ABSTRACT
Objective To investigate the protective effects and the possible mechanisms of mild hypothermia against liver L02 cells hypoxic-ischernia reperfusion injury by using mild hypothermia pretreatment.Methods L02 cells were randomly divided into three groups:normal control group (N group),hypoxic-ischemia reperfusion group (control group) and hypoxic-ischemia reperfusion with mild hypothermia pretreatment group (experimental group).Before hypoxic-ischemia reperfusion,cells in experimental group were pretreated with mild hypothermia for 6 h,while the other groups were given the normal culture.Thereafter,the hypoxic-ischemia reperfusion models of L02 cells were performed by a tri-gas incubator to hypoxic-ischemia culture for 12 h,followed by reperfusion with normal conditions for 4 hours.Cells in N group were cultured in normal conditions.The temperature of experimental groups was set to 32 C.The samples were collected,and the cell injury,the cell vitality,the cell apoptosis and the expression of JNK in different groups were detected.Results Compared to N group,the levels of alanine aminotransferase (ALT),aspartate transaminase (AST) and lactic dehydrogenase (LDH) were significantly increased,the cell vitality was significantly decreased,the cell apoptosis and the expression of p-JNK were significantly increased in control and experimental groups (P ＜ 0.05).Compared to control group,all these changes were significantly ameliorated in experimental group.The levels of ALT,AST and LDH in control group were (30.0 ± 4.6),(26.3 ± 3.8) and (1129.0 ± 134.3) U/L,and those in the experimental group were (21.0 ± 2.7),(18.7 ± 2.1)and (898.3 ± 79.2),respectively.The cell vitality in control group and experimental group was (64.33 ± 2.32)％ and (78.17± 3.01)％ respectively.The cell apoptosis in control group and experimental group was (32.4 ± 2.3) ％ and (18.8 ± 1.4) ％ respectively.The expression of p-JNK in experimental group was significantly decreased.All these differences were statistically significant (P＜0.05).Conclusion Mild hypothermia pretreatment could significantly attenuate liver L02 cells hypoxicischemia reperfusion injury probably by inhibiting JNK activation.
ABSTRACT
Objective To investigate the protective effects and the possible mechanisms of mild hypothermia against liver L02 cells hypoxic-ischernia reperfusion injury by using mild hypothermia pretreatment.Methods L02 cells were randomly divided into three groups:normal control group (N group),hypoxic-ischemia reperfusion group (control group) and hypoxic-ischemia reperfusion with mild hypothermia pretreatment group (experimental group).Before hypoxic-ischemia reperfusion,cells in experimental group were pretreated with mild hypothermia for 6 h,while the other groups were given the normal culture.Thereafter,the hypoxic-ischemia reperfusion models of L02 cells were performed by a tri-gas incubator to hypoxic-ischemia culture for 12 h,followed by reperfusion with normal conditions for 4 hours.Cells in N group were cultured in normal conditions.The temperature of experimental groups was set to 32 C.The samples were collected,and the cell injury,the cell vitality,the cell apoptosis and the expression of JNK in different groups were detected.Results Compared to N group,the levels of alanine aminotransferase (ALT),aspartate transaminase (AST) and lactic dehydrogenase (LDH) were significantly increased,the cell vitality was significantly decreased,the cell apoptosis and the expression of p-JNK were significantly increased in control and experimental groups (P ＜ 0.05).Compared to control group,all these changes were significantly ameliorated in experimental group.The levels of ALT,AST and LDH in control group were (30.0 ± 4.6),(26.3 ± 3.8) and (1129.0 ± 134.3) U/L,and those in the experimental group were (21.0 ± 2.7),(18.7 ± 2.1)and (898.3 ± 79.2),respectively.The cell vitality in control group and experimental group was (64.33 ± 2.32)％ and (78.17± 3.01)％ respectively.The cell apoptosis in control group and experimental group was (32.4 ± 2.3) ％ and (18.8 ± 1.4) ％ respectively.The expression of p-JNK in experimental group was significantly decreased.All these differences were statistically significant (P＜0.05).Conclusion Mild hypothermia pretreatment could significantly attenuate liver L02 cells hypoxicischemia reperfusion injury probably by inhibiting JNK activation.
ABSTRACT
Objective To explore the changes of genes associated with the nuclear factor of kappa B(NF-?B) signaling pathway in neonatal rats with early hypoxic-ischemic reperfusion brain damage(HIRBD).Methods Twenty-four SD rats at age of 7 days,with male to female of 1212,were randomized into normal control group(group A,n=8),hypoxic-ischemia reperfusion for 2 h(group B,n=8) and hypoxic-ischemia reperfusion for 4 h(group C,n=8).The tissues of hippocampus were taken for complete RNA extraction.Gene chip inspection and biological signal analysis technique were used to detect the expression of 113 involved signal molecules of NF-?B pathway.Results Compared with group A,the up-regulated expression was found in Chemokine(C-C motif) ligand 2,Dual specificity phosphatase 1,FBJ osteosarcoma oncogene(Fos) and Toll-like receptor 9.Whereas the expressions of Caspase-1,8,Mitogen-activated protein kinase kinase 6,Mitogen activated protein kinase 3 and Ras homolog gene family member a from Ras-gene famimly was found down-regulated in group B.The up-regulated expression was in Fos,IL-1? and Toll-like receptor 6,but that of down-regulation was found in Caspase-1,Extracellular matrix protein 1,Lysophosphatidic Acid G-protein-coupled receptor 2,Mucosa associated lymphoid tissue lymphoma translocation gene 1,Inhibitor of kappa B kinase epsilon and Ras homolog gene family member c.Conclusions At the early stage of HIRBD,the Toll-like receptors may induce NF-?B activation,leading to the coordinated induction of multiple genes,which is involved in inflammatory,apoptosis and cell proliferation.Genes induced by NF-?B are responsible for the physiopathological process of early brain damage in neonatal rats with HIRBD.
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Objective To explore the effect of exogenous adrenomedullin(ADM) on expressions of glutathion in plasma and brain tissue inneonatal rats with hypoxic-ischemia reperfusion brain damage(HIRBD) and the mechanism of action.Methods Fifty-six cases of 7 d SD rats were randomly divided into 4 groups including normal control group(without any treatment),HIRBD group(the model with hypoxia for 2 h and ischemia for 1 h),primed group(abdomen infusion of ADM at 0.5 h before making model,the other was same to the HIRBD group)and treatment group(abdomen infusion of ADM at onces after making model,the other was same to the HIRBD group).The neonatal rats in 4 groups were derived blood and brain tissue after decapitation at either 4 h or 24 h after reperfusion.The levels of gtutathion(GSH) in plasma and brain tissue were determined by using chromatometry.Results In HIRBD group,the affection areas at 24 h after reperfusion enlarged compared with those at 4 h after reperfusion.Meanwhile,the affection of punctiform degeneration or necrosis at 4 h after reperfusion transformed into the affection of lamellar or diffuse degeneration or necrosis at 24 h after reperfusion.The levels of GSH in plasma and brain tissue in HIRBD group at either 4 h or 24 h after reperfusion were significantly lower than that in normal control group(Pa0.05).Meanwhile the pathology score of brain section in primed group and treatment group were significantly lower than that in HIRBD group at either 4 h or 24 h after reperfusion(Pa0.05).Conclusion Exogenous ADM can induce the neuroprotection in HIRBD by adjusting the expression of GSH.