有一定的关联。展开更多
文摘In order to provide us new clues to induce some endogenous protective molecular mechanisms, the changes in gene expression profile induced by ischemia-reperfusion in pulmonary tissues of rats were investigated and the dynamic mechanism of pulmonary ischemia-reperfusion injury was elucidated. Thirty male Wistar rats were randomly divided into 6 groups： 5 ischemia-reperfusion （I/R） groups （I/R 0-h, I/R 1-h, I/R 3-h, I/R 6-h, I/R 24-h） and control group （n=5 in each）. An in situ ischemia-reperfusion lung injury rat model was established by occluded hilus of lung. The RatRef-12 Expression Beadchip （22 226 gene probes per array） was used to analyze the pattern of gene expression in all groups. The results showed that 648, 340, 711, 1279 and 641 genes were differentially expressed in I/R 0-, 1-, 3-, 6- and 24-h groups respectively. The differentially expressed genes were classified as following 7 functional categories： cytokine, adhesion molecule, growth factor and apoptosis-related factor, oxidation and antioxidation molecule, metabolic enzyme, ion channel and aquaporin, signal transduction molecule. It was suggested that gene chip technology was an effective and quick method for screening differentially expressed genes. Many differentially expressed genes with different functions interacted each other to result in pulmonary ischemia-reperfusion injury.
基金supported by New Medical Technology Import Project in Henan Province(No 2011020113)
文摘Objective:To investigate the effect of sevoflurane on tissue permeability of lung ischemiareperfusion injury(LIRI)in rats.Methods:A total of 45 wistar rats were randomly divided into3 groupsⅠ,Ⅱ,Ⅲ.Modified Eppinger method was adopted to establish the rat lung ischemiareperfusion injury model.GroupⅠserved as the control group,groupⅡas ischemia reperfusion group,groupⅢas sevoflurane ischemia-reperfusion group.Blood gas index,lung permeability index(LPI)change,lung tissue pathology change and lung water content were observed and compared between groups of rats at different time points.Results:During ischemia reperfusion,all rats kept balance of the MAP during different time points,SPO_2 of groupⅡandⅢdecreased significantly thanⅠgroup(P<0.05);after reperfusion lung permeability index in GroupⅡandⅢwas higher than the control group significantly(P<0.05),120 min after reperfusion LPI change and iujury of groupⅢwas significantly lower thanⅡgroup(P<0.05);interstitial and alveolar cavity effusion in of groupⅢwere lower than that of groupⅡ.Conclusions:Sevoflurane pretreatment can reduce the lung tissue permeability,and LIRI plays a protective role in LIRI.
文摘Objective：To observe the protective effects of safflor Injection（SI） and extract of Ginkgo biloba（EGB） on lung ischemia-reperfusion injury（LIRI） and investigate its mechanism.Methods：In vivo rabbit model of LIRI was reconstructed.Forty rabbits were randomly and equally divided into four groups：sham-operation group（sham group）,ischemia-reperfusion group（model group）,ischemia-reperfusion plus SI group（safflor group） and ischemia-reperfusion plus EGB injection group（EGB group）.Malondialdehyde（MDA） content,superoxide dismutase（SOD） and xanthine oxidase（XO） activity in serum were measured.The wet/dry weight ratio（W/D） of the lung tissue and activity of myeloperoxidase（MPO） were also tested.Ultrastructure change of the lung tissue was observed by the electron microscope.The expression of intercellular adhesion molecule-1（ICAM-1） was measured by immunohistochemistry（IHC）.Results：In the model group,MDA and XO increased and SOD decreased in serum compared with the sham group（P〈0.01）.The values of W/D,MPO and ICAM-1 of the model group were higher than those of the sham group（P〈0.01）,but those of the safflor group and EGB group were significantly lower than those of the model group（P〈0.01）.The IHC demonstrated that ICAM-1 expression in lung tissue of the model group was significantly higher than those of the safflor group（P〈0.01）.Compared with safflor group,in the EGB group MDA,XO,MPO decreased,SOD and ICAM-1expression increased（P〈0.05）,but the change of W/D was not statistically significant（P〉0.05）.Conclusions：SI and EGB may attenuate LIRI through antioxidation,inhibition of neutrophil aggregation and down-regulation of ICAM-1expression.But EGB had more effect on the antioxidation,while SI did better on regulating ICAM-1 expression.
基金This work was supported by a grant from theNational Natural Science Foundation of China(No.30200272).
文摘BACKGROUND: Toll-like receptor 2 and 4 (TLR2/4) may play important roles in ischemia-reperfusion (I/R) injury, and N-acetylcysteine (NAC) can prevent the generation of reactive oxygen species (ROS) induced by I/R injury. This study aimed to investigate the changes in TLR2/4 gene expression in the liver and lung after I/R injury with or without NAC pretreatment. METHODS: BALB/c mice were used in a model of partial hepatic I/R injury and randomly assigned to a sham-operated control group (SH), a hepatic ischemia/reperfusion group (I/R) or a NAC pretreated, hepatic I/R group (I/R-NAC). The levels of TNF-alpha in the portal vein and plasma alanine aminotransferase (ALT) were measured at 1 and 3 hours after reperfusion. The lung wet-to-dry ratio was measured, and the expression of TLR2/4 mRNA and protein in the liver and lung were assessed with RT-PCR and Western blotting at the same time points. RESULTS: Compared with the I/R group, the expression of TLR2/4 mRNA and protein in the liver and lung in the I/R-NAC group was decreased at the same time point (P<0.05). The levels of portal vein TNF-a and plasma ALT increased continuously in the l/R group at I and 3 hours of reperfusion compared with the SH group; however, they declined significantly in the group pretreated with NAC (P<0.05). The extent of lung edema was relieved in the I/R-NAC group compared with the I/R group (P<0.05). CONCLUSIONS: TLR2/4 was activated in the liver and lung in the process of partial hepatic I/R injury. NAC inhibited the activation of TLR2/4 and the induction of TNF-alpha resulting from I/R injury via modulating the redox state, thus it may mitigate liver and lung injury following partial hepatic I/R in mice.
文摘Objective To study the effects of isoflurane on ischemia-reperfusion(IR)-induced injury in isolated rat lungs.Methods This study was performed on an isolated buffer-perfused rat lung model.There were four groups:CON group(n=6):perfusion for60min without ischemia;IR group(n=6):after perfusion for30min,then interruption of perfusion and ventilation for45min followed by reperfu-sion for30min;ISO1group(n=6):1.38%isoflurane was administered for30min before45min ischemia,then followed by30min reper-fusion;ISO2group(n=6):1.38%isoflurane was administered during the period of reperfusion.The Myeloperoxidase(MPO)activity of lung,neutrophils counts,tumor necrosis factor-α(TNF-α),superoxide dismutase(SOD)activity,malondialdehyde(MDA)in perfusate,and the Wet-to-Dry lung weight ratios were measured.Results IR caused significant increases in the wet-to-dry lung weight ratios,the activity of lung MPO,the contents of MDA and TNF-αin perfusate,but decreasess in the SOD activity and neutrophils counts.Administration of isoflu-rane(both ISO1and ISO2groups)significantly protected against IR-induced injury the via inhibiting increases of MPO activity and contents of MDA and TNF-αin perfusate.Isoflurane significantly increased the SOD activity and neutrophils counts in perfusate.No difference was found between ISO1and ISO2groups.Conclusion Our results suggest that isoflurane protects the lungs against IR-induced injury in isolated rat lung model.
文摘Objective To investigate the expression of bradykinin as a substrate of CD26 /DPP IV in rats with ischemia/reperfusion injury following lung transplantation ( LTx) . Methods Thirty - six syngeneic male SD rats were randomly allocated into control group and experimental group ( n = 18 each) ,and 36 rats served as do-
文摘目的探讨长链非编码RNA(long non-coding RNA,lncRNA)肺腺癌转录子1(MALAT1)以及下游调控蛋白高迁移率族蛋白B1(High-mobility group protein box-1,HMGB1)在缺血后处理降低大鼠心肌缺血-再灌注损伤(ischemia/reperfusion injury,IRI)中的作用。方法将24只大鼠饲养7天后,随机分成3组:假手术(Sham)组、缺血再灌注(ischemia/reperfusion,IR)组、缺血后处理(ischemic post-conditioning,IPO)组。模型构建完毕24 h进行检测大鼠血清中心肌肌钙蛋白I(cTnI)和白介素6(IL-6)表达水平,取材检测大鼠心肌梗死面积,检测大鼠心肌组织中MALAT1转录表达水平的差异,HMGB1、Toll样受体4(Toll-like receptor4,TLR4)蛋白含量差异。结果与Sham组比较,IR、IPO组血清中cTnI、IL-6水平明显升高,心肌梗死面积明显增加,心肌组织中MALAT1表达水平显著上调,HMGB1、TLR4水平明显升高(P<0.05)。与IR组比较,IPO组cTnI浓度显著降低,心肌梗死面积显著减小,心肌组织中lncRNA-MALAT1相对表达量降低,HMGB1、TLR4蛋白含量降低(P<0.05)。结论及时的缺血后处理可有效减缓大鼠心肌缺血-再灌注的损伤程度,其相关机制可能与抑制MALAT1调节控制HMGB1、TLR4表达水平之间有一定的关联。
