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Objective To explore the effects of cannabinoid receptor agonist WIN55,212-2 preconditioning on spinal cord ischemia reperfusion injury in rats.Methods A total of 32 male Sprague-Dawley rats was randomly divided into four groups (n =8):sham group,control group,dimethyl sulfoxide(DMSO) group which was given intraperitoneally DMSO 0.3 ml 30 min before ischemia reperfusion,and WIN group which was given intraperitoneally WIN55,212-2 1 mg/kg 30 min before ischemia reperfusion.Each rat was neurologically assessed at 24 h and 48 h after reperfusion by Tarlov scale,and the number of normal motor neurons at anterior horn of the spinal cord was recorded.Res uits The Tarlov scale of WIN group was significantly higher than that control and DMSO groups (P ＜ 0.05).There were more normal motor neurons at anterior horn of the spinal cord in WIN group than those in control and DMSO groups (P ＜ 0.05).Conclusions Cannabinoid receptor agonist WIN55,212-2 preconditioning might attenuate spinal cord ischemia reperfusion injury.
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Objective To study the protective effects of propofol pretreatment on ischemia-reperfusion injury in rabbit heart. Methods Forty New Zealand white rabbits (40 male, weighting 2. 5 ± 0. 36kg) were randomly assigned to 4 groups, including sham operation group, ischemia reperfusion (IR)group, IR + ischemia preconditioning (IP) group and IR + Propofol preconditioning (PP) group (n =10 each). The myocardial ischemia-reperfusion model of rabbits was established by coronary artery ligation.The levels of high energy phosphates (ATP, ADP and AMP) in myocardial tissue were measured by HPLC.The activities of serum lactate dehydrogenase (LDH), serum creatine kinase-MB (CK-MB) superoxide dismutase (SOD) and malondiadehyd (MDA) in myocardial tissue were assayed. Results The content of ATP, ADP, AMP, and the activity of SOD in PP group and IP group were higher than that of IR group, and the content of LDH, MDA and CK-MB in injured myocardial tissue in PP group and IP group were obviously lower than that of IR group (P ＜0. 05, P ＜0. 01). No difference was found in PP group and IP group(P＞0. 05). Conclusion Propofol preconditioning as well as ischemia preconditioning protected the myocardial tissues from the ischemia-reperfusion injury by improving the myocardial energy metabolism, the debasement of the oxyradical level and the antagonism the reaction of lipid peroxides.
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Objective To study the protective effects and mechanisms of adenosine on lung ischemia-reperfusion injury in rabbit. Methods The rabbit ltng model of ischemia-reperfusion was constructed.Thirty Chinese rabbits were random divided into three groups: Group A (no surgery), group B (ischemiareperfusion) and group C (Adenosine + ischemia-reperfusion). The MDA content,SOD content of the plasma, wet-dryrate (W/D) and the pathology of lung tissue and the index of quantitative assessment of histologic lung injury (IQA) were measured after 60 min reperfusion. Results After 60min reperfusion, the value of W/D, MDA and IQA in group B were significantly higher than those in group A (q = 7. 06,13.71,18. 62, P ＜0.01), while the concentration of SOD were lower than those in group A (q = 14. 33, P ＜0.01). In contrast with group B, W/D,MDA and IQA in group C was obviously lower (q =5.23 ,8. 51, 9.99,however, the concentration of SOD were higher than those in group B (q = 7.73, P ＜ 0. 01). In contrast with group A and C ,the expression of CD11b/CD 18 of group B was significantly increased after 60min reperfusion (q =8.59,9.56, P ＜0. 01). Conclusion Adenosine can prevent ischemia-reperfusion injury in rabbit lung in vivo by inhibiting the expression of CD-11b/CD18 on PMNs and dropping oxygen free radicals level.
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Objective To study the feasibility and safety of limb remote ischemic preconditioning (RIPC) in infants and explore the protective effect on myecardium ischemia reperfusion injury for infants undergoing cardiac operation under cardiopulmonary bypass. Methods 60 infants weight less than 7 kilograms with ventricular septal defect were enrolled into the study. 30 of them (RIPC group) were ischemic preconditioned two times (24 hours and 1 hour preoperatively) by three cycles of iscbemia (5 minutes for each) and reperfusion on the left upper arm using a blood pressure cuff. Serum lactate dehydrogenase (LDH), creatine kinase (CK) and its isoenzyme (CK-MB), and tro-ponin I (TnI) ; malondialdehyde (MDA) and superoxide dismutase (SOD) was preoperatively detected. The expression of heat shock pro-tein 70 (HSP 70) in cardiomyocytes was determined by western blot analysis. The surgical outcome including limb movement and sensory function was also recorded. Results No limb disability or sensory disturbance or no other surgical complications was found in all infants. LDH, CK, TnI at the beginning of operation in RIPC group was higher than those in control group. After operation, leakage of heart enzymes were attenuated in RIPC group, and the serum concentration of enzymes were lower than those in the control group. The RIPC group had low coronary sinus venous concentration of MDA but high SOD. The expression of HSP70 was upregulated in cardiomyocytes of RIPC group. Conclusion The limb RIPC can be done easily and safety in infants, and BIPC can reduce the leakage of myocardial enzymes and upregu-late the expression of HSP, which possess protective effect on myocardial IRI.
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Objective To observe the protective effect of magnesium gluconate on myocardial apoptosis by ischemia reperfusion injury in isolated rat hearts, and study the possible mechanism. Methods The hearts of 48 Sprague-Dawely rats were isolated, linked to Lange-ndorff perfusion apparatus, and randomly divided into 3 equal groups(n = 16 each) : Control group, ischemia/reperfusion (I/R) group and magnesium gheonate group. 8 rats in each group were perfused. Control group was pedused with modified KH buffer for 110min. I/B group was perfuesd with modified KH buffer for 20 min, then exposed to iscbemia for 30 min, and then reperfused with modified KH buffer for 60 min. Magnesium gheonate group was perfumed with modified KH buffer with magnesium gluconate for 20 min, then exposed to isohemia for 30 min and then reperfused with modified KH buffer with magnesium glueonate for 60 min. Lacate dehydrogenase (LDH) and ereatine kinase (CK) in the effluent liquid from the heart were measured after reperfusion. The concentration of Ca2+ and NO in the left ventricle were determined. The other 8 rats in each group were reperfused for 120 minutes as the method described before. After repeffusion, the myoeyte apoptosis was examined by Annexin-V-FITC/PI. After the two experiments the incidence of ventrieular arrhytlunias during reperfusion was assessed. Results Compared with I/R, magnesium glueonate decreased the incidence of ventricular an'hythmias(P <0. 01). The contents of CK and LDH in the effluent liquid from the heart in magnesium glueonate group was lower than that of I/R group (P <0. 01). The contents of Ca2+ and NO in the left ventricle in magnesium gluconate group was decreased than that of I/R group (P <0. 01). The index of myocyte apoptosis were significanfly lower in magnesium glueonate group than that of I/R group (apoptosis index :27.79±1.59 vs 33.61±2.10, P < 0. 01) . Conclusion Magnesium glueonate has protective effect on myocardial isohemia reperfusion injury in rats. The protective effect may be related to decreasing myocyte apoptosis by increasing the content of NO and relieving calcium overload.
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Objective To explore protective effects of curcumin on lung injury in the early hepatic ischemia/reperfsion (reperfusion for 1 and 3 hour) inrats. Methods Wistarratswererandom]y divided into the fo]]owinggroups: GroupA (shamoperation), group B (control group) and group C (cureumin applied). Contents of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA), myeloperoxidase (MPO) in lung tissues were determined to evaluate the protective effect of eurcumin on lung injury in the injury of isehemia/ reperfusion. Results Curcumin relieved edema of diaphragmatic wall and exudation of blood cell and white cell in pulmonary alveoli. Curcumin increased the contents of SOD, CAT and decreased contents of MDA, MPO in lung tissue. Conclusion By repressing the generation of oxygen free radical and infiltration of polymorphonuclear leukocyte in lung tissue, curcumin can relieve lung injury in the early hepatic ischemia/repeffusion.
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Objective In this study we investigated the expression and protective mechanisms of Hsp22 and VEGF in brain tissue following cerebral ischemic reperfusion in gerbils and whether they are correlative. Method Forty five gerbils were randomly divided into there groups: Normal Group (n =5) ,Sham-operated Group and Ischemia-Reperfusion Group (I/R). Sham-operated Group and I/R Group were divided into four subgroups (each group has five animals) : 6 hours group, lday group, 3days group, 7days group. Histological analysis of tissue injury was carried out by staining with haematoxylin and eosin haematoxylin and eosin (HE). Result The tissues of normal group and sham-operated group was integrated, but that of I/R were changed with gliocyte hyperplasia and hypertrophia, interstitial edema, cellular edema, gliocyte and neuron edema , neuron necrosis. The data presented here provided a positive correlation between expression of Hsp22 and VEGF. Conelusions There was a positive correlation between expression of Hsp22 and VEGF after gerbils brain I/R injury.
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Objective To investigate the mechanisms of Chinese traditional medicine mixture protection of vascular endothelial cell from apoptosis in cerebral ischemia-reperfusion injury. Methods Healthy, clean SD rats were randomly divided into 4 groups: Sham opera-tion group (SOG), cerebral ischemia reperfusion injury group (IRG), cerebral ischemia preconditioning group (IPG) and Chinese tradi-tional medicine mixture preconditioning group (CPG). Furthermore, IRG, IPG and NPC were divided into 4 sub-groups: 1 d, 7d, 14d, 21d subgroup, according to the different time point since ischemia-reperfusion took place. And in CPG, Naotai formula extract was used. Cere-bral vascular endothelial cells of rats were removed and Hoechst 33258 staining and the DNA gradient bands were used to detect the apoptosis of these cells. Then the influence of Naotai formula extract on caspase-3, 8 and 9 activation, and Bid lysis was examined by Western-blot, and the mechanisms of Chinese traditional medicine mixture protection of vascular endothelial cell were investigated from apoptosis signal pathway. Result Naotai formula extract can inhibit the apoptosis of endothelial cells in ischemia-reperfusion injury, and it also can inhibit the activation of caspase-3, 8 and 9, thus inhibit the lysis of Bid into tBid. Conclusion Naomi formula extract inhibit the apoptosis of endo-thelial ceils in ischemia-reperfusion injury via apoptosis signal pathway.
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Objective To study the mechanism of monophosphoryl lipid A (MPLA) protecting liver ischemia-reperfusion injury in rats, and explore the hemeoxygenase-1-carbon monoxide-cyclic guanosine monophosphate (HO-1-CO-cGMP) pathway whether involved in MPLA enhance calcitonin gene-related peptides (CGRP) releasing or not. Methods Male SD rats were randomly divided into control group, sham-operated group, hepatic ischemia-reperfusion group, MPLA low, medium and high dose groups (hepatic ischemia-reperfusion + MPLA0. 2,0. 5,1.0 mg/ kg). Hepatic isehemia-reperfusion model was constructed, followed by observation of cell ultrastructure through electron microscope. Serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) and liver tissue levels of CO were determined. HO-1 expression in liver tissue was detected by immunohistochemic, CGRP, eGMP concentration in liver tissue was detected by RIA assay. Results Compared with hepatic isehemia-reperfusion group, the cell damage in MPLA group were relatively minor, and ALT, AST, LDH were significantly decreased (P <0.05), while HO-1, CO, cGMP, CGRP levels were signifi-cantly increased (P < 0.05). HO-1 and CO, CO and cGMP, cGMP and CGRP were obviously positive correlated (P <0.05). Conclu-sion MPLA enhanced CGRP synthesis and release through HO-1-CO-cGMP pathway in liver ischemia / reperfusion, which may be one of the mechanisms of MPLA reducing hepatic ischemia-reperfusion injury in rat.
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Objective To study the effect of procyanidin on neural cell apoptosis and the expression of Caspase-3 of cerebral ische-mia reperfusion(I/R) injury in rats. Methods 40 rats were randomly divided into 4 groups, which were sham operated group, I/R group, low dose procyanidin treated group and high dose procyanidin treated group. The focal middle cerebral artery occlusion (MCAO) model was made by suture-occluded method. After MCAO for 90min following 24h of reperfusion, neural cell apoptosis and the expression of caspase-3 was investigated with TUNEL and immunohistochemistry. HE staining and Trc staining was also used. Result Compared with sham opera-ted group, neural cell apoptosis rate and the expression of caspase-3 were increased at the 24th hour of reperfusion in the ischemic territory(P < 0.05) . Compared with I/R group, low and high dose procyanidin treated group reduced expression of caspase-3 and neural cell apopto-sis rate in a dose-dependent manor (P <0.05). The change of ischemic impairment in procyanidin treated group was less than that of I/R group, and the change of high dose procyanidin treated group was less than that of low dose procyanidin treated group. Compared with that of I/R group, cerebral infarction volume of procyanidin treated group was decreased in a dose-dependent manor (P < 0.05). Conclusion Procyanidin may reduce cerebral ischemia-reperfusion injure by reducing expression of caspase-3 and neural cell apoptosis.
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lsartan could reduce the release of p-selectin.Conclusions Valsartan could relieve myocardial ischemia reperfusion injury of rat, which may be through reducing p-seleetin of plasma.
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Objective To study the protective effects of propofol against ischemia/reperfusion injury in rat lung. Methods Rat model of pulmonary ischemia/reperfusion injury was used in this study. Rats were randomly divided into three groups, including sham opera-tion group (group A), iachemia/reperfusion group (group B) and propofol group (group C), 15 rats in each group. The concentration of tumor necrosis factor -α and interleukin-6 in bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay (ELISA). Then blood gas analysis, lung wet/dry (W/D) weight ratio were detected in each group. Results Propofol could significantly improve PaO2, reduce the W/D value and the contents of TNF-α and IL-6 in BALF. Conclusion Propofol effectively suppressed the pro-duction and release of inflammatory cytokine, therefore it can protect the lung from isehemia/reperfusion injury.
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Objective To study the protective effect of Octreotide against ischemia-reperfusion injury when liver was resected Methods Using the routine Pringle's maneuver hepaticvaseular occlusion,thirty patients for resection of liver with cirrhosis were random divided into two groups:octreotide group(n=15)and physiologic saline group(n=15).In octreotide group,the patients with hepatecto15),the patients were injected 1ml saline in the same way.The variations of postoperative liver function were measured.Plasma MDA and TNF-α after reperfusion for 1h were measured and the hepatic histopathologic alterations were also examined.Results The levels of ALT and AST from the octreotide group increased less than those of the physiologic saline group(P＜0.01).Meanwhile,Plasma MDA and TNF-α from the octreotide group was slightly increased(P＜0.01)and the hepatic histopathologic alterations were significantly decreased.Conclusions Given octreotide by subcutaneous injection before blocking portabepatis show all important protective effect against the hepatic isehemia-repedusion injury for resection of liver.
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Objective To study the nerve protective mechanism of puerarin on ischemic brain injured and observe the expression change of TNF-α cytokines in ischemic brain area. Methods 90 healthy male SD(Spraque-Dawley)rats were used to built the animal model of brain medium sized artery focal cerebral ischemia reperfusion with the patching methods, and the rats were randomly divided into three groups: Sham operation group(n=30),operation group(n=30),operation with puerarin interfered group(n=30).There were five different observing time in every group(6h,12h,24h,48h,72h after operation).The operation with puerarin group rats were treated with puerarin solution, the sham operation and operation group rats were injected the same volume Sodium Chloride. To observe the expression of TNF-α cytokines in different time, immunohistochemistry staining in ischemic region was used. Results Compared with the sham operation group. the expression of TNF-α cytokine in cerebral isehemic reperfusion brain tissue in the operation and the operation with puerarin interfered groups was higher(P＜0.01).Compared with the operation group, the expression of TNF-αcytokine was significantly decreased in different time after cerebral ischemic-reperfusion in the operation with puerarin interfered group(P＜0.01 or P＜0.05).Conclusions The puerarin can restrain the expression of the TNF-α cytokine.
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Objective To study the effect of tanshinone ⅡA on the expression of P-selectin and ICAM-1 after cerebral ischemia reperfusion (I/R)injury in rats. Methods Rats were randomly divided into 4 groups: Sham operated group, I/R group, low dose Tan ⅡA treated group and high dose Tan ⅡA treated group. The focal middle cerebral artery occlusion (MCAO) model was made by suture-occluded method. Rats were pretreated with Tan ⅡA, ig for 3d,respectively before MCAO. After 90min MCAO following 24 hours of reperfusion, the expression of P-selectin and ICAM-1 was detected with using immunohistochemistry method. Result Compared with sham operated group, the expression of P-selectin and ICAM-1 increased after reperfusion for 24 hours in the ischemic territory(all P＜0.01).Compared with I/R group, the expression of P-selectin and ICAM-1 decreased in a dose dependent manner in low and high dose Tan ⅡA treated group(P＜0.01).Compared with that of I/R group, cerebral infarction volume was decreased in a dose dependent manner in low dose Tan ⅡA treated group and high dose Tan ⅡA treated group(all P＜0.01).The change of ischemic impairment in low or high dose Tan ⅡA treated group was less than that in IR group, and the change of ischemic impairment in high dose Tan ⅡA treated group was less than that in low dose Tan ⅡA treated group. Conclusion Tan ⅡA may reduce cerebral ischemia-reperfusion inflammation injure by decreasing the expression of p-selectin and ICAM-1.Tan ⅡA plays protective effect on cerebral ischemia injury, especially when high dose of Tan ⅡA(30mg/kg)was used.