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

Objective To investigate the influence of injection carthamus tinctorius D. (1C) on the expression of intercellular adhesion molecule-1(ICAM-1) during the ischemia-reperfusion injury of lung (LIRI) in rabbits and its potential mechanism. Method Single lung ischemia-reperfusion animal model was induced in rabbits. A total of 30 Japanese white rabbits were randomly divided into sham-operation group (S group, n =10), ischemia-reperfusion group (I/R group, re = 10) and ischemia-reperfusion plus 1C group (1C group, n = 10) .The rabbits of 1C group received 1C 2.0 ml/kg injected intravenously just at 20 min before ligation of artery involved and the same dose of 1C instantly at the initiation of reperfusion. Malondialdehyde (MDA) , superoxide dismutase (SOD) and xanthine oxidase(XO) in serum were measured. The lung tissue was sampled and assayed wet/dry weight ratio (W/D), contents of myeloperoxidase (MPO) at the end of the experiment, and ultrastructure changes were observed under electron microscope. The expression of ICAM-1 was measured by using immunohistochemistry(IHC) . snd one-way ANOVA was used for statistical analysis. Results In I/R group, serum XO and MDA increased and SOD decreased, whereas the same pattern of changes but less magnitude happened in 1C group ( P < 0.01). The values of W/D and MPO were much higher in I/R group, but lower in 1C group. Under electron microscope, the ultrastructure of lung tissue showed pathological changes in the rabbits of I/R group,and these changes were greatly attenuated in the rabbits of 1C group . The IHC showed that ICAM - 1 in lung tissue of I / R group was (2.94±0.48) which was significantly higher than that of 1C group(1.75 (P < 0.01). Conclusions Injection Carthamus tinctorius D. may meliorate the ischemia-reperfusion injury of lung by way of suppressing the expression of ICAM-1, inhibiting neutrophil aggregation, lowering oxygen free radical level and decreasing lipid peroxidation.

Objective To evaluate the role of CCAAT/enhancer-binding protein homologous protein (CHOP) in ischemia-reperfusion induced lung injury, and clarify the potential molecular mechanism.Methods Fifty mice of C57BL/6J were randomly divided into five groups, 10 mice in each group, including Sham operation group(sham group),ischemia/reperfusion group (I/R group), I/R +PBS+Lipofectamine group(I/R+PBS+Lipo group) , I/R+scramble siRNA group( I/R+siRNASCR group) , I/R+CHOPsiRNA group( I/R+siRNACHOP group).The content of total lung water (TLW), wet-to-dry weight ratio (W/D) of lung and index of quantitative assessment of histologic lung injury (IQA) were detected, CHOP mRNA and protein expression were detected by RT-PCR and Western blot.Results Compared with Sham group, W/D, TLW and IQA were significantly elevated in I/R group,I/R+PBS+Lipo group and I/R+siRNASCR group (P<0.05).Moreover, the W/D,TLW and IQA reduced with CHOP-siRNA treatment, respectively(P<0.01).Compared with Sham group, CHOP mRNA and protein expressions were significantly elevated in I/R group,I/R+PBS+Lipo group and I/R+siRNASCR group, Moreover, the CHOP mRNA and protein expressions reduced with CHOP-siRNA treatment, respectively(P<0.01). Conclusion I/R could cause excessive unfolded protein response in lung tissue, and induce apoptosis by CHOP signal pathway, damage lung tissue. The inhibition of CHOP pathway could alleviate lung ischemia-reperfusion injury.

According to current situation of the undergraduates'scientific research,proposal of establishing the systematic research capacity training program was given,and this program's effects on undergraduates at our school were analyzed.

AIM: To explore the effects of fluctuant high blood glucose and stable high blood glucose on apoptosis and the expression of Bax and Bcl-2 in glomerular endothelial cells and renal tubular epithelial cells in diabetic rats. METHODS: 24 SD rats were divided into 3 groups: control group, stable high blood glucose group and fluctuant high blood glucose group. Diabetic rats were induced by intraperitoneal injection of STZ, and the fluctuant high blood glucose animal model was induced by intraperitoneal injection of aspart and glucose at different time points every day. Apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL), and immunohistochemistry was used to detect apoptosis associated gene bax and bcl-2 expression in kidney. RESULTS: After 4 experimental weeks, a significant increase in cell apoptosis, up-regulation of Bax protein expression in kidney tubular epithelial cell and down-regulation of Bcl-2 in glomerular endothelial cell in fluctuant high blood glucose rats were observed compared with stable high blood glucose rats.CONCLUSION: Fluctuant high blood glucose induces more apoptosis in renal tubular epithelial cells than that in stable high blood glucose diabetic rats.

Objective To evaluate dexmedetomidine-induced cardioprotection in a mouse model of lung ischemia-reperfusion (I/R) and the relationship with endoplasmic reticulum stress.Methods Forty healthy SPF male C57BL/6J mice,weighing 20-24 g,aged 8-10 weeks,were divided into 4 groups (n=10 each) using a random number table:sham operation group (Sham group),lung I/R group (I/R group),dexmedetomidine group (Dex group) and dexmedetomidine plus atipamezole (specific α2-adrenergic receptor antagonist) group (DA group).The model of lung I/R injury was established by clamping the left hilum of lung for 30 min followed by 180 min of reperfusion.In group Sham,only sternotomy was performed,the hilum of lung was not clamped,and the mice were mechanically ventilated for 210 min.In Dex and DA groups,dexmedetomidine 20 μg/kg and dexmedetomidine 20 μg/kg plus atipamezole 250 μg/kg were injected intraperitoneally,respectively,at 30 min before establishment of the model.At 180 min of reperfusion,blood samples were collected from the orbit for determination of creatine kinase-MB (CK-MB) and lactic dehydrogenase (LDH) activities in serum.The animals were then sacrificed,and hearts were removed for determination of apoptosis in cardiomyocytes (by TUNEL) and expression of phosphorylated c-Jun N-terminal kinase (p-JNK),caspase-12,CCAAT/enhancer-binding protein homologous protein (CHOP) and glucose-regulated protein 78 (GRP78) in myocardial tissues (by Western blot),and expression of JNK,caspase-12,CHOP,GRP78 mRNA in myocardial tissues (by real-time polymerase chain reaction).Apoptosis index was calculated.Results Compared with Sham group,the serum CKMB and LDH activities and apoptosis index were significantly increased,the expression of p-JNK,JNK mRNA,and caspase-12,CHOP and GRP78 protein and mRNA was up-regulated in I/R,Dex and DA groups (P＜0.01).Compared with I/R group,the serum CK-MB and LDH activities and apoptosis index were significantly decreased,the expression of p-JNK,JNK mRNA,and caspase-12 and CHOP protein and mRNA was down-regulated,the expression of GRP78 protein and mRNA was up-regulated in group Dex,and the expression of GRP78 protein and mRNA was significantly up-regulated (P＜0.01),and no significant change was found in the other parameters in group DA (P＞0.05).Compared with DEX group,the serum CK-MB and LDH activities and apoptosis index were significantly increased,the expression of pJNK,JNK mRNA,and caspase-12 and CHOP protein and mRNA was up-regulated (P＜0.01),and no significant change was found in the expression of GRP78 protein and mRNA in DA group (P＞0.05).Conclusion Dexmedetomidine can reduce myocardial injury induced by lung I/R,and the mechanism may be related to activation of α2-adrenergic receptors and inhibition of endoplasmic reticulum stress in myocardial cells of mice.

Objective To observe the clinical effect of therapy of budesonide/formoterol powder for inhalation in treatment of adult with bronchial asthma.Methods 90 cases with bronchial asthma and were divided into observation group and control group randomly from February 2014 to February 2015.45 cases in each group.Control group was treated with budesonide inhalants +formoterol inhalants, observation group was given budesonide/formoterol powder inhalation.Changes of related indicators were followed up and recorded.Results After treatment, IL-5, IL-12 and IFN-γwere (60.2 ±9.7)pg/mL,(31.4 ±3.1)pg/mL,(1.6 ±0.2) ng/mL of observation group were better than control group (72.8 ±10.7)pg/mL,(38.5 ± 5.6)pg/mL,(2.3 ±0.3) ng/mL (P<0.05).After treatment,total effective rate in observation group was 68.9%, which was better than control group (48.9%)(P<0.05).Conclusion Clinical effect of budesonide/formoterol powder for inhalation in treatment of patients with bronchial asthma is accurate, and there is no obvious adverse reaction.

AIM: To investigate the effect of dexmedetomidine (DEX) on renal injury induced by lung ischemia/reperfusion (I/R) in mice and its relationship with endoplasmic reticulum stress response.METHODS: Healthy SPF male C57BL/6J mice, weighing 20~24 g, aged 8~10 weeks, were randomly divided into 5 groups (n=10 each): sham operation group (sham group), I/R group, atipamezole (Atip) group, DEX group, and DEX+Atip group.In vivo lung I/R model was established by occlusion of the left pulmonary artery for 30 min followed by 180 min of reperfusion in the mice.The Atip (250 μg/kg), DEX (20 μg/kg) and DEX+Atip were intraperitoneally infused into the mice before left pulmonary hilus was blocked in Atip group, DEX group and DEX+Atip group, and other operations were the same as I/R group.After experiment, the mice were killed, and the renal tissues were harvested to observe the morphological changes.The enzymatic activity of caspase-3, serum creatinine and blood urea nitrogen, and cell apoptotic index of the renal cells were also analyzed.The expression of c-Jun N-terminal kinase (JNK), caspase-12, CCAAT/enhancer-binding protein homdogous protein (CHOP) and glucose-regulated protein 78 (GRP78) at mRNA and protein levels in the renal tissues was determined by RT-PCR and Western blot.RESULTS: Compared with sham group, the enzymatic activity of caspase-3, serum creatinine and blood urea nitrogen, renal cell apoptotic index, and the mRNA and protein levels of JNK, caspase-12, CHOP and GRP78 in I/R group were significantly increased (P<0.01), and the renal tissues had obvious damage under light microscope.Compared with I/R group, Atip group and DEX+Atip group, the enzymatic activity of caspase-3, serum creatinine and blood urea nitrogen, renal cell apoptotic index, and the mRNA and protein levels of JNK, caspase-12 and CHOP in DEX group were significantly decreased, and the expression level of GRP78 significantly increased (P<0.01).Furthermore, the renal tissue damage was obvious reduced.CONCLUSION: DEX effectively relieves the renal injury induced by lung I/R in mice, which may be associated with exciting α2-adrenergic receptor and inhibiting endoplasmic reticulum stress response.

AIM: To investigate the effects of safflor injection(SI) on expression of cyclooxygenase-2 mRNA during lung ischemia/reperfusion injury(PIRI) in rabbits.METHODS: Rabbit lung model of ischemia/reperfusion injury was constructed in vivo.The rabbits were randomly divided into three groups: sham-operation group(group S),ischemia-reperfusion group(group I/R) and ischemia/reperfusion plus safflor injection group(group SI).The lung tissue sampled at the end of the experiment was assayed for wet/dry weight ratio(W/D),injured alveoli rate(IAR) and observed ultrastructure changes under electron microscope.The expressions of COX-1 and COX-2 were measured by immunohistochemistry(IHC).The expression of COX-1 mRNA and COX-2 mRNA were observed by in situ hybridization(ISH).RESULTS: The value of W/D and IAR was much higher in I/R group,but decreased in SI group.Electron microscope showed obvious ultrastructure injury brought by PIRI in I/R group,which was greatly attenuated in SI group.The IHC and ISH demonstrated that COX-2 and COX-2 expressions in pulmonary tissue of I/R group were significantly higher than those in S group(P

Objective To investigate the change of caspase-3 in rabbits after lung ischemia-reperfusion injury(LIRI) and the effect of puerarin(葛根素).Methods Thirty healthy rabbits used for unilateral lung ischemia-reperfusion model were randomly divided into 3 groups(each n=10): control group(C group),lung ischemia-reperfusion group(I/R group) and puerarin group.The activity of serum superoxide dismutase(SOD),the contents of serum malondialdehyde(MDA) and nitric oxide(NO),the wet to dry weight(W/D) ratio of lung tissue and the index of quantitative assessment of histological lung injury(IQA) were measured respectively in different groups;the pneumocyte apoptosis index(AI) was achieved by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling(TUNEL);caspase-3 protein and mRNA expression were studied by using in situ hybridization(ISH) and immunocytochemistry(IHC) techniques in the groups mentioned above.Results The activity of SOD and content of NO were significantly lower in I/R group than those in C group(both P