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Objective To evaluate the efficacy and safety of mNGF to peripheral neuropathy induced by n-bexane. Methods 54 cases were treated with mNGF (18 μg i. m qd.) and the period of treatment is 56 days. 15 severe cases treated with two periods of treatment. Subjects received symptoms and signs of nerve system and activi-ties of daily living (ADL) scale were examined before and every 14 days after treated, The efficacy of mNGF was as-sessed by score increase of each index before and after treatment himself. To evaluate the safety, subjects received Is-boratory examinations before and every 28 days after treated, recorded adverse events everyday. Results During the trial, The indexes had improved remarkably in two weeks after the treatment , There were highly significant differ-ences in score increase after 4 ～ 8 weeks of treatment(P < 0. 01). It indicated that treatmented with mNGF was effec-tive. There were no severe adverse events (SAE) found among 54 trial subjects. There were no evident abnormalities in laboratory examinations before and after treatment. Pains of the injected sites are the main ADR, the incidence was 68.5% (37/54). Conclusion The results of the research indicated that mNGF clinical application could be consid-ered as safe and effective.
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Aim To investigate the effects of fasudil on neuronal apoptosis after cerebral ischemia/reperfusion(I/R) injury in rats.Method Focal cerebral ischemia/reperfusion model in rats was made by transient occlusion of the middle cerebral artery for 90 minutes followed by 24 h reperfusion.The number of neural apoptotic cells was measured by the method of TUNEL staining;Bcl-2,Bax,Caspase-3 protein expressions were observed by immunohistochemical staining;the expression of phospho-MYPT and phospho-Akt protein was determined by Western blot.Result Compared with the MCAO group,fasudil could decrease the number of neural apoptotic cells,upregulate the expression of Bcl-2 and phospho-Akt protein and inhibit the expression of Bax,Caspase-3 and phospho-MYPT protein significantly(P
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Objective To investigate the effects of pre-ischemic administration of L-NAME on brain protective effects of simvastatin against focal cerebral ischemic/reperfusion injury in rats. Methods ① Animals were subjected to transient 2-hour middle cerebral artery occlusion(MCAO)with the use of the intraluminal filament method previously described by Zea Longa. ② 54 male rats were treated with simvastatin or vehicle by gavage two weeks before MCAO, and L-NAME was injected into laterar ventricle of rats 45 minutes before MCAO. After neurological deficit was assessed at 22 hours of reperfusion, rats were killed, and the brains were rapidly removed. The coronal sections of the brains were prepared and stained with 2% TTC, and the infarct volumes were determined. Another 54 male rats were performed as description above except that the brain tissues were made into homogenate at 22 hours of reperfusion, and the contents of lactic acid(LA) and MDA, and the activities of superoxide dismutase(SOD) in the brain tissues were also measured. Results Administration of simvastatin significantly reduced the size of brain infarct, improved neurological deficits, decreased the contents of LA and MDA and increased the activities of SOD, but L-NAME could abrogate these effects. Conclutions L-NAME could abrogate the protection of simvastatin against ischemic/reperfusion injury,which may be by inhibiting the expression and activity of endothelial NO synthase(eNOS) up-regulated by simvastatin.
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AIM:To observe the effects of fasudil on inflammatory reaction in cerebral ischemia/reperfusion rats.METHODS:Focal cerebral ischemia/reperfusion model in rats was made by transient occlusion of middle cerebral artery for 1.5 h followed by 24 h reperfusion.Fasudil was injected intraperitoneally before operation and 12 h after operation.The neurological function was scored and the infarct volume was measured after operation.The water content of brain was measured with dry-wet weight;The myeloperoxidase(MPO)activity was determined by spectrophotometer;The permeability of the blood brain barrier was evaluated by measurement of the Evans Blue(EB)content in the brain with spectrophotometer;The brain content of IL-8 was evaluated with ELISA;The level of NF-?B p65 mRNA expression was determined by RT-PCR;The expressions of ICAM-1,VCAM-1 and NF-?B p65 protein were observed by immunohistochemistry;The MCP-1 and the expression of NF-?B p65 protein in the nuclear extracts were detected by western blotting.RESULTS:Fasudil improved the neurological function,decreased the infarct size,reduced the permeability of blood brain barrier and brain water content,inhibited the MPO activity,decreased the content of IL-8 and the protein expressions of ICAM-1,VCAM-1 and MCP-1 in brain tissue,inhibited the expressions of NF-?B p65 mRNA and protein and reduced the content of NF-?B p65 protein in the nuclear extracts significantly(P
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Some immune responses induced by atherosclerosis may aggravate the state of the illness by inducing persistent arterial inflammation, whereas others may inhibit arterial inflammation and atherosclerosis.Thus, the prevention and treatment of atherosclerosis may be achieved by the method of immunomodulation, by which selectively suppress proatherogenic immune responses or activate antiatherogenic ones.
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Aim To Study the inhibition mechanism of edelfosine on cytokinesis in Schizosaccharomyces pombe. Methods To observe the inhibition of cytokinesis and growth, the experiments of inhibition of cyto-kinesis and parallel growth were carried out. To explore the inhibition mechanism of edelfosine, the experiment of retransfection of yeast genes was carried out. Results Edelfosine inhibited the cytokinesis of S.pombe in low dosage and cell growth in high dosage. The mid2△、spm1△ and pmp1△ strains were resistant to edelfosine in high dosage. However, these strains retrieved the sensitive to edelfosine in high dosage by retransfected the relevant genes, respectively. A reciprocal action, which was the Mid2p induced the phosphorylated Spm1, while the Pmp1 dephosphorylated Spm1, existed among the Spm1、Mid2 and Pmp1 in S.pombe treated with edelfosine. Conclusion The inhibition of edelfosine on cytokinesis and cell growth due to the effect of Spm1、Mid2 and Pmp1.
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Aim To investigate whether ischemic postconditioning could induce ischemic tolerance to focal cerebral reperfusion injury and comparison with ischemic preconditioning. Methods A reversible middle cerebral artery occlusion (MCAO)was used in this study. Fifty male Sprague-dawley rats were randomized into five groups(n=10): sham-operated group,MCAO group,preconditioning group, postconditioning group and nimodipin group . The neurological function was scored and the infarct volume was measured after operation. The grouping,experimental methods and procedures of another fifty rats were as above except that ipsilateral brain of infarction was dissected and made into homogenate,then the contents of MDA,SOD,GSH and LA were quantitatively measured. Results The postconditioning and preconditioning improved the neurological function,reduced the cerebral infarction volumes and cerebral swelling significantly compared with those of the MCAO group. Contents of LA and MDA were lower, while the activity of SOD in the brain tissues were higher in preconditioning group and postconditioning group than those of the MCAO group. Conclusion Postconditioning could induce brain tolerance, and increase the antioxidant activity, which might be an important mechanism of induction of brain tolerance.