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Aim To investigate the effect of Salidroside on the focal celebral ischemia/reperfusion injury in rats and its underlying mechanism. Methods Adult male Sprague-Dawley rats, weighing 260-300 g, were ran-domly divided into three groups: sham, MCAO, MCAO+salidroside ( Sal ) groups. The rats were sub-jected to local celebral ischemia reperfusion with su- ture-occluded method. The rats of MCAO +Sal group were treated intraperitoneally with salidroside ( 50 mg ·kg-1 ) for 6 days. Neurological deficit testing was performed with Longa’ s Scale. The mRNA expressions of Neun,Nogo-A,and NgR were detected by RT-qPCR in ischemic brain. The protein expressions of Neun, NGF , BDNF , Nogo-A and NgR were determined by Western blot. Results Compared with MCAO group, salidroside significantly improved the neurological defi-cit,promoted the expressions of Bcl-2,Neun,NGF,BD-NF, and inhibited the expressions of Nogo-A, NgR. Conclusion Salidroside can reduce neurological defi-cit, increase the number of Nissl’ s Body and the ex-pression of Neun, and protect rats against focal cele- bral ischemia/reperfusion injury,which may be accom-plished by increasing the expressions of Bcl-2, NGF, BDNF, and inhibiting the expressions of Nogo-A, NgR.
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Aim To investigate the effects of baicalin on cognitive function in global cerebral ischemia reper-fusion rats, and the probable mechanism involved. Methods Sixty male Sprague-Dawley(SD) rats were randomly divided into Sham operation group ( S group) , global cerebral ischemia reperfusion group ( I/R group) , global cerebral ischemia reperfusion + ba-icalin treatment group ( I/RB group) , twenty in each. Model was induced via the bilateral occlusion of the common carotid arteries plus hemorrhagic hypotension. 12 h after reperfusion, rats in I/RB group were given baicalin (100 mg·kg-1 ) saline solution by intragas-tric administration twice per day for 7 days. Rats in S group and I/R group were given the corresponding dose of saline infusion at the same time. Morris water maze test was employed to detect spatial learning and memo-ry. BrdU immunohistochemistry was used to detect the proliferation of neural precursor cells ( NPCs ) in the brain. Expression of COX-2 in the brain tissue was measured by Western blot. Results Compared to I/R group, baicalin improved spatial learning and memory damage ( P nitive function in the rats with global cerebral ischemia reperfusion, which might be associated with its inhibi-tory effects on the expression of COX-2 , thereby in-creasing the proliferation of NPCs in the brain.
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AIM:To investigate the role of PI3K/Akt and JAK2/STAT3 pathways in the protection of sulfur dioxide (SO2) against limb ischemia/reperfusion (I/R)-induced acute lung injury (ALI) in rats.METHODS:ALI was induced by limb I/R in the SD rats.Na2 SO3 (0.54 mmol/kg, ip)/NaHSO3 (0.18 mmol/kg, ip) as SO2 donor was injec-ted at 20 min before reperfusion.The inhibitors of JAK2/STAT3 and PI3K/Akt pathways, Stattic (3 mg/kg, iv) and LY294002 (40 mg/kg, iv), respectively, were injected at 1 h before reperfusion.Peripheral blood and lung tissues were collected for determining the contents of the cytokines, the protein levels of the molecules related to the signaling pathways, apoptosis and histopathologic changes by ELISA, TUNEL and Western blot.RESULTS:Compared with control group, the content of MDA, the activity of MPO, lung coefficient, apoptotic index, cytokine expression, and the protein levels of p-Akt and p-STAT3 in I/R group all increased significantly, and administration of Na2 SO3/NaHSO3 attenuated the damage in the lung.Besides, the results of Western blot showed that the rat lung tissues expressed p-STAT3 protein and p-Akt pro-tein.After I/R, the protein levels of p-STAT3 and p-Akt were increased.After using Na2 SO3/NaHSO3 , p-Akt was in-creased, but p-STAT3 was decreased (P<0.05).CONCLUSION:Both JAK2/STAT3 and PI3K/Akt pathways are like-ly involved in the protective effect of SO2 against limb I/R-induced ALI in rats.The activation of JAK2/STAT3 signaling pathway increases I/R injury.Reversely, the activation of PI3K/Akt signaling pathway reduces I/R injury.Besides, JAK2/STAT3 and PI3K/Akt signaling pathways may have crosstalk during I/R-induced ALI and JAK2/STAT3 pathway may have an impact on the P13K/Akt pathway.
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AIM: To investigate the effects of fluvas-tatin on expression of intercellular adhesion molecule-1 after myocardial ischemia-reperfusion in rabbits with hyper-lipidemia. METHODS: 30 rabbits which were gastric perfusion administered intralipid were randomly divided into 3 groups ( n - 10 in each) : IR ( ischemia-reperfusion) group, S (sham-operation) group and F (fluvastatin 10 mg?kg-1 ) group. Electrocardiography and cardiac function were recorded during the experiment. At the end of reperfusion, ischemic area and infarct size were defined by Evans blue and triphenyltetrazolium chloride staining. The expression of ICAM-1 in myocardium was measuredby RT-PCR. RESULTS: After ischemia-reperfusion, the expression of ICAM-1 mRNA in myocardial and infarct size decreased and cardiac function significantly improved in F group compared with IR group. CONCLUSION: The increase of expression of ICAM-1 mRNA in myocardial may be one of the important factors in inducing myocardial ischemia-reperfusion injury. The myocardial protective mechanism of fluvastatin maybe attribute to its effect on decreasing the expression of ICAM-1 mRNA in myocardial .
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Aim To study the protective effects of Rhynchophyll a of total alkaloids ( RTA ) on cerebral ischemia/reperfusion injury and the possi ble mechanism of action. Methods The effects of RTA on decapit ated gasping model and model of middle cerebral artery ischemia 2 h/reperfusion 22 h were observed. The neurological scores, cerebral infarct volume and cerebr al water content after ischemia/reperfusion were observed in rats respectively. The activities of NOS and SOD and the content of MDA in rat's brain tissue were measured. Neuron apoptosis in ischemia penumbral area were detected by terminal depoxynucleotidyl transferase mediated dUTP-biotin nick end labeling ( TUNEL ) . Results The average gasping times in mice treated with RTA 50 , 75 mg?kg -1 was significantly prolonged. The cerebral infarct volume and cerebral water content in rats treated with RTA 40, 60 mg?kg -1 were sign ificantly decreased in ischemic rats. RTA 40, 60 mg?kg -1 increased the ac tivity of SOD ,and decreased the activity of NOS and the content of MDA in the i schemic brains of rats. The number of apoptotic neurons in ischemia penumbral ar ea of cerebral tissue of rats treated with RTA 40, 60 mg?kg -1 was signif icantly lower than that in control rats. Conclusions RTA has pr otective effect on cerebral ischemia/reperfusion injury; this may be related to inhibit the activity of NOS and lipoperoxidation, and increasing the activity of SOD and decreasing neuron apoptosis.
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By using the model of ischemia-reperfusion injury in the isolated working rat heart,the change of free amino acid concentrations in myocardium and the effect of taurine on the heart were investegated. It was found that concentrations of 17 free amino acids in myocardium, except Cys,decreased,and that 20mM taurine was able to ameliorate the ischemia-reperfusion injury of the heart ;e. g. , the improvement of recovery of cardiac mechanical functions, the decrease in the leakage of LDHand CK from myocardium,in the accumulation of lipid peroxides and calcium,and in the loss of free amino acids in myocardium,as well as the decrease in the occurence rate of ventricular arrhythmias during the reperfusion phase. So, it may be suggested that exogenous taurine has some protective effects against the myocardial is-chemia-reperfuaion injury.
