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1.
AIM: To study the change of myocardial ceramide during myocardial ischemia/reperfusion and the relationship between ceramide and apoptosis and oxidative stress. METHODS: After inducing myocardial ischemia/reperfusion (I/R) injury in mice with pituitrin (Pit), myocardial SOD activity and MDA content were measured. DNA agarose gel electrophoresis and fluorescent staining of DAPI were done to check up apoptosis. The content of myocardial ceramide (μg/kg) was measured through HPTLC and scan of thin plate. RESULTS: The myocardium of I/R model group had the phenomenon of DNA ladder. Apoptosis index and ceramide content in I/R model group were higher than those in normal control group (P<0.01). SOD activity in I/R modal group was lower than that in normal control group (P<0.01). The apoptosis index and ceramide content in I/R model group were positive correlative (r=0.970，P<0.01). The myocardial content of ceramide and MDA were positively correlative too (r=0.974, P<0.01). CONCLUSION: The results indicate that there are apoptosis, oxidative stress and increase in ceramide content in ischemia/reperfusion myocardium.  相似文献   

2.
AIM: To investigate the expression of calcium sensing receptor(CaSR) during myocardial injury induced by ischemia/reperfusion and disclose the relationship between CaSR and myocardial ischemia/reperfusion. METHODS: The experimental model was established by the 30 min ligating and 1 h, 2 h, 4 h, 6 h reperfusing the left descending coronary artery (LAD) in rats. Wistar rats were randomly divided into 5 groups: sham group, ischemia/reperfusion 1 h, 2 h, 4 h, 6 h groups (I/R 1 h, 2 h, 4 h, 6 h group). CaSR mRNA expression was detected by RT-PCR. Left ventricular function was recorded. The levels of plasma lactate dehydrogenase (LDH), alondialdehyde (MDA) and superoxide dismutase (SOD) were measured. The change of ultrastructure in the ischemia/reperfusion myocardium of rats was observed by electron microscopy. RESULTS: LVSP,±dp/dtmax and SOD activity decreased gradually with the reperfusion time prolonged. LDH and MDA peaked at 2 h. The ultramicro-structural injury at the 1 h and 2 h was more serious than that at 4 h and 6 h. The expression of CaSR increased significantly after reperfusion of 1 h and 2 h, and decreased after 4 h and 6 h. CONCLUSION: The increased expression of CaSR mRNA and serious injure of myocardium were observed. CaSR may be associated with the myocardial ischemia/reperfusion injury.  相似文献   

3.
AIM: To investigate the effect of dexamethasone (DEX) preconditioning on reperfusion arrhythmia. METHODS: 46 Sprague-Dawley rats were divided randomly into DEX and control (CON) group, the rats were pretreated with DEX or sodium chloride before their hearts were separated for Langendorff perfusion and for ischemia/reperfusion. The reperfusion arrhythmias were observed dynamically after 60 min reperfusion following 30 min ischemia. The expression of HSP72 in myocardium was examined by Western blotting and immunohistochemistry at reperfusion 60 min. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) and the activities of Na+-K+-ATP ase, Ca2+-Mg2+-ATPase on myocardial plasma membrane were detected. RESULTS: Compared with control group, the accumulated points and persistence time of ventricular arrhythmia were reduced significantly in DEX group (P<0.05), the expression of HSP72 was significant upregulated (P<0.05), the level of MDA was reduced significantly, the activities of SOD, CAT, GSH-Px and Na+-K+-ATPase were significantly higher (P<0.05). CONCLUSION: Dexamethasone pretreatment markedly reduces the reperfusion ventricular arrhythmias in rats, which may be attributed to upregulation of HSP72, SOD, CAT, GSH-Px , Na+-K+-ATPase and inhibition of lipid peroxidation.  相似文献   

4.
AIM: To explore the protective effect of riboflavin preconditioning on hepatic ischemia/reperfusion injury in rats. METHODS: Twenty-four Sprague-Dawley rats wererandomly divided into 3 groups (n=8): sham group, ischemia/reperfusion (I/R) group and riboflavin preconditioning (R+I/R) group. The rats in sham group and I/R group received a standard chow,while the rats in R+I/R group received a chow supplemented with riboflavin. After 4 weeks, portal vein and hepatic artery supplying the middle and left hepatic lobes were clamped with a traumatic vascular clip for induction of partial hepatic ischemia in the rats in I/R group and R+I/R group. After 1 h of ischemia, 1 h of reperfusion was conducted by removal of the clip. The activity of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) in serum,the activity of superoxide dismutase (SOD) and the level of malondialdehyde (MDA) in serum and liver were measured. Western blotting was employed to examine the protein expression of heme oxygenase-1(HO-1) in the liver. RESULTS: The results showed that ischemia/reperfusion injury markedly increased the activity of AST and ALT in serum, decreased the activity of SOD, and elevated the level of MDA and the activity of HO-1 in the liver as compared with sham group (P<0.01). The riboflavin pretreatment significantly decreased the activity of AST and ALT in serum, increased the activity of SOD and decreased the levels of MDA in serum and liver as compared with I/R group (P<0.01). In addition, the protein expression of HO-1 and the activity of HO-1 were elevated in R+I/R group (P<0.01). Cytoplasmic vacuolation and swelling of the hepatocytes were observed in I/R group. Treatment with riboflavin markedly alleviated the changes of liver structure. CONCLUSION: Riboflavin preconditioning has protective effect on hepatic ischemia/reperfusion injury. The mechanism may be correlated with enhancing the anti-oxidation and alleviating the reaction of lipid peroxidation.  相似文献   

5.
AIM: To observe the effect of exogenous spermine (low concentration) on myocardial ischemia/reperfusion injury in rats.METHODS: 40 Wistar rats were randomly divided into 4 groups: sham- operation group (Sham), ischemic reperfusion group (I/R), spermine group (Sp) and natural saline group (NS). The model of ischemic/reperfusion injury was established by ligating rat coronary artery. In Sp group, spermine (0.5 mmol/L, 2 mL/kg) was injected slowly into rat vein. During the process, we recorded the electrocardiogram and the LV functional parameters, assayed the levels of SOD, LDH, NO and MDA in serum, and examined the ultrastructure of the myocardium. RESULTS: In I/R group, the incidence of arrhythmia was 90%, myocardial ultrastructure was injured seriously, values of LVSP and ±dp/dtmax decreased, levels of LDH, NO and MDA increased while SOD activity decreased (P<0.05 or P<0.01, compared with Sham group). Compared with I/R and NS group, all those indexes in Sp group changed significantly (P<0.05 or P<0.01). CONCLUSION: Exogenous spermine alleviates myocardial ischemia/ reperfusion injury in rats. The mechanism may be related to its antioxidant effect and relieving the injury caused by oxygen free radical.  相似文献   

6.
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   

7.
AIM: To study the effects and the possible mechanisms of exogenous spermine on the rats with acute transient focal cerebral ischemia/reperfusion (I/R) injury.METHODS: The rat model of focal cerebral ischemia/reperfusion was established by middle cerebral artery occlusion (2 h) and reperfusion (2 h). Healthy adult SD rats were divided into 5 groups;sham group,I/R group and spermine(4,20 and 40 mmol/L)groups.The degree of cerebral injury was evaluated by neurological deficit score, infracted volume, superoxide dismutase (SOD) activity and malondialdehyde (MDA) content. The morphological changes of the brain were observed by HE staining and electron microscopy. RESULTS: Compared with I/R group, the neurological deficit score, infracted volume and the content of MDA were decreased, the SOD activity was increased and the ultrastructural changes were improved in spermine-treated groups. CONCLUSION: Exogenous spermine has a protective effect against acute focal cerebral ischemia/reperfusion injury. The mechanisms may be related to scavenging free radical by spermine.  相似文献   

8.
AIM: To investigate the protective effects and mechanism of tacrolimus on renal ischemia/reperfusion(I/R) injury in rats.METHODS: Sixty male Wistar rats were randomly divided into 3 groups: sham-operated group, I/R group and tacrolimus group. After the renal I/R injury model was established, the serum content of creatinine(Cr), tumor necrosis factor-α(TNF-α)and malondialdehyde(MDA) and activity of superoxide dismutase(SOD) were measured at reperfusion time points of 0.5 h, 2 h, 6 h and 24 h. The renal histopathological lesions and the expression of Fas and caspase-3 were observed by the methods of microscopy and immunohistochemistry, respectively.RESULTS: At all the 4 time points, the levels of Cr, TNF-α and MDA in tacrolimus group were lower than those in I/R group(P<0.05). The SOD activity in tacrolimus group was higher than that in I/R group. Compared with I/R group, the renal histopathological lesions were improved, and the levels of Fas and caspase-3 were significantly decreased in tacrolimus group(P<0. 05).CONCLUSION: Tacrolimus inhibits the production of free radical, the expression of TNF-α and apoptosis of renal tubular epithelial cells in renal I/R injury in rats, indicating that tacrolimus has protective function against renal I/R injury.  相似文献   

9.
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   

10.
AIM: To investigate the protective effect of recombinant SCR15-18 domain of human complement receptor type 1 (CR1-SCR-15-18) on intestinal ischemia and reperfusion in a rat model. METHODS: Sprague-Dawley rats were randomly divided into 3 groups: sham operation(SO) group, ischemia and reperfusion (I/R) group and CR1-SCR15-18 treatment group. The superior mesenteric artery of the rats was clamped for 30 min followed by 60 min of reperfusion. PBS alone or CR1-SCR15-18 protein (30 mg/kg) in PBS was intravenously administered 5 min before reperfusion. Intestinal vascular permeability, myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD) were measured. The histopathological changes of intestinal mucosa were examined by HE staining and complement 3 was detected by immunohistochemical analysis. RESULTS: Compared with SO group, the vascular permeability, the activity of MPO and the content of MDA in I/R group were significantly increased, and the activity of SOD was decreased. HE staining demonstrated that I/R induced severe intestinal histological damages and the increased amount of complement 3 and its derivates were deposited in the necrosis area. Compared with I/R group, the vascular permeability, the activity of MPO and the content of MDA were decreased and the activity of SOD was significantly increased in CR1-SCR15-18 treatment group. CR1-SCR15-18 also significantly attenuated intestinal histological injury, and reduced the deposition of complement 3 and its derivates in the necrosis zone. CONCLUSION: sCR1-SCR15-18 protein exerts a protective effect against intestinal I/R injury in rats, possibly by inhibiting the activation of complement.  相似文献   

11.
AIM:To observe the protective effect of non-wounded ischemic preconditioning on ischemic/reperfusion injury in isolated rat hearts. METHODS: 25 male SD rats, weighting (250±30) g, were randomly divided into three groups: control group (C,n=8), anoxia/reoxygenation group (A,n=8) and non-wounded legs ischemic preconditioning group (N-WIP,n=9).Hearts were isolated from rats and perfused on a Langendorff apparatus with a normal Krebs-Henseleit buffer (saturation 95% O2+5% CO2) at a constant pressure (8.33 kPa) and temperature (37 ℃) in C group; Following 15 min equilibration, hearts were subjected to 15 min of global ischemia and 15 min reperfusion (37℃) in A group; Rats were subjected to non-wounded leg repeated-brief ischemic preconditioning, and then treated in procedure similar to A group in N-WIP group.The activities of superoxide dismutase (SOD) and Ca2+-Mg2+-ATPase, malondialdehyde (MDA) content of efflux from coronary vessel and myocardium, myocardium monophasic action potential and contractile force were measured before ischemia, 15 minutes after ischemia and 5, 15 minutes after reperfusion. RESULTS:Compared with A group, non-wounded legs ischemic preconditioning reduced the incidence of reperfusion arrhythmias (P＜0.05), decreased the content of MDA of myocardium (P＜0.01), enhanced the activities of SOD (P＜0.01) and stabilized myocardial membranous potential,the activity of Ca2+-Mg2+-ATPase and contractile function. CONCLUSION:These results indicate that non-wounded leg ischemic preconditioning has a protective effect on ischemia-reperfusion injury in isolated rat hearts. The mechanism may be related to the strength of antioxidation, the stability of Ca2+-Mg2+-ATPase activity and membranous structure in myocardium.  相似文献   

12.
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13.
AIM:To study the impacts of the myocardial connexin 43 degradation on conduction velocity during acute myocardial ischemia.METHODS: Studies were carried out in 16 dogs which were randomly divided into control group(n=4) and ischemia group(n=12). The acute myocardial ischemia was induced by ligation of the left anterior descending coronary artery. The conduction velocity of ischemic myocardium was determined. The content of Cx43 of the ischemic myocardium was examined by laser confocal microscopy with a double-label immunohistochemistry technique. RESULTS:(1)The Cx43 degraded rapidly during acute myocardial ischemia, and the conduction velocity of ischemic myocardium declined greatly; (2)The conduction velocity correlated positively with the Cx43 pixel density in each small region of ischemic myocardium; (3) The Cx43 pixel density decreased over 50% in the region which occuring permanent conduction block.CONCLUSION: These data suggest the degradation of Cx43 decreases the conduction velocity greatly during acute short time myocardial ischemia, and severe degradation of Cx43 would lead to permanent conduction block.  相似文献   

14.
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   

15.
AIM: To investigate the effect and mechanism of liver ischemia/reperfusion (I/R) injury on the changes of cardiac energy metabolism and structure.METHODS: 48 healthy Wistar male rats were randomly divided into 6 groups as follows (n=8 in each group): control group (CTL), simply ischemia for 30 min without reperfusion(I group); reperfusion following ischemia for 30 min (I/R group); 2 h reperfusion following ischemia for 30 min (I/R 2 h group); 4 h reperfusion following ischemia for 30 min (I/R 4 h group) and 6 h reperfusion following ischemia for 30 min (I/R 6 h group). The level of serum endotoxin was measured. The levels of insulin and insulin antibody in heart were detected by radioimmunoassay. The contents of MDA, MPO and lactic acid in heart were also determined. RESULTS: During the process of liver I/R injury, the level of endotoxin increased in I group and I/R group and declined gradually for long time during reperfusion, but was still longer than that in CTL group (P<0.05). The level of MDA obviously increased in I group and in all reperfusion groups compared to CTL (P<0.05). The obvious significant differences among I/R 2 h group, I/R 4 h group, I/R 6 h group with CTL were observed (P<0.05). The activities of MPO obviously increased in all reperfusion groups, there was also an obvious significant difference compared with CTL and I group (P<0.05). The level of lactic acid obviously increased with prolongation in reperfusion (P<0.05), but decreased in I/R 6 h group (P<0.05). The level of insulin decreased in I/R 4 h group and I/R 6 h group (P<0.05). No difference of insulin antibody was observed among all groups (P>0.05). CONCLUSION: During the process of liver I/R injury, endotoxin is absorbed from intestine and impairment of liver detoxication leads to endotoxemia, which might play a role in the changes of the energy metabolism and structure in heart.  相似文献   

16.
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17.
AIM: To investigate the effect of diazoxide (D) postconditioning on Cardiac function and mitochondrial cardiolipin in isolated rat heart and to explore the protective effect of ATP sensitive potassium channel on diazo-xide postconditioning myocardium. METHODS: The myocardial ischemia/reperfusion injury model in isolated rat hearts was established by Langendorff apparatus. The isolated rat hearts were randomized into 4 groups (n=8): control group (control), myocardial ischemia/reperfusion injury group (I/R), diazoxide postconditioning group (I/R+D), 5- hydroxy decanoic acid (5-HD) plus diazoxide postconditioning group (I/R+5-HD+D). The hearts in each group were started with 20 min perfusion for equilibration. The hearts in control group perfused for 70 min; The hearts in I/R group was global ischemia for 40 min after ischemia reperfusion at 4 ℃ ST. Thomas cardioplegia, then reperfusion for 30 min; The hearts in I/R+D group were treated with diazoxide (50 μmol/L) in K-H perfusion for 5 min after global ischemia for 40 min, then reperfusion for 25 min; The hearts in I/R+5-HD+D group were treated with 5-HD (100 μmol/L) in K-H perfusion for 5 min before diazoxide postconditioning, then reperfusion for 20 min. The heart rate, coronary outflow volume, heart function, myocardial enzymes and myocardial mitochondrial cardiolipin at the end of perfusion in each group were determined. RESULTS: Compared with control group and I/R+D group, the heart rate, the concentration of heart phospholipid and the coronary outflow volume were reduced, the heart function was significantly impaired the contents of myocardial enzymes were increased in I/R group. However, no significant difference between I/R group and I/R+5-HD+D group was observed. CONCLUSION: The diazoxide postconditioning protects the myocardium by increasing mitochondrial cardiolipin content, reducing the release of myocardial enzymes, improving heart function and reducing myocardial reperfusion injury. The myocardial protective effect of diazoxide is completely blocked by 5- hydroxy decanoic acid.  相似文献   

18.
AIM: To investigate the mechanisms underlying the protective effect of kidney ischemic preconditioning on rabbit myocardium in case of ischemia-reperfusion and the possible role of oxygen free radicals in the process. METHODS: Animals were divided into four groups: ischemia/reperfusion(I/R), classical ischemic preconditioning(CIPC), kidney ischemic preconditioning (KIPC) and superoxide dismutase in combination with kidney ischemic preconditioning(SOD+KIPC). The endo genous myocardial pretective material, nitric oxide(NO) and 5'-nucleotidase(5'-NT) were checked in four groups. RESULTS: As compared with I/R group, both CIPC and KIPC could ameliorate left ventricular function, reduce plasma PLA2 activity and arrhythogenic rate also, the myocardial 5'-NT and NO production were significantly higher than that of the rabbit of I/R group. However, the protective effect on rabbit myocardium was significantly weakened by the SOD administration before the ischemic preconditioning. CONCLUSION: Protective effect of KIPC on myocardium may be due to increase in endo genous myocardial protective materials, oxygen free radicals may play an important role in the endo genous myocardial protective material release.  相似文献   

19.
AIM: To investigate the effects of human urotensin II (hUII) on ischemia/reperfusion (I/R) injury in isolated rat hearts. METHODS: In the ischemia/reperfusion (I/R) model of isolated perfused rat hearts, the effects of hUII pretreatment on cardiac function was monitored with cardiac function software of MFL Lab200. ATP, total calcium, and malondialdehyde (MDA) content in myocardium were detected. The coronary perfusion flow (CPF) and lactate dehydrogenase (LDH) activity in coronary effluent were measured during reperfusion. RESULTS: In the hUII pretreated group, the release of LDH from myocardium was lower [(78.3±18.1)U/L] than I/R group [(109.3±23.9) U/L, P< 0.05], with decreased contents of MDA and calcium in myocardium (decreased by 24% and 27%, respectively, P< 0.05) and an increased myocardial ATP content [(3.8±0.4)μmol/g dw vs (2.2±0.4)μmol/g dw, P< 0.05)]. At the same time, hUII pretreatment increased CPF [(5.4±0.7) mL/min vs (3.8±0.8) mL/min in I/R group, P< 0.05], reduced left ventricular end-diastolic pressure (LVEDP) by 20% ( P< 0.05) with increased±d p /d t max [(217±38) kPa/s and (119±18) kPa/s vs (173±29) kPa/s and (82±25) kPa/s in I/R groups, respectively, P< 0.05]. hUII pretreatment also increased natrite/natrate (NO2-/NO3-) content in coronary effluent [(52.2±12.0)μmol/L vs (32.1±10.2)μmol/L in I/R group, P< 0.05)]. CONCLUSION: hUII pretreatment attenuated I/R injury in isolated perfused rat hearts. The protective mechanism might be associated with NO-mediated coronary vasodilation.  相似文献   

20.
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   

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