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Objective To investigate the effect of B7-H3 protein,a collaborative signal molecule,on macrophage-inflammatory protein 2 (MIP-2) mRNA level in Streptococcus pneumococcal meningitis mouse models.Methods Forty-eight healthy male BALB/C mice at the age of 1.5-2.0 months were randomly divided into 4 groups:9 g/L saline group(NS group),B7-H3 protein group(B7-H3 group),Streptococcus pneumoniae group(SP group),and Streptococcus pneumoniae plus B7-H3 protein group(combination group),12 mice in each group.Mouse models were established by intracerebral ventricular injection with 9 g/L saline,B7-H3 protein,Streptococcus pneumoniae type 3 or Streptococcus pneumoniae type 3 plus B7-H3 protein.Neurobehavior of different groups was evaluated according to loeffler rule after injection for 6 h and 24 h,then the mice were sacrificed and MIP-2 mRNA levels were tested by Real-time PCR.The results were analyzed by SPSS 18.0 software.Results Neurobehavior scoring results showed that there were no significant differences between B7-H3 group and NS group (P ＞ 0.05) after infection for 6 h and 24 h,while the score of SP group was decreased compared with that of NS group (P ＜ 0.05),and the score of combination group was significantly decreased compared with that of SP group (P ＜ 0.05).Real-time PCR results showed that,compared with the NS group,the relative MIP-2 mRNA level in SP group increased after injection for 6 hours (1.210 ±0.932 vs 1.000 ± 0.008),but the difference was not significant (P ＞ 0.05),while at 24 h post infection,the relative MIP-2mRNA expressions in SP group were significantly increased compared with that of NS group(12.880 ± 7.792 vs 1.000 ±0.091),the difference was significant (P ＜ 0.05).At 6 h post infection,SP + B7-H3 treatment enhanced the MIP-2mRNA production compared to SP infection alone,but the difference was not significant [(1.240 ± 0.804) vs (1.210 ± 0.932)] (P ＞ 0.05) ; while at 24 h post infection,the difference was significant (38.760 ± 6.601 vs 12.880 ± 7.792) (P ＜ 0.05).Conclusion Collaborative signal molecule B7-H3 protein may increase MIP-2 mRNA level in Streptococcus pneumococcal meningitis mouse model,and exaggerate the clinical disease condition.
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<p><b>BACKGROUND</b>Glucocorticoid receptor (GR) is believed to be a major factor in brain maturation and in modulation of a series of brain activity. Hippocampal neurons are abundant in glucocorticoid receptor, and there is significant change in GR expression under certain pathological state. Epilepsy is a special pathological state of the central nervous system. This study aimed to explore the role of GR in epilepsy by observing the change and functions of GR in hippocampus with a basolateral amygdale-electrical kindled rat epilepsy model.</p><p><b>METHODS</b>Firstly, we established the basolateral amygdale-electrical kindled rat epilepsy model. Then GR mRNA expression in the hippocampus was assayed by semi-quantitative reverse transcription-PCR in this experiment. In addition, the processes of epileptic seizures were observed and electroencephalograms were recorded. One-way analysis of variance (ANOVA) was employed for comparing means of multiple groups, followed Fisher's least significant difference (LSD) for paired comparison.</p><p><b>RESULTS</b>The rats were successfully kindled after an average of (13.50 ± 3.99) times electrical stimulation, in which it was showed that GR mRNA expression reduced obviously as compared with the control group and the sham groups (P < 0.001). The down-regulation of GR mRNA expression was abated or reversed by some anti-epilepsy drugs (P < 0.001 compared with the epilepsy group), accompanied by attenuation of seizures and improvement of electroencephalograms.</p><p><b>CONCLUSIONS</b>Down-regulation of hippocampal GR mRNA expression may be related to the kindling. Anti-epilepsy drugs exposure can retard this change.</p>
Subject(s)
Animals , Male , Rats , Amygdala , Metabolism , Epilepsy , Genetics , Kindling, Neurologic , Genetics , Rats, Sprague-Dawley , Receptors, Glucocorticoid , Genetics , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
0.05).Conclusion FT3 ,T3 play some potentially roles in the pathogenesis of ADHD and TSH may not be related to it.
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0.05).However,the level of PRG-1 protein in cerebral cortex of experimental group was significantly higher than that of control group at 7 d(t=2.347,P=0.041).Conclusion The up-regulated expression of PRG-1 in cerebral cortex may be associated with the recurrent neonatal seizure-induced brain damage.