Preventive and therapeutic effect of simvastatin on secondary inflammatory damage of rats with cerebral hemorrhage

Objective:To investigate the preventive and therapeutic effect and mechanism of simvastatin on secondary inflammatory damage of rats with cerebral hemorrhage.Methods:Sixty SD rat aged 9-12 weeks were chosen and divided into the control group,model group and simvastatintreated group randomly with 20 rats in each group.Rats in the model group and simvastatintreated group were infused with autologous fresh uncoagulated blood to the right brain tissue of the basal ganglia to build the cerebral hemorrhage model,while rats in the control group were treated with the same amount of normal saline.Then,rats in the simvastatin-treated group were given a gavage of 3 mg/kg of simvastatin once a day after modeling.Rats in the three groups were given nerve dysfunction score(NDS) and wet-dry weighting method was used to detect the brain water content(BWC) of brain tissues around the lesion of the rats.Then Nissl staining was conducted and the undamaged neurons were counted.Immunohistochemical SP method was applied to count the number of NF-d the immuno fluorκB,TLR4 and IL-1escence method wasβ positive cells in brain tissues around the lesions,an employed to determine the expression levels of NF-κB,TLR4 and IL-1me points were aβ proteins.Results:The NDS results of the simvastatin-treated group at all till significantly higher than those of the model group(P < 0.05);the BWC values of the simvastatin-treated group at all time points were all significantly lower than those of the model group at the same periods(P < 0.05);the number of the undamaged neurons around the lesions of the simvastatin-treated group at all time points were all significantly higher than those of the model group(P < 0.05);seven days after treatment,the number of the NF-κB,TLR4 and IL-1β positive cells in brain tissues around the lesions of the simvastatin-treated group were all significantly lower than those of the model group(P < 0.05),and its expression levels of NF-ower than those of the model group(κB,TLR4 and IL-1P < 0.05).Conclusioβ protein were also significantly lns:Simvastatin can inhibit the expressions of NF-κB,TLR4 and IL-1β proteins in rats with cerebral hemorrhage,and protect neurons and reduce secondary inflammatory damages by down-regulating the above protein-mediated inflammatory responses.

Nerve protective effect of rhTPO and G-CSF on hypoxic ischemic brain damage in rats

Objective:To observe the protection effect of rhTPO and granulocyte colony stimulating factor(G-CSFi on brain nerve after hypoxic ischemic brain damage(HIBD)in neonatal rats,exploring new ways for the laboratory basis of treatment for hypoxic ischemic encephalopathy,and provide for possible.Methods:A total of 120 newborn SD rats aging 7 d were randomly divided into control group,model group,TPO group and G-CSF group,using the method of blockingleft carotid artery to establish HIBD model.The left carotid artery was only seperated rather than blocked in the control group;after modeling,saline injection,rhTPO treatment and G-CSF treatment were adopted in the model group,TPO group and C-CSF group respectively.Then 10rats of 4 groups were executed at Day 3,7,14 after modeling,brain tissue was extracted to observe the brain damage:Immunohistochemical method was used to observe the histopathological changes of brain tissue and changes of nest protein(nestin)expression.Results:Injured brain mass of model group,TPO group and G-CSF group were significantly higher than that of control group at corresponding time point(P<0.05).Injured brain mass of TPO group and G-CSF group were significantly lower than that of model group(P<0.05),and with the increase of age,more significant increasing trend.At Day 3 after modeling,the expression of nestin positive cells in cerebral cortex of model group,TPO group and G-CSF gnmp increased significantly than that of control group{P<0.05);nestin positive cells of G-CSF group outnumbered TPO group significantly(P<0.05).Conclusions:The early TPO,G-CSF treatment of HIBD rats can improve brain function after hypoxia ischemia by neural protection.G-CSF can promote the differentiation of neural cells proliferation,and reduee degeneration and necrosis of nerve cells.