| Objective To investigate the effects of recombinant human granulocyte colony-stimulating factor(rhG-CSF) on the expression of nuclear factor-kappaB(NF-ΚB) and induciable nitricoxide synthase(iNOS) in rats with focal cerebral ischemia/reperfusion. To explore the anti-inflammatory mechanisms of rhG-CSF, and to provide a new theoretical basis for clinical application.Methods Thirty-six male Sprague-Dawley rats were randomly divided into the sham-operated group, the model group and the rhG-CSF-treatment group (treatment group), and12rats were included in each group. The left middle cerebral artery occlusion was established by the Longa suture method. In the treatment group, a single dose of50μg/kg rhG-CSF was injected subcutaneously2hours after cerebral ischemia. The sham-operated group and model group received the same volume of saline. After24hours of reperfusion, the neurologic impairment evaluation scores were recorded on Longa5-point scale, and then all the rats were killed. The rat brain tissue sections were stained by TTC staining and the infarction volume was measured by the BI-2000Medical image analysis system.The positive cell expression of the nuclear transcription factor-KB p65(NF-KB p65) and the inducible nitric oxide synthase (iNOS) in each rat brain tissue was observed after immunohisto-chemistry(PV-6001two-step method) staining.The BI-2000Medical image analysis system was used to measure the positive cells average gray value of NF-ΚB p65and iNOS.Measurement datas were expressed using mean±standard deviation and analyzed by spss13.0.When the value of "P" is lower than0.05,it has significance.Results1.The rats of sham-operated group had no neurologic impairment and the neurological outcome score was0.The rats of other two groups had neurologic impairment in various degree,the neurological outcome score of the treatment group(1.25±0.45) was lower than the model group(2.58±0.67)(P<0.01).2. TTC staining can clearly show the range of the white infarction. The brain tissue of sham-operation group had no infarction. The white infarction of the left middle cerebral artery territory was found in the model group and treatment group,and compared with the model group [(31.05±1.49)%], the infarction volume was significantly small in the treatment group [(24.04±1.49)%)(P<0.01).3.Compared with the sham-operated group (161.86±4.27), the mean gray values of the expression of NF-ΚB p65was significantly decreased in the model group (96.67±3.94)(P<0.01). Compared with the model group, the mean gray values of the expressions of NF-ΚB p65was significantly increased in the treatment group (136.18±5.26)(P<0.01).4.Compared with the sham-operated group (163.99±4.08), the mean gray values of the expressions of iNOS was significantly decreased in the model group (109.73±6.07)(P<0.01). Compared with the model group, the mean gray values of the expressions of iNOS was significantly increased in the treatment group(128.05±3.19)(P<0.01). Infarction was not found in the sham-operated group.Conclusions1.rhG-CSF can decrease neurological function scores and promote the recovery of limb functions after the CI/RP.2.The effects of rhG-CSF can reduce infarction volume after CI/RP.3.rhG-CSF can decreased the expressions of NF-κB p65and iNOS after theCI/RP. The mechanism of rhG-CSF neuroprotection may be achieved by decreasing the expressions of NF-ΚB and iNOS and inhibiting the inflammatory response. |
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