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Objective To explore the effect of sufentanil postconditioning on the focal cerebral is-chemia reperfusion injury in diabetic rats. Methods An intraperitoneal injection of 50 mg/kg streptozotocin was used to induce diabetes in rats. Meanwhile,the diabetes mellitus model was confirmed by the blood glu-cose level over 16. 7 mmol/L. The diabetes mellitus male SD rats,weighting 250-300 g,were randomly divid-ed into 3 groups:sufentanil postconditioning diabetic group (SP-DM),ischemia reperfusion diabetic group (IR-DM),sham operation diabetic group(sham-DM),with 12 in each group. The non-diabetic rats were randomly divided into 3 groups:sufentanil postconditioning non-diabetic group(SP-NDM), ischemia reperfu-sion non-diabetic group(IR-NDM),sham operation non-diabetic group(sham-NDM),with 12 in each group. All rats in the IR-NDM/DM group and SP-NDM/DM group were exposed to the right middle cerebral artery occlusion for 90 minutes followed by 24 hours reperfusion. The sufentanil 1 μg/kg were injected into the rats in SP-NDM/DM group via tail vein at 5 minutes before reperfusion. Normal saline was injected into the rats in sham-NDM/DM group and IR-NDM/DM group at 5 minutes before reperfusion. At 24 hours after reperfu- sion,the neurological deficit scores( NDS) were assessed,then all the rats were sacrificed. Infarct volume, which was determined by 2,3,5-triph-enyltetrazolium ( TTC) staining,and water content of right hemisphere for brain edema were also measured. Results All rats showed neurological deficit,brain infarction and brain edema after focal cerebral ischemia reperfusion. (1) At 24 hours after reperfusion,the neurological deficit score in IR-DM group(3. 4±0. 4) was significantly higher than that in the IR-NDM group(2. 8± 0. 5) ( t=2. 313,P<0. 05),there was no significant difference in neurological deficit score between the SP-DM group (3. 3±0. 4) and the IR-DM group(t=1. 546,P>0. 05). (2) At 24 hours after reperfusion,the infarct volume in IR-DM group((58. 3±2. 1)%) was significantly higher than that in the IR-NDM group((32. 1±2. 6)%) (t=2. 912, P<0. 05), there was no significant difference in infarct volume between the SP-DM group ((56. 9±2. 1)%) and the IR-DM group(( 58. 3 ± 2. 1)%) ( t=1. 633,P>0. 05). ( 3) At 24 hours after reperfusion,the water content of the right hemisphere in IR-DM group(( 89. 3± 3. 5)%) was significantly higher than that in the IR-NDM group((82. 6±3. 9)%)(t=2. 218,P<0. 05),there was no significant differ-ence in water content of the right hemisphere between the SP-DM group(( 87. 5±3. 4)%) and the IR-DM group(t=1. 730,P>0. 05). Conclusion Sufentanil postconditioning loses neuroprotection against focal cer-ebral ischemia reperfusion injury in diabetic rats.
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Aim To investigate the protective effects and mechanism of aspirin against focal cerebral ischemia-reperfusion in rats. Methods Right middle cerebral artery was occluded by inserting a thread through internal carotid artery for 2 h, and then reperfused for 72 h. 60 mg?kg -1 dose of aspirin was intragastric administrated at 0 h and 6 h after reperfusion. The brain injured area, the mortality, and cerebral edema were estimated. The apoptotic cells of brain tissue were detected by terminal deoxynucleotidyl transferase mediated dUTP-biotin nick-end labeling (TUNEL) method. Bcl-2 and Bax were detected by immunohistochemical staining method. The activity of calcineurin (CaN) in brain tissue was determined by the inorganic phosphorus method. The content of adenosine 5′-triphosphate (ATP) in brain tissue was separated by capillary electrophoresis. Results By using of aspirin 60 mg?kg -1, all indications were dramatically improved. The injured area of brain [from (10.51?1.12)% to (0.94?0.08)%], the cerebral edema of occluded side [from (82.43?2.0)% to (76.29?0.77)%], and the mortality [from 28% to 0%] were dramatically reduced. In brain tissue of occluded side, 60 mg?kg -1 aspirin helped to reduce the number of apoptotic cells from (26.43?2.0) to (17.53?0.44), increase the ratio of Bcl-2/Bax from (0.61?0.05) to (1.01?0.15), inhibit the activity of CaN from (6.03?1.5) to (3.47?0.96), and improve the ATP level from (10.26?1.02) to (25.65?3.45). Conclusion The neuroprotective effects of aspirin on focal cerebral ischemia-reperfusion injury in rats for 72 h might be attributed to its effects by anti-apoptosis, increasing the ratio of Bcl-2/Bax, inhibiting the activity of CaN, and improving the energy metabolism.
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Aim To investigate the protective effect of zileuton,a 5-lipoxygenase inhibitor,on focal cerebral ischemia-reperfusion injury in rats.Methods The right middle cerebral artery of the rat was occluded by inserting a thread through internal carotid artery for 2 h,and then reperfused for 24 h.Zileuton(10,50 mg?kg~(-1)) was orally administered 2 h before ischemia and 0,5,10 h after reperfusion.After 24 h reperfusion,the content of malondialdehyde(MDA) and nitric oxide(NO),the activities of glutathion peroxidase(GSH-PX),myeloperoxidase(MPO) and nitricoxide synthase(NOS) were measured.Results Compared with vehicle group,the infarct size,content of NO and NOS of the brain were significantly reduced in 10 and 50 mg?kg~(-1) zileuton groups;zileuton 50 mg?kg~(-1) also reduced the content of MDA,increased the activity of GSH-PX,and inhibited the increase of MPO in brain tissue.Conclusion Zileuton possesses the neuroprotective effects on focal cerebral ischemia-reperfusion injury in rats.