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Objective To investigate the effect of cyclin-dependent kinase 2 (cdk2) recombinant lentivirus in rats with lipopolysaccharide (LPS)-induced acute lung injury (ALI).Methods Thirty-six adult SD rats were divided into control group, LPS model group and gene intervention group according to the random number table, with 12 rats per group.Rats with LPS-induced ALI were established by intratracheal injection of LPS.Saline solution (60 μL/kg) was injected in control group at the time point of 0, 24, 48 h respectively.Control-lentivirus (60 μL/kg) and cdk2 recombinant lentivirus (60 μL/kg) were injected respectively in LPS model group and gene intervention group at the time point of 0 h and 24 h.After 48 h, LPS (60 μL/kg) with isotonic saline solution were injected in both LPS model group and gene intervention group.Lung tissue samples from right-lower areas were collected at 24 h postinjury to evaluate the pathological changes with HE staining.Expressions of cdk2, clara cell secretory protein (CCSP), phospholipase A2(PLA2) and p-C/EBP β protein were detected by Western blot.Inflammatory factors of tumor necrosis factor-α(TNF-α), interleukin (IL)-1β, IL-6 and IL-10 in serum were measured with ELISA method.Results Inflammatory infiltration and damage to the alveolar structure were serious in LPS model group than control group, while inflammatory infiltration decreased significantly and alveolar structure tended to be normal in gene-intervention group.Expression of Cdk2 in control group (1.00±0.21) and LPS model group (0.93±0.17) were similar, but both were lower than that in gene intervention group (4.29±0.73) (P<0.05).Expression of CCSP in gene intervention group (3.19±0.38) was significantly higher than that in control group (1.00±0.20) and LPS model group (0.32±0.19) (P<0.05).Expression of PLA2 in LPS model group (4.49±0.51) was higher than that in control group (1.00±0.13) and gene intervention group (1.76±0.26) (P<0.05).Meanwhile, the variation of p-C/EBPβ concentration among the groups was similar to CCSP.Expression of TNF-α in LPS model group[(196.34±30.17)pg/ml] was higher than that in control group [(71.24±5.13)pg/ml] and gene intervention group[(86.32±11.02)pg/ml](P<0.05).Changes in IL-1β, IL-6 and IL-10 among the groups were similar to TNF-α.Conclusions Over-expression of Cdk2 plays a protective role for LPS-induced ALIby up-regulating CCSP and down-regulating inflammatory factors such as PLA2, TNF-α, IL-1β, IL-6 and IL-10, as may relate to the phosphorylation of C/EBPβ.
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Objective To evaluate the effects of unilastatin on brain injury in children undergoing aortic arch surgery under cardiopulmonary bypass (CPB).Methods Twenty ASA physical status Ⅲ or Ⅳ children of both sexes,aged 1-24 months,weighing 3-12 kg,undergoing repair of coarctation of aorta or interrupted aortic arch complicated with intracardiac malformations under CPB,were randomly divided into 2 groups (n =10 each):control group (group C) and ulinastatin group (group U).Ulinastatin 20 000 U/kg was diluted into 10 000 U/ml with normal saline and it was then injected intravenously in 3 parts (1/3 was injected via the internal jugular vein after induction of anesthesia; 1/3 at the beginning of CPB and 1/3 at 5 min before aortic unclamping).In group C the equal volume of normal saline was given instead of ulinastatin.Blood samples were taken from the radial artery after induction of anesthesia (T1),at 10 min after aortic clamping (T2),at 10 min after aortic unclamping (T3),at the end of CPB (T4),and at 6 and 24 h after termination of CPB (T5,T6) for determination of plasma S100B protein and neuron-specific enolase (NSE) concentrations.Results There was no significant difference in plasma levels of S100B protein and NSE at T1 between the two groups (P ＞ 0.05).Plasma S100B protein and NSE levels were significantly increased at T2-5 as compared to the baseline values at T1 in both groups (P ＜ 0.05).Plasma S100B protein and NSE levels were significantly lower at T2-5 in group U than in group C (P ＜ 0.05).Conclusion Ulinastatin can attenuate brain injury in children undergoing aortic arch surgery under CPB.
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OBJECTIVE:To investigate the protective effect of Polydatin on acute lung injury following endotoxic shock in rats.METHODS:Using a rat endotoxic shock model,animals were randomly divided into4groups∶sham operation group,en?dotoxic shock group,Polydatin treatment group and Polydatin pretreatment group.MAPs(mean artery pressures)were mea?sured at given time points.At the end of the experiment,the serum,the lung tissue,and the bronchoalveolar lavage fluid(BALF)were collected.The levels of lung coefficient,lung penetrating index(LPI),the protein concentration of BALF and the content of NOS in the lung tissue were measured.Furthermore,the histologic changes of the lung were observed under light micro?scope.RESULTS:In addition to prohibiting the dropping of MAP,Polydatin could mitigate the acute lung injury induced by endotoxin which increased the levels of lung coefficient,LPI,the protein concentration of BALF and the content of NOS in lung tissue.Enough morphological evidence could be found in pathological sections.Especially,the protective effects were more ob?vious in Polydatin pretreatment group.CONCLUSION:Polydatin has prophylactic and therapeutical effects on acute lung injury following endotoxic shock and the prophylactic effect is more marked than the therapeutic one.