Résumé
Aim To explore the mechanism of Buyang huanwu decoction attenuating cerebral ischemia-reper- fusion injury in rats by regulating autophagv through AMPK/mTOR/ULKl signaling pathway.Methods Left eerebral ischemia model in rats was established by modified thread ocelusion method, then the rats in each group were given medieine onee every 24 hours for 3 times.After 72 hours of reperfusion, the nerve injury and the changes of cerebral infarction volume were observed; the morphology, number and apoptosis of nerve cells were observed by Nissl staining and TUNEL staining; the expression of autophagy protein and AMPK/mTOR/LJLKl autophagy signaling pathway related proteins were detected by Western blot.Results Buyang huanwu decoction could improve the neurological deficit of rats, reduce the volume of cere bral infarction and neuronal apoptosis, reduce the pathological injury of brain tissues, inhibit the phosphorylation activation of AMPK, relieve the inhibition of AMPK on downstream mTOR and LJLK1 , promote the phosphorylation activation of both, and inhibit autophagy.AMPK agonist metformin increased the level of autophagy and reversed the protective effect of Buyang huanwu decoction on cerebral ischemia-reperfusion injury in rats.Conclusion Buyang huanwu decoction mediates AMPK/mTOR/ULKl autophagy signaling pathway to play a neuroprotective effect on cerebral is- chemia-reperfusion injury in rats.
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Objective To quantitatively evaluate the diagnostic value of blood oxygen leveldependent (BOLD) MRI in the diagnosis of different degrees of liver warm ischemia-reperfusion injury (WIRI) in rabbits and evaluate the intervention effect of liposomal prostaglandin E1 (Lipo-PGE1).Methods Seventy healthy adult New Zealand white rabbits were randomly divided into sham -operated group (A0),thermal ischemic groups (A1～A3) and intervention groups (A4～A6).All experimental rabbits were scanned by routine MR and BOLD MRI after 6-hour reperfusion.R2* images were calculated by two radiologists.The levels of alanine aminotransferase (ALT),asparate aminotransferase (AST) and lactate dehydrogenase (LDH) were examined.And liver pathological sectioning was performed.All data were processed by one-way,Spearman's correlation and receiver operating characteristic curve analyses.Results The intraclass correlation coefficient (ICC) was 0.805 of two measurements suggesting that the repeatability of the outcome was decent.R2* values among sham-operated,thermal ischemia and intervention groups were statistically significant (P＜0.05).R2 * values in sham-operated and ischemia groups were statistically significant (P＜0.05).As warm ischemia time elapsed,R2* value showed a rising trend.R2* values in sham-operated and intervention groups were statistically significant (P＜0.05).R2* values of sham-operated group at the same timepoint of thermal ischemia and intervention groups were statistically significant (P＜0.05).Under the same ischemic time,R2* values of intervention groups were smaller than those of thermal ischemia groups.With the prolongation of ischemia time,reduction of R2* values became more pronounced.However,it did not reach the level of A0 group.R2* values were significantly positively correlated with ALT,AST and LDH (r＞0.5,P＜0.05).ROC analysis indicated that R2* had an excellent diagnostic performance.Conclusions BOLD MRI may be applied for noninvasive assessment of liver ischemia-reperfusion injury in different degrees.Lipo-PGE1 alleviates ischemia -reperfusion injury and BOLD MRI can evaluate the relieving degree of Lipo-PGE1.
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Aim To investigate the effect of isocorydine on arrhythmia in rats induced by myocardial ischemia/reperfusion injury. Methods SD rats were randomly divided into 6 groups: sham group, myocardial ische-mia/reperfusion group, verapamil group and isoc-orydine group of 2. 5 , 5 , 10 mg · kg-1 , each group having 16 rats. Left anterior descending ( LAD ) was tied up to establish the injury model of myocardial is-chemia. ECG was recorded for analysis. The ischemic and infarction area was measured and indexes of SOD, MDA, GSH-Px in the myocardial were determined. Re-sults Isocorydine could significantly reduce the inci-dence of arrhythmia induced by ischemic/reperfusion, including VT, VF;and reduce ischemic and infarction area. Further study demonstrated that isocorydine could increase myocardial SOD and GSH-Px, but de-crease myocardial MDA. Conclusion Isocorydine has a protective effect on the myocardial ischemia/reperfu-sion injury, which might be related to its anti-oxidative function.
Résumé
Aim To study the effect of adiponectin ( APN) on myocardial ischemia reperfusion( IR) injury in diabetic rats and to explore the role of oxidation-an-tioxidation system. Methods Male Sprague Dawley rats were randomly divided into control group( NS) , IR group ( NIR ) , diabetes group ( DS ) , DS + IR group (DIR), DS +APN +IR group(APN). Experimental diabetes was induced in the animals by a single intrap-eritoneal injection of streptozotocin at a dose of 55 mg ·kg-1 . The IR and NIR group were subjected to myo-cardial I/R injury. APN group was administered APN through intravenous injection 10 min before the reper-fusion, the others were administered normal saline. The rats were considered diabetic and used for the study only if their glucose levels were higher than 15 mmol·L-1. Results All the diabetic rats exhibited increased levels of blood glucose and reduction of body weight ( P <0. 05 ) . Compared with those of NS and DS groups, the myocardial infarct size, cardiomyocyte apoptosis, MDA concentration and ROS in NIR and DIR groups were remarkably increased, activities of SOD and NO were decreased(P<0. 05 or P<0. 01). APN decreased oxidative stress product generation and myocardial apoptosis induced by diabetic myocardial I/R injury ( P <0. 05 ) . Conclusion APN exerts pro-tective effect on myocardial I/R injury in diabetic rats through anti-oxidative mechanism.