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1.
AIM: To evaluate the role of calreticulin (CRT) in myocardial protection of remote preconditioning against myocardial ischemia/reperfusion injury. METHODS: Thirty SD rats were randomly divided into 5 groups: ischemia reperfusion group (IR), ischemia preconditioning group (IP), remote preconditioning group Ⅰ (RPI), remote preconditioning group Ⅱ (RPII) and pseudo-operation group (PO). The ischemia/reperfusion model was established in vivo. Hemodynamic changes of heart function were observed. Serum cardiac troponin T (cTnT), superoxide dismutase (SOD), malondialdehyde (MDA) and the expression of calreticulin in myocardium were detected. RESULTS: Hemodynamic data, serum cTnT, DA, SOD and the expression of CRT in RPI and IR group were not statistically different (P>0.05). SOD level in IP and RPII group was higher than that in IR group (P<0.05). Accordingly, cTnT, MDA and the expression of CRT in these two groups were lower than those in IR group (P<0.05). CONCLUSION: Remote preconditioning may mimic the protective effect of ischemic preconditioning. Remote preconditioning attenuates myocardial ischemia/reperfusion injury in vivo possibly through down-regulation of CRT expression in rats.  相似文献   

2.
AIM: To investigate the effect of ischemic preconditioning (IP) on myocardial Bcl-2 expression and mitochondrial structure during heart valve replacement surgery under cardiopulmonary bypass. METHODS: Fifty-four patients were prospectively randomized to receive or not ischemic preconditioning (IP) before cold cardioplegic arrest. Ischemic preconditioning in the IP patients (n=22) was induced by a single 2-min ischemia followed by 3-min reperfusion just before aortic clamping and cold crystalloid cardioplegia for myocardial protection. The control group (n=32) received no ischemic preconditioning before cold cardioplegic arrest. The levels of ejection fraction (EF), fractional shortening(FS) and stroke volume (SV) in both groups were measured and compared. troponin T (c-TnT) level, Bcl-2 protein expression and microscopic changes of myocardial mitochondrial structure were recorded for each group before and after surgery. RESULTS: The level of EF, FS and SV in IP group was higher than those in control group (P<0.05). No significant difference in preoperative c-TnT levels between two groups was observed. The level of c-TnT in IP group was lower than that in control group and with a declining trend over time of 6 h, 24 h, 48 h, 72 h and 5 d after surgery, respectively. The preoperative positive unit of Bcl-2 expression between two groups showed no statistical difference (P> 0.05). Postoperatively, the positive unit of Bcl-2 expression in IP group was 19.85±5.88, significantly increased as compared to the preoperative value (P<0.05). In control group, the positive unit of Bcl-2 expression was 14.17±3.39, showed no statistically significant difference to the preoperative value (P>0.05). Postoperative Bcl-2 expression between two groups showed a significant difference (P<0.05). In the control group, microscopic observation revealed swollen mitochondrion, with a hardly visible or disrupted membrane for some mitochondrion; mitochondrial crista were obviously dissolved and loose with a large number of vacuoles formation. However in IP group, myocardial mitochondrion appeared with intact membrane, concentrated mitochondrial cristae with high electron density and no vacuoles formation was observed. CONCLUSION: IP may up-regulate the expression of myocardial anti-apoptotic protein Bcl-2 to protect the mitochondrion, thus protecting cardiocytes and cardiac functions.  相似文献   

3.
AIM: To study the alteration and role of apelin in myocardial ischemic preconditioning and ischemia/reperfusion injury of rats.METHODS: Forty-five SD rats were randomly divided into three groups: ischemia/reperfusion group (IR),ischemia pre-conditioning group (IP) and sham operation group.ECG was continuously used to evaluate the score of arrhythmias.The protein levels of apelin-36 in myocardium and plasma were detected by radioimmunoassay.The expression of apelin was observed by immunohistochemistry.RESULTS: (1) The scores of arrhythmias in IP group (2.1±0.5) was only 58.3% of IR group (3.6±0.8) ( P<0.01).(2) The apelin-36 protein level of plasma and myocardium in IR group were respectively lower by 36.1% and 45.6% than those in SH group (P<0.01),and those in IP group were lower by 23.8% and 24.7% than those in SH group (P<0.01),but higher than those in IR group (18.9% and 38.5%,respectively,P<0.05).(3) The staining absorbance of apelin in IR,SH and IP group was (7.87±2.41),(22.53±2.54) and (14.23±2.15),respectively.There were significant differences between IR and SH (P<0.01) and between IP group and SH group (P<0.05).(4) The scores of arrhythmias in IP and IR were negatively correlated with the protein level of apelin-36 in myocardium (r= 0.847,P <0.01).CONCLUSION: The down-regulation of apelin-36 in the plasma and myocardium of rats indicates that apelin has an important role in myocardial ischemic preconditioning and ischemia/reperfusion injury.  相似文献   

4.
AIM:To observe the effects of ligustrazine ferulate on the apoptosis of myocardial cells in rats with myocardial ischemia-reperfusion injury, and to explore its possible mechanism. METHODS:Sixty male SD rats were randomly divided into five groups: sham-operation group, ischemia-reperfusion group, ligustrazine (4 mg/kg) group, low-dose (4 mg/kg) ligustrazine ferulate group and high-dose (8 mg/kg) ligustrazine ferulate group. The rat myocardial ischemia-reperfusion model was established by 30 min of myocardial ischemia followed by 120 min of reperfusion. Drugs were administered to the rats by jugular vein injection 10 min before reperfusion. After the reperfusion was finished, the biochemical indicators in serum and the histological indexes in myocardium were detected. RESULTS: Compared with ischemia-reperfusion group, ligustrazine ferulate lowered the serum levels of creatine kinase MB form, lactate dehydrogenase, cardiac troponin I and malondialdehyde, elevated the activity of total superoxide dismutase in serum and the expression of Bcl-2 protein in myocardium, decreased the expression of Bax protein and myocardial apoptotic index, and increased the Bcl-2/Bax ratio (all P<0.01). All the indicators in ligustrazine ferulate groups were dose-dependently superior to those in ligustrazine group (P<0.05 or P<0.01). CONCLUSION: Ligustrazine ferulate protects rats against myocardial ischemia-reperfusion injury. Its anti-apoptotic effect may be related to up-regulation of Bcl-2 and down-regulation of Bax.  相似文献   

5.
AIM: To examine the effect of pretreatment with low-concentration of 11, 12-epoxyeicosatrienoic acid(EET) on myocardial ischemia/reperfusion injury in rats. METHODS: After tracheotomy, myocardial ischemia/reperfusion was produced by occlusion and release of the left anterior descending artery(LAD) of the rats. Ischemic preconditioning(IP) was made by two times of ischemia(5 min)/reperfusion(5 min). The experiment was conducted in three groups: control,IP and pretreatment with 11,12-EET(6.24×10-8 mol/L), and each group was subdivided into two subgroups:A,the rats were subjected to ischemia(10 min)/reperfusion(10 min) and arrhythmias during the whole periods were monitored; The rats in B were subjected to ischemia(60 min)/reperfusion(30 min) and arrhythmias, cardiac funtion and myocardial infarction size were documented. RESULTS: Both IP and pretreatment with 11,12-EET could protect the heart against arrhythmias, cardiac disfunction and myocardial infarction. CONCLUSION: Pretreatment with 11,12-EET had protective effect on myocardium in case of ischemia/reperfusion, which was similar to ischemic preconditioning.  相似文献   

6.
AIM: To investigate the effects of ethane 1,2-dimethanesulfonate (EDS) preconditioning on renal ischemia/reperfusion (I/R) injury in male Sprague-Dawley (SD) rats. METHODS: Male SD rats (n=48) were randomly assigned to 6 groups: blank, sham, I/R, EDS+I/R, EDS+testosterone (TST)+I/R, and castration (Cast)+I/R. The renal pedicles were bilaterally occluded with a microvascular clamp for 45 min to establish renal I/R-induced injury model. Bilateral orchiectomy was conducted 2 weeks before surgery. EDS (75 mg/kg) was intraperitoneally injected 5 d before operation. Blood samples were collected 24 h after reperfusion from the vena orbitalis posterior plexus. Luteinizing hormone (LH), TST, serum creatinine (SCr), blood urea nitrogen (BUN), and kidney injury molecule-1 (KIM-1) were detected. The renal tissues were harvested to measure the level of TNF-α and the expression of Fas mRNA and caspase-3 protein. RESULTS: Serum TST levels in EDS+I/R group and Cast+I/R group were below the minimum detectable threshold. Compared with other groups, the rats in EDS+I/R group and Cast+I/R group had higher levels of SCr, BUN and KIM-1 (P<0.05). SCr and BUN levels showed no significant difference between EDS+I/R group and Cast+I/R group (P>0.05), but KIM-1 level in EDS+I/R group was lower than that in Cast+I/R group (P<0.05). After reperfusion for 24 h, the levels of TST and LH in EDS+I/R group, Cast+I/R group and EDS+TST+I/R group were lower than those 1 h before operation (P<0.05). Compared with Cast+I/R and I/R group, the TNF-α level and expression of Fas mRNA and caspase-3 protein were significantly decreased in EDS+I/R group (P<0.05). CONCLUSION: EDS preconditioning substantially reduces the serum TST level, thus attenuating I/R-induced acute renal injury. TNF-α-induced Fas/FasL pathway may be involved in this process.  相似文献   

7.
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8.
AIM: In order to study the relationship between the ERK and p38 MAPK activation and the protection of 11, 12-epoxyeicosatrienoic acid (11, 12-EET) and ischemia preconditioning (IP), the effects of 11, 12-EET and ischemic preconditioning on phosphorylated ERK and p38 MAPK during ischemia and reperfusion in rat myocardium were examined. METHODS: The rat heart was subjected to ischemia for 5 min by ligating the left anterior descending coronary artery followed by reperfusion for 5 min (two times) to undergo ischemia preconditioning. The rats were divided into 5 groups: (1) control; (2) sham group; (3) ischemia/reperfusion (I/R) group, in which the rat heart suffered from 60 min ischemia followed by 30 min reperfusion; (4) IP plus I/R group; (5) EET plus I/R group, in which 6.28×10-8 mol/L 11, 12-EET was injected intravenously 20 min before I/R. The heart function was examined, and phosphorylated ERK and p38 MAPK were detected by Western blot. RESULTS: At 30 min reperfusion, +dp/dtmax, -dp/dtmax and LVDP decreased significantly in I/R group compared with sham group, IP plus I/R group and EET plus I/R group; Phosphorylated ERK1/2 level was higher in I/R group than sham group, but was lower in I/R group than IP plus I/R group and EET plus I/R group; Phosphorylated p38 MAPK level was lower in control, sham, IP plus I/R and EET plus I/R group than I/R group. CONCLUSION: 11,12-EET protects rat heart against ischemia/reperfusion injury, the mechanism may be related to activation of ERK1/2 and inhibition of p38 MAPK.  相似文献   

9.
AIM:To investigate the protective effect of ischemic preconditioning (IPC) on hepatic ischemia-reperfusion(I/R) injury in cirrhotic rats and its possible mechanism. METHODS:Hepatic I/R was induced by Pringle maneuver. The cirrhotic rats were randomized into three groups: Group A: before 30 min of ischemia, a short period of 5 min ischemia and 5 min reperfusion were given; Group B: before 30 min of ischemia, a short period of 10 min ischemia and 10 min of reperfusion were given; Group C: 30 min ischemia only. The serum alanine transferase (ALT), hepatic Fas-mRNA, caspase-3 activity and hepatocyte apoptosis were analyzed. RESULTS:The 7-day survival rate in the group A and B were 100%, respectively. However, it was only 62.5% in the group C. After 6 h of reperfusion, the ALT levels in both group A and B were significantly lower than that of in group C, P＜0.01. The ALT level of group A was also lower than that of group B, P＜0.01. The hepatic Fas-mRNA expression, caspase-3 activity and apoptotic hepatocyte in group A were significantly lower than those of in group C, P＜0.01. CONCLUSIONS:IPC has significant protective effect against hepatic I/R injury. An IPC with 5 min of ischemia and 5 min of reperfusion has the maximal protective effect. The protective mechanism of IPC against hepatic I/R injury is via down-regulation of Fas-mRNA expression, inhibiting caspase-3 activity and subsequently inhibiting hepatocyte apoptosis.  相似文献   

10.
AIM: To study the effects of norepinephrine preconditioning(NE-P) and ischemic preconditioning (IP)on apoptosis and Bcl-2, Bax expression in rat myocardial cells in myocardial ischemic reperfusion (I/R). METHODS: The model of rat ischemic-reperfusion was used to conduct NE-preconditioning. Apoptotic myocytes were detected with TUNEL. Bcl-2, Bax expression were detected with immunohistochemistry. RESULTS: The rate of apoptosis cells in I/R group was higher, the rate of apoptosis cells in NE-P group and IP was lower significantly than that in I/R group(P＜0.01). The expression of Bcl-2 in I/R group was lower, but the expression of Bax was higher, the expression of Bcl-2 in NE-P group was higher significantly than that in I/R group(P＜0.01), the expression of Bax in NE-P group was lower than that in I/R group(P＜0.01). There was no significantly difference between NE-P and IP group in the above parameters (P＞0.05). CONCLUSION: NE-P reduced myocyte apoptosis by I/R in rats; The expression of Bcl-2 ,Bax genes played an important role in myocardial apoptosis.  相似文献   

11.
AIM: To investigate the protective effect of lactulose preconditioning on intestinal ischemia-reperfusion (IR) injury in rats. METHODS: Thirty Sprague-Dawley rats were randomly divided into 3 groups: sham operation group, IR group and IR plus lactulose preconditioning group. Lactulose was intragastrically administered in lactulose group 7 days prior to operation, and the equal volume of saline was administered in the other 2 groups. The intestinal IR injury was induced in IR group and IR+lactulose group using bulldog clamps on superior mesenteric artery by 30 min of ischemia followed by 60 min of reperfusion. Following reperfusion, the serum samples were collected for estimating the levels of interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and IL-1β. Segments of terminal jejunum were rapidly fixed in 4% paraformaldehyde, and HE staining was applied to assess the histopathology. Apoptosis in intestinal epithelium was determined by the technique of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL). The samples of terminal jejunum were also taken for measuring malondialdehyde,superoxide dismutase and the expression of cleaved caspase-3. RESULTS: Lactulose preconditioning significantly attenuated the severity of intestinal IR injury, with inhibition of IR-induced apoptosis. Moreover, lactulose preconditioning significantly limited the release of cytokines and lipid oxidation. CONCLUSION: Lactulose preconditioning has a protective effect on intestinal ischemia reperfusion by inhibiting IR-induced apoptosis and oxidative stress.  相似文献   

12.
AIM: To study the effects of noninvasive delayed limb ischemia preconditioning (NDLIP) on animal cardiac function, myocardial morphology and myocardial apoptosis after myocardial infarction (MI). METHODS: Healthy SD male rats[n=45, weighing (250±10) g] were randomly divided into 3 groups:MI group:the animal model of MI was established by surgical ligation of left anterior descending artery (LAD) after 2 weeks; NDLIP group:after the success of the MI animal model, NDLIP was carried out every other day until the 4th, 6th and 8th weeks; sham group:as the negative control group, the animals were taken heart LAD threading but no ligation. All rats were fed conventionally. At the end of the 4th, 6th and 8th weeks, all rats were made ventricular intubation, and then the hemodynamic parameters were recorded. The blood samples were withdrawn from the abdominal aorta and the serum was separated via centrifugation. The serum contents of Bcl-2 and Bax were measured by ELISA. Left ventricular anterior wall was homogenized. The mitochondrial respiratory chain complexes Ⅰ, Ⅱ, Ⅲ and Ⅳ in the myocardial tissues were detected by ELISA. RESULTS: At the end of the 4th, 6th and 8th weeks, compared with MI group, left ventricular systolic pressure in NDLIP group was significantly increased, while left ventricular end-diastolic pressure in NDLIP group was significantly decreased (both P<0.05). Mitochondrial respiratory chain complexesⅠ, Ⅱ, Ⅲ and Ⅳ in NDLIP group were significantly increased (P<0.05). The serum level of Bcl-2 in NDLIP group was significantly increased and Bax level was reduced remarkably (both P<0.01). CONCLUSION: NDLIP improves the hemodynamic indexes, promotes the mitochondrial respiratory function and inhibits cell apoptosis, thus improving the prognosis of MI.  相似文献   

13.
AIM：To investigate whether hydrogen sulfide (H2S) protects the hearts against inflammatory responses induced by acute myocardial ischemia in isolated rat hearts. METHODS：Rat acute myocardial ischemia injury was induced by ligation of the left anterior descending coronary artery for 4 h, and the normal perfusate was replaced with NaHS (5 μmol/L, 10 μmol/L and 20 μmol/L) perfusate accordingly in NaHS groups 2 h after ischemia. The changes of cardiac function in the myocardial ischemic injury rats were observed. The mRNA expression of TNF-α, IL-1β, IL-6, IL-10 and ICAM-1 was detected by real-time PCR. The protein level of nuclear factor-κB (NF-κB) in the myocardial tissues was detected by Western blotting. RESULTS：The cardiac function in ischemia group was lower than that in sham group (P<0.01). Compared with ischemia group, perfusion of NaHS resulted in the improvement of the cardiac function (P<0.05 or P<0.01). Compared with sham group, the mRNA expression of TNF-α, IL-1β, IL-6 and ICAM-1 in the cardiac tissues was significantly increased, and the mRNA expression of IL-10 in the cardiac tissues was significantly decreased in ischemia group (P<0.01). Compared with ischemia group, the perfusion of NaHS significantly decreased the mRNA expression of TNF-α, IL-1β, IL-6 and ICAM-1 (P<0.05 or P<0.01). The perfusion of NaHS at concentrations of 10 μmol/L and 20 μmol/L significantly increased the mRNA expression of IL-10 (P<0.01). The protein level of NF-κB in ischemia group was markedly higher than that in sham group (P<0.01). Compared with ischemia group, the perfusion of NaHS at concentrations of 10 μmol/L and 20 μmol/L significantly decreased the expression of NF-κB (P<0.05 or P<0.01). CONCLUSION：H2S protects the hearts against acute ischemia injury through inhibition of NF-κB activation and subsequent down-regulation of NF-κB-dependent inflammatory gene expression.  相似文献   

14.
AIM: To investigate the effects of heptanol preconditioning on the changes of structure, function and connexin 43 (Cx43) content in mitochondria in a rabbit model of myocardial isehemia-reperfusion (IR) injury. METHODS: In anesthetized open-chest rabbits, the left anterior descending artery (LAD) was occluded for 30 min and reperfused for 4 h. Sixty-four rabbits were randomly divided into 4 groups (n=16 in each group): sham operation group (sham group), ischemia-reperfusion group (IR group), ischemic preconditioning group (IP group) and heptanol preconditioning group (HT group). All rabbits in the 4 groups were killed 4 h after reperfusion. Myocardial infarct size was determined at the end of the experiment. Mitochondria was isolated by centrifugations. The ultrastructural changes of the mitochondria were observed under electronic microscope. The mitochondrial membrane potential, Ca2+ concentration, MDA content and SOD activity of myocardial mitochondria were also examined. The content of mitochondria Cx43 was detected by Western blotting. RESULTS: Compared to IR group, the myocardial infarct size was significantly reduced in IP (18.97%±2.80%) and HT (19.97%±3.80%) groups, the damage of mitoehondrial ultrastructure was milder (P<0.05), mitochondrial membrane potential was significantly higher and Ca2+ concentration was much lower (P<0.01) in IP group and HT group. No significant difference of MDA content and SOD activity in myocardial mitochondria between IR group and HT group was found. However, MDA content were much lower and SOD activity was significantly higher in IP group as compared to IR group (P<0.01). Compared to sham group, the mitochondria Cx43 expression was distinctly decreased compared to IR group (P<0.05) and no significant difference was found between IP group and HT group (P>0.05). CONCLUSION: Heptanol preconditioning protects myocardium from ischemia-reperfusion injury. The mechanism may be related to increasing in mitochondrial membrane potential, alleviating Ca2+ overload in myocardial mitochondria and attenuating the decrease in mitochondria Cx43 expression induced by isehemia-reperfusion.  相似文献   

15.
GUO Xiao-Fang  GU Qin  LIU Ning  YU Sun 《园艺学报》2012,28(11):1971-1975
AIM: To investigate the relationship between renal cell apoptosis induced by ischemia/reperfusion injury and the activation of P53. METHODS: Eighteen mice were randomly divided into 3 groups: sham operation group, acute kidney injury (AKI) group and pifithrin-alpha(PFT-α) treatment group. The AKI model was established by clamping bilateral renal arteries for 45 min and then performing reperfusion. The mice in PFT-α group were intraperitoneally injected with PFT-α at dose of 2.2 mg/kg 5 min before AKI model was established. The changes of serum creatinine and urea nitrogen were determined and renal pathological changes were observed 48 h after AKI. The P53 expression in the kidney was evaluated by Western blotting and immunofluorescence methods. Apoptosis of the renal cells was observed by TUNEL assay. The protein expression of tumor necrosis factor receptor (TNFR), caspase-3 and Bcl-2 was detected by immunohistochemical method. RESULTS: The levels of serum creatinine and urea nitrogen in AKI group and PFT-α group were higher than those in sham operation group. Compared with AKI group, the levels of serum creatinine and urea nitrogen were significantlydecreased in PFT-α group. No pathological change of the kidney was observed in sham operation group. In AKI group, the pathological changes such as shedding of brush border, vacuolus and dropwise degeneration in the renal tissues were observed. These pathological changes were attenuated in PFT-α group as compared with AKI group. The protein was expression level of P53 and the apoptotic cells were much higher in AKI group than those in sham operation group, and P53 protein was mainly expressed in the renal cortex, while those were significantly decreased in PFT-α group as compared with AKI group. Compared with sham operation group, the expression levels of TNFR and caspase-3 were increased and the Bcl-2 levels was decreased. Compared with AKI group, the expression level of TNFR and caspase-3 decreased and Bcl-2 expression was increased. CONCLUSION: P53 protein is mainly expressed in the renal cortex and induces apoptosis by increasing the expression of caspase-3 and regulating the expression of TNFR and Bcl-2 in the kidney following ischemia/reperfusion injury.  相似文献   

16.
AIM: To establish and evaluate a rat model of heart ischemia-reperfusion injury in vivo. METHODS: Seventy-two male Sprague-Dawley rats weighing(250±50)g were randomly divided into sham operation group(sham), ischemia-reperfusion group(I/R) and normal group. The animals were anesthetized and heparinized. Myocardial ischemia-reperfusion was induced by ligating the left anterior descending coronary artery with "U-shape tube" for 35 min followed by 120 min or 240 min reperfusion in vivo. The heart infarct size was measured by triphenyltetrazolium chloride(TTC) staining. The myocardial cell apoptotic index was determined by the method of terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling(TUNEL). Immunohistochemical method was used to detect the expression of Bcl-2 and Bax in rat ischemia myocardium. The blood level of MB isoenzyme of creatine kinase(CK-MB),cardiac troponin I(cTnI),nitric oxide(NO),malondialdehyde(MDA), total superoxide dismutase(T-SOD)and glutathione peroxidase(GSH-Px) were detected after reperfusion for 2 h and 4 h. RESULTS: Compared with normal group and sham group, there were obvious changes of ST-T segment and Q wave in the electrocardiogram of I/R group. The blood level of CK-MB, cTnI, NO, MDA and GSH-Px in I/R group increased(P<0.05,P<0.01) after reperfusion for 2 h and 4 h, and the blood level of T-SOD in I/R group after reperfusion for 2 h and 4 h also increased(P<0.05). The heart infarct size in I/R group was the largest as compared to other groups. Among these groups, the apoptotic index of I/R group was the highest and the Bcl-2/Bax ratio in I/R group decreased(P<0.01).CONCLUSION: The rat model of heart ischemia-reperfusion injury in vivo can be successfully established with the "U-shape tube". There are obviously changes of heart infarct size, blood level of CK-MB, cTnI, NO, MDA, T-SOD and GSH-Px, myocardial apoptotic index and Bcl-2/Bax ratio between I/R rats and control animals.  相似文献   

17.
AIM: To investigate whether excessive endoplasmic reticulum stress (ERS) is involved in the protective mechanism of Panax quinquefolium saponins (PQS) against ischemia/reperfusion (I/R) injury in rat myocardium. METHODS: The model of myocardial I/R injury in vivo was made by ligating the left anterior descending artery for 45 min followed by 24 h of reperfusion in SD rats. The hemodynamics and serum content of cardiac troponin T (cTnT) were measured. The myocardial infarct size was measured by Evans blue and 2, 3, 5-triphenyltetrazolium chloride (TTC) staining. Cardiomyocyte apoptosis was detected using in situ TDT-mediated dUTP nick end labeling (TUNEL). The protein levels of glucose-regulated protein 78 (GRP78), calreticulin (CRT), C/EBP homologous protein (CHOP), caspase-12, apoptosis-associated proteins Bax and Bcl-2 were determined by Western blotting. RESULTS: Compared with I/R group, the mean arterial pressure in PQR+IR group was decreased by 32.0%, and left ventricular±dp/dtmax was increased by 64.0% and 35.0%, respectively.The serum content of cTnT was decreased by 53.3%, the percentage of area of necrosis (AN)/area at risk (AAR) was reduced by 65.5% and the apoptosis rate was decreased by 54.9%.The myocardial pathological changes were improved. Bcl-2 protein expression was increased by 110.0% and that of Bax was decreased by 47.8%. CRT protein expression was decreased by 43.4 %, CHOP protein expression and the protein level of cleaved caspase-12 were decreased by 38.6% and 23.7% in PQS+I/R group. CONCLUSION: PQS alleviates I/R injury in myocardium by inhibition of excessive ERS.  相似文献   

18.
AIM: To investigate the cardio-protective mechanism of ischemic preconditioning (IP) during heart valve replacement of the perspective of architectural changes of myocardial gap junction. METHODS: Fifty-four patients were prospectively randomized to receive or not ischemic preconditioning before cold cardioplegic arrest. The IP protocol in IP patients (n=22) consisted of a single 2-minute ischemia followed by 3-minute reperfusion just before aortic clamping and cold crystalloid cardioplegia for myocardial protection. The control group (n=32) received no ischemic preconditioning prior to cold cardioplegic arrest. The parameters including arrhythmias occurrence, Cx43 expression (immunohistochemistry SABC method) and myocardial structure and intercalated discs observed under electronic microscope were recorded before and after surgery in each group. RESULTS: In IP group, one case (4.55%) of ventricular arrhythmia (sporadic ventricular premature beat), 11 cases (50.00%) of supraventricular arrhythmia (atrial fibrillation, atrial flutter, supraventricular tachycardia, atrioventricular block) and 10 cases (45.50%) of ischemic ST-T changes were observed. In control group, there were 14 cases (43.75%) of ventricular arrhythmia (ventricular premature beat, tachycardia), 18 cases (56.25%) of supraventricular tachycardia and 28 cases (87.50%) of ischemic ST-T changes. No statistical difference in preoperative positive unit of Cx43 expression between the two groups was found (P>0.05). Postoperatively, the positive unit of Cx43 expression in IP group was 16.15±4.40, but the difference was not significant compared to the preoperative value (P>0.05). In control group, Cx43 expression was 11.92±1.26, significantly lower than that of the preoperative value (P<0.05). Cx43 expression between the two postoperative groups showed a significant difference (P<0.05). In control group, electronic microscopic observation revealed disrupted intercalated discs, with some partially or even totally ruptured and disintegrated. Enormous necrotic structural changes of myocardial fibers were also observed, including swelling, dissolution and disorganization of myofilaments and fibers, widening of the Z striae and disorganization. However in IP group, the intercalated discs appeared intact, continuous with normal myocardial structure. CONCLUSION: IP maintains normal expression of the myocardial junctional gap protein Cx43, which preserves a seamless intercellular gap junction and a normal myocardial electric conduction activity.  相似文献   

19.
AIM: To determine the effects of different-term streptozotocin(STZ)-induced diabetes on ischemia/reperfusion (I/R) injury and cell apoptosis in rats myocardial via alterations in myocardial peroxynitrite.METHODS: The models of I/R injury were induced by occlusion and reperfusion of the left descending coronary artery (LDCA) in rats.I/R-induced infarct size was determined using triphenyltetrazolium chloride (TTC) staining.Quantified caspase-3 expression was used to represent apoptosis by Western blotting analysis.Peroxynitrite formation as indicated by nitrotyrosine level was measured by morphometric analysis.RESULTS: Two weeks after STZ treatment,infarct size (35.00%±3.00%) was smaller in 2 weeks diabetic hearts (2WKD) as compared with time-matched control group (2WKC) (51.00%±3.30%),whereas after 16 weeks of diabetes (16WKD),the infarct size (61.00%±3.00%) was bigger in the diabetic hearts as compared with the 16WKC group (50.00%±2.00%,P<0.05).After I/R,caspase-3 expression was lower in 2WKD+I/R group (A value：481±77) than that in 2WKC+I/R group (A value：1033±46),while caspase-3 was higher in the 16WKD+I/R group (A value：1206±78) than that in 16WKC+I/R group (A value：940±72,P<0.05).Nitrotyrosine was lower in 2WKD hearts (A value：211±13) than that in controls (A value：409±12),but was higher in 16WKD group (A value：506±37) compared with controls (A value：378±46,P<0.05).CONCLUSION: Short- and long-term STZ induced diabetes exerts opposite influences on myocardial I/R injury and cell apoptosis,and these contradictory influences may depend on different alterations in myocardial peroxynitrite.  相似文献   

20.
AIM：To investigate the protective effect of β-asarone against hypoxia/hypoglycemia and reperfusion injury in primary rat hippocampal neurons. METHODS：Cell viability, the activity of caspase-3, the protein expression of p-JNK and Bcl-2, and the mRNA expression of Bcl-2 and caspase-3 were determined by MTT assay, spectrophoto-metry, Western blotting and real-time PCR. RESULTS：Compared with normal control group, the cell viability decreased and the activity of caspase-3 increased obviously, the expression of p-JNK protein and caspase-3 mRNA increased obviously, and the expression of Bcl-2 protein decreased obviously in model group (P<0.05). Compared with model group, different doses of β-asarone inhibited the changes of the above indexes (P<0.05). CONCLUSION：β-asarone inhibits JNK-mediated chondrosome signaling pathway, thereby attenuating the process of hippocampal neuron apoptosis after hypoxia/hypoglycemia and reperfusion.  相似文献   

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