目的观察安神补脑液(ASBN)对失眠大鼠海马体γ-氨基丁酸受体(GABA)、钠-钾-氯协同转运蛋白表达的影响及其催眠作用机制。方法采用腹腔注射对氯苯丙氨酸(PCPA)复制大鼠失眠模型,将复制成功的失眠模型大鼠随机分为氟西汀(Fluoxetine)组,...目的观察安神补脑液(ASBN)对失眠大鼠海马体γ-氨基丁酸受体(GABA)、钠-钾-氯协同转运蛋白表达的影响及其催眠作用机制。方法采用腹腔注射对氯苯丙氨酸(PCPA)复制大鼠失眠模型,将复制成功的失眠模型大鼠随机分为氟西汀(Fluoxetine)组,模型组,ASBN高、中、低剂量(ASBN-H、M、L)组,另取15只正常大鼠作为正常组。各给药组连续7 d给予相应药物口服灌胃,模型组和正常组连续灌胃7 d 0.9%生理盐水,观察各组大鼠的一般活动状态。采用qPCR检测海马体中GABA_ARγ2和Na+-K+-Cl-协同转运蛋白(NKCC1)的表达,采用免疫组化染色(IHC)-P检测大鼠海马体中GABA_ARα1的表达。结果ASBN可提高海马体中GABA_ARα1、GABA_ARγ2表达,降低NKCC1表达。结论ASBN可以通过调节失眠大鼠海马体中GABA_ARα1、GABA_ARγ2和NKCC1表达量来改善大鼠的睡眠状态。展开更多
As a leading cause for morbidity and mortality in young adults,traumatic brain injury（TBI）,along with the poorly understood TBI-related seizures inducing their predispositions,pose a major health and socioeconomic p...As a leading cause for morbidity and mortality in young adults,traumatic brain injury（TBI）,along with the poorly understood TBI-related seizures inducing their predispositions,pose a major health and socioeconomic problem in the world（Huang,2013）.展开更多
Sodium-potassium-chloride cotransporter 1 (NKCC1) and potassium-chloride cotransporter 2 (KCC2) are associated with the transmission of peripheral pain.We investigated whether the increase of NKCC1 and KCC2 is associa...Sodium-potassium-chloride cotransporter 1 (NKCC1) and potassium-chloride cotransporter 2 (KCC2) are associated with the transmission of peripheral pain.We investigated whether the increase of NKCC1 and KCC2 is associated with peripheral pain transmission in dorsal root ganglion neurons.To this aim,rats with persistent hyperalgesia were randomly divided into four groups.Rats in the control group received no treatment,and the rat sciatic nerve was only exposed in the sham group.Rats in the chronic constriction injury group were established into chronic constriction injury models by ligating sciatic nerve and rats were given bumetanide,an inhibitor of NKCC1,based on chronic constriction injury modeling in the chronic constriction injury + bumetanide group.In the experiment measuring thermal withdrawal latency,bumetanide (15 mg/kg) was intravenously administered.In the patch clamp experiment,bumetanide (10 μg/μL) and acutely isolated dorsal root ganglion neurons (on day 14) were incubated for 1 hour,or bumetanide (5 μg/μL) was intrathecally injected.The Hargreaves test was conducted to detect changes in thermal hyperalgesia in rats.We found that the thermal withdrawal latency of rats was significantly decreased on days 7,14,and 21 after model establishment.After intravenous injection of bumetanide,the reduction in thermal retraction latency caused by model establishment was significantly inhibited.Immunohistochemistry and western blot assay results revealed that the immune response and protein expression of NKCC1 in dorsal root ganglion neurons of the chronic constriction injury group increased significantly on days 7,14,and 21 after model establishment.No immune response or protein expression of KCC2 was observed in dorsal root ganglion neurons before and after model establishment.The Cl^– (chloride ion) fluorescent probe technique was used to evaluate the change of Cl^– concentration in dorsal root ganglion neurons of chronic constriction injury model rats.We found that the relative optical density of N-(et展开更多
文摘目的观察安神补脑液(ASBN)对失眠大鼠海马体γ-氨基丁酸受体(GABA)、钠-钾-氯协同转运蛋白表达的影响及其催眠作用机制。方法采用腹腔注射对氯苯丙氨酸(PCPA)复制大鼠失眠模型,将复制成功的失眠模型大鼠随机分为氟西汀(Fluoxetine)组,模型组,ASBN高、中、低剂量(ASBN-H、M、L)组,另取15只正常大鼠作为正常组。各给药组连续7 d给予相应药物口服灌胃,模型组和正常组连续灌胃7 d 0.9%生理盐水,观察各组大鼠的一般活动状态。采用qPCR检测海马体中GABA_ARγ2和Na+-K+-Cl-协同转运蛋白(NKCC1)的表达,采用免疫组化染色(IHC)-P检测大鼠海马体中GABA_ARα1的表达。结果ASBN可提高海马体中GABA_ARα1、GABA_ARγ2表达,降低NKCC1表达。结论ASBN可以通过调节失眠大鼠海马体中GABA_ARα1、GABA_ARγ2和NKCC1表达量来改善大鼠的睡眠状态。
文摘As a leading cause for morbidity and mortality in young adults,traumatic brain injury（TBI）,along with the poorly understood TBI-related seizures inducing their predispositions,pose a major health and socioeconomic problem in the world（Huang,2013）.
基金supported by the National Natural Science Foundation of China,No.30160026(to JQS)the High Level Talent Research Project of Shihezi University of China,No.RCSX201705(to YW)
文摘Sodium-potassium-chloride cotransporter 1 (NKCC1) and potassium-chloride cotransporter 2 (KCC2) are associated with the transmission of peripheral pain.We investigated whether the increase of NKCC1 and KCC2 is associated with peripheral pain transmission in dorsal root ganglion neurons.To this aim,rats with persistent hyperalgesia were randomly divided into four groups.Rats in the control group received no treatment,and the rat sciatic nerve was only exposed in the sham group.Rats in the chronic constriction injury group were established into chronic constriction injury models by ligating sciatic nerve and rats were given bumetanide,an inhibitor of NKCC1,based on chronic constriction injury modeling in the chronic constriction injury + bumetanide group.In the experiment measuring thermal withdrawal latency,bumetanide (15 mg/kg) was intravenously administered.In the patch clamp experiment,bumetanide (10 μg/μL) and acutely isolated dorsal root ganglion neurons (on day 14) were incubated for 1 hour,or bumetanide (5 μg/μL) was intrathecally injected.The Hargreaves test was conducted to detect changes in thermal hyperalgesia in rats.We found that the thermal withdrawal latency of rats was significantly decreased on days 7,14,and 21 after model establishment.After intravenous injection of bumetanide,the reduction in thermal retraction latency caused by model establishment was significantly inhibited.Immunohistochemistry and western blot assay results revealed that the immune response and protein expression of NKCC1 in dorsal root ganglion neurons of the chronic constriction injury group increased significantly on days 7,14,and 21 after model establishment.No immune response or protein expression of KCC2 was observed in dorsal root ganglion neurons before and after model establishment.The Cl^– (chloride ion) fluorescent probe technique was used to evaluate the change of Cl^– concentration in dorsal root ganglion neurons of chronic constriction injury model rats.We found that the relative optical density of N-(et
