Breviscapine,extracted from the herb Erigeron breviscapus,is widely used for the treatment of cardiovascular diseases,cerebral infarct,and stroke,but its mechanism of action remains unclear.This study established a ra...Breviscapine,extracted from the herb Erigeron breviscapus,is widely used for the treatment of cardiovascular diseases,cerebral infarct,and stroke,but its mechanism of action remains unclear.This study established a rat model of traumatic brain injury induced by controlled cortical impact,and injected 75 μg breviscapine via the right lateral ventricle.We found that breviscapine significantly improved neurobehavioral dysfunction at 6 and 9 days after injection.Meanwhile,interleukin-6 expression was markedly down-regulated following breviscapine treatment.Our results suggest that breviscapine is effective in promoting neurological behavior after traumatic brain injury and the underlying molecular mechanism may be associated with the suppression of interleukin-6.展开更多
Cold-inducible RNA-binding protein（CIRP）, a key regulatory protein, could be facilitated by mild hypothermia in the brain, heart and liver. This study observed the effects of mild hypothermia at 31 ± 0.5℃ on t...Cold-inducible RNA-binding protein（CIRP）, a key regulatory protein, could be facilitated by mild hypothermia in the brain, heart and liver. This study observed the effects of mild hypothermia at 31 ± 0.5℃ on traumatic brain injury in rats. Results demonstrated that mild hypothermia suppressed apoptosis in the cortex, hippocampus and hypothalamus, facilitated CIRP m RNA and protein expression in these regions, especially in the hypothalamus. The anti-apoptotic effect of mild hypothermia disappeared after CIRP silencing. There was no correlation between mitogen-activated extracellular signal-regulated kinase activation and CIRP silencing. CIRP silencing inhibited extracellular signal-regulated kinase-1/2 activation. These indicate that CIRP inhibits apoptosis by affecting extracellular signal-regulated kinase-1/2 activation, and exerts a neuroprotective effect during mild hypothermia for traumatic brain injury.展开更多
Interleukin-6 has been shown to be involved in nerve injury and nerve regeneration, but the effects of long-term administration of high concentrations of interleukin-6 on neurons in the central nervous system is poorl...Interleukin-6 has been shown to be involved in nerve injury and nerve regeneration, but the effects of long-term administration of high concentrations of interleukin-6 on neurons in the central nervous system is poorly understood. This study investigated the effects of 24 hour expo-sure of interleukin-6 on cortical neurons at various concentrations （0.1, 1, 5 and 10 ng/mL） and the effects of 10 ng/mL interleukin-6 exposure to cortical neurons for various durations （2, 4, 8, 24 and 48 hours） by studying voltage-gated Na＋ channels using a patch-clamp technique. Volt-age-clamp recording results demonstrated that interleukin-6 suppressed Na＋ currents through its receptor in a time- and dose-dependent manner, but did not alter voltage-dependent activation and inactivation. Current-clamp recording results were consistent with voltage-clamp recording results. Interleukin-6 reduced the action potential amplitude of cortical neurons, but did not change the action potential threshold. The regulation of voltage-gated Na＋channels in rat corti-cal neurons by interleukin-6 is time- and dose-dependent.展开更多
[Objectives]This study was conducted to investigate the effects of remifentanil pretreatment on inflammatory factors in rats with acute cerebral ischemia.[Methods]Sixty SD rats were randomly divided into the normal co...[Objectives]This study was conducted to investigate the effects of remifentanil pretreatment on inflammatory factors in rats with acute cerebral ischemia.[Methods]Sixty SD rats were randomly divided into the normal control group,sham operation group,ischemic brain injury group,and remifentanil pretreatment group.Except the normal control group,each group was divided into three subgroups(six in each group)according to the sampling time points of 6,12 and 24 h after execution.After modeling,the rats were scored for neurological deficit,and observed for pathological changes of neurons in the brain tissue by HE staining and the brain infarct volume by TTC staining,and the expression levels of TNF-α,IL-6 and IL-8 were detected by RT-PCR.[Results]HE staining:No significant changes were observed in the pathological morphology of the brain tissue in the blank group and sham operation group;and the neuronal structure of rats in the acute cerebral ischemia group was obviously damaged,and the neuronal damage in the remifentanil pretreatment group was less than that in the acute cerebral ischemia group at each time point.TTC staining:The gray brain infarct area in the remifentanil pretreatment group was significantly smaller than that in the cerebral ischemia group(P<0.05).RT-PCR detection results:The expression levels of TNF-α,IL-6 and IL-8 in the blank group and sham surgery group did not show significant changes at different times(P>0.05);and compared with the cerebral ischemia group,the expression levels of TNF-α,IL-6,and IL-8 in the remifentanil pretreatment group were significantly reduced at all time points(P<0.05).[Conclusions]Remifentanil pretreatment could protect the brain by reducing the expression of inflammatory factors after cerebral ischemia injury.展开更多
文摘Breviscapine,extracted from the herb Erigeron breviscapus,is widely used for the treatment of cardiovascular diseases,cerebral infarct,and stroke,but its mechanism of action remains unclear.This study established a rat model of traumatic brain injury induced by controlled cortical impact,and injected 75 μg breviscapine via the right lateral ventricle.We found that breviscapine significantly improved neurobehavioral dysfunction at 6 and 9 days after injection.Meanwhile,interleukin-6 expression was markedly down-regulated following breviscapine treatment.Our results suggest that breviscapine is effective in promoting neurological behavior after traumatic brain injury and the underlying molecular mechanism may be associated with the suppression of interleukin-6.
基金supported by the National Natural Science Foundation of China,No.81303091
文摘Cold-inducible RNA-binding protein（CIRP）, a key regulatory protein, could be facilitated by mild hypothermia in the brain, heart and liver. This study observed the effects of mild hypothermia at 31 ± 0.5℃ on traumatic brain injury in rats. Results demonstrated that mild hypothermia suppressed apoptosis in the cortex, hippocampus and hypothalamus, facilitated CIRP m RNA and protein expression in these regions, especially in the hypothalamus. The anti-apoptotic effect of mild hypothermia disappeared after CIRP silencing. There was no correlation between mitogen-activated extracellular signal-regulated kinase activation and CIRP silencing. CIRP silencing inhibited extracellular signal-regulated kinase-1/2 activation. These indicate that CIRP inhibits apoptosis by affecting extracellular signal-regulated kinase-1/2 activation, and exerts a neuroprotective effect during mild hypothermia for traumatic brain injury.
基金supported by a grant from the National Natural Science Foundation of China,No.30972766,31170852,81001322,81172795,81173048the Specialized Research Fund for the Doctoral Program of Colleges and Universities,No.20094402110004
文摘Interleukin-6 has been shown to be involved in nerve injury and nerve regeneration, but the effects of long-term administration of high concentrations of interleukin-6 on neurons in the central nervous system is poorly understood. This study investigated the effects of 24 hour expo-sure of interleukin-6 on cortical neurons at various concentrations （0.1, 1, 5 and 10 ng/mL） and the effects of 10 ng/mL interleukin-6 exposure to cortical neurons for various durations （2, 4, 8, 24 and 48 hours） by studying voltage-gated Na＋ channels using a patch-clamp technique. Volt-age-clamp recording results demonstrated that interleukin-6 suppressed Na＋ currents through its receptor in a time- and dose-dependent manner, but did not alter voltage-dependent activation and inactivation. Current-clamp recording results were consistent with voltage-clamp recording results. Interleukin-6 reduced the action potential amplitude of cortical neurons, but did not change the action potential threshold. The regulation of voltage-gated Na＋channels in rat corti-cal neurons by interleukin-6 is time- and dose-dependent.
基金Supported by Science and Technology Planning Project of Health Commission of Jiangxi Province(SKJP220229249)Science and Technology Planning Project of Jiangxi Provincial Administration of Traditional Chinese Medicine(2019A149).
文摘[Objectives]This study was conducted to investigate the effects of remifentanil pretreatment on inflammatory factors in rats with acute cerebral ischemia.[Methods]Sixty SD rats were randomly divided into the normal control group,sham operation group,ischemic brain injury group,and remifentanil pretreatment group.Except the normal control group,each group was divided into three subgroups(six in each group)according to the sampling time points of 6,12 and 24 h after execution.After modeling,the rats were scored for neurological deficit,and observed for pathological changes of neurons in the brain tissue by HE staining and the brain infarct volume by TTC staining,and the expression levels of TNF-α,IL-6 and IL-8 were detected by RT-PCR.[Results]HE staining:No significant changes were observed in the pathological morphology of the brain tissue in the blank group and sham operation group;and the neuronal structure of rats in the acute cerebral ischemia group was obviously damaged,and the neuronal damage in the remifentanil pretreatment group was less than that in the acute cerebral ischemia group at each time point.TTC staining:The gray brain infarct area in the remifentanil pretreatment group was significantly smaller than that in the cerebral ischemia group(P<0.05).RT-PCR detection results:The expression levels of TNF-α,IL-6 and IL-8 in the blank group and sham surgery group did not show significant changes at different times(P>0.05);and compared with the cerebral ischemia group,the expression levels of TNF-α,IL-6,and IL-8 in the remifentanil pretreatment group were significantly reduced at all time points(P<0.05).[Conclusions]Remifentanil pretreatment could protect the brain by reducing the expression of inflammatory factors after cerebral ischemia injury.
