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AIM:To observe the effects of edaravone on high glucose-induced apoptosis of SH-SY5Y cells and its potential mechanism .METHODS:The SH-SY5Y cells were cultured in the DMEM medium with 100 mmol/L glucose and 100μmol/L edaravone for 24 h.The viability of the SH-SY5Y cells was detected by MTT assay .The levels of ROS in the cells were determined by DCFH-DA fluorescent probing .The apoptotic rates of the cells were analyzed by flow cytome-try.The protein expression of Bax and Bcl-2 in the cells were detected by Western blot .The expression levels of micro-RNA-25 (miR-25) were determined by real-time PCR.To further clarify the target sites of edaravone on inhibiting apopto-sis induced by high glucose , miR-25 inhibitor was applied to the SH-SY5Y cells and the activity of caspase-3 was meas-ured.RESULTS:Compared with control group , the cell viability was decreased significantly in model group , and the ROS level was increased significantly .The protein expression of Bax was up-regulated significantly , while the expression levels of Bcl-2 and miR-25 were significantly down-regulated .Compared with model group , the cell viability was increased signifi-cantly in edaravone group .The ROS level was decreased significantly .Meanwhile, the expression of Bax was down-regula-ted, while the expression of Bcl-2 and miR-25 was up-regulated with statistical significance .The caspase-3 activity of the cells incubated with 100 mmol/L glucose and miR-25 inhibitor was increased .However, no alteration of caspase-3 activity with edaravone added simultaneously was observed .CONCLUSION: Edaravone inhibits the apoptosis of SH-SY5Y cells induced by high glucose with the potential target site of miR-25.
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OBJECTIVE:To study the effect of Shenkang injection on the irbesartan pharmacokinetics in rats in vivo. METH-ODS:18 SD rats were randomly divided into control group(normal saline)and Shenkang injection(calculated by crude drug as 4 g/kg),9 in each group,which were intraperitoneally injected twice a day,for 7 d. After 1 h of last administration,25 mg/kg irbe-sartan was intragastrically administrated. 0.3 mL sample blood was taken in fundus venous plexus before administration of irbesartan and after 0.25,0.5,1,2,4,8,12,24,32,48,56,72,96 h of administration. Using biphenyl diester as inner standard,HPLC was adopted to determine the plasma concentration of irbesartan in plasma of rats,and pharmacokinetic parameters were calculated by using non-compartmental model in Phoenix WinNolin? 6.1 pharmacokinetic software. RESULTS:After intragastrically adminis-trated irbesartan in rats in control group and Shenkang injection group,AUC0-96 h were (28.82 ± 10.49),(35.64 ± 9.99) mg·h/L;cmax were(0.64±0.15),(0.76±0.33)mg/L;tmax were(13.07±16.70),(10.23±3.97)h;CLZ/F were(0.85±0.35),(0.63±0.21) L/(h·kg);VZ/F were (38.24 ± 24.87),(30.99 ± 9.75) mL/kg respectively,with no statistical significances (P>0.05). CONCLU-SIONS:Shenkang injection will not affect the in vivo pharmacokinetics process of irbesartan in normal dose on rats.
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Oxidative stress is one of the important pathological mechanisms of neuron damage in ischemic stroke.Antioxidant therapy has become one of the important measures for ischemic brain injury.This article reviews the advances in research on the antioxidant therapy of ischemic stroke.
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Objective To investigate the effect of cocaine-amphetamine-regulated transcript peptide (CART) on the content of 4-hydroxy-2-noneral (HNE) and infarct volume after cerebral ischemia/reperfusion in mice.Methods A total of 96 healthy male mice were randomly divided into four groups:ischemia/reperfusion (n =27),CART (n =27),normal saline control (n =27) and sham operation (n =15) groups.A middle cerebral artery occlusion (MCAO) model was induced.Two hours after MCAO,CART 55-102 and equivalent normal saline were injected respectively via the tail veins of mice in the CART group and the normal saline control group,and then they were injected every other 24 hour.The neurological scores,infarct volume and the HNE content of lipid metabolism of oxidative stress were performed and detected respectively at 12,24,48 and 72hours after reperfusion.Results CART could significantly improve the neurological deficit scores (all P ＜0.05) and reduce infarct volume (all P＜0.05) at different time points after ischemia/reperfusion.The content of HNE was upregulated (all P＜0.05) at different points after referfusion.CART could significantly down-regulate the increased HNE levd in brain after ischemia (all P＜0.05).Conclusions CART may protect ischemic brain injury in mice by inhibiting lipid peroxidation.