Effect of Electroacupuncture on TRPM7 mRNA Expression after Cerebral Ischemia／reperfusion in Rats via TrkA Pathway

TRPM7 ion channel protein is a member ofthe transient receptor potential (TRP) cation chan-nel superfamily .It is an unusual bifunctional pro-tein that contains anα-kinase domain fused to aCa2 +-permeable cation channel . Aarts and col-leagues provide evidence that TRPM7 initiatesCa2 +overload. TRPM7 may play a key role in an-oxic neuronal death[1]. Electroacupuncture (EA)has been shown to be an effective treat ment onstroke . The detailed mechanisms mediating thebeneficial effects of…     

第二掌骨侧穴位治疗胆囊结石诱发“气至病所”探析

目前不少临床与实验研究表明耳穴与体穴并用是针灸治疗胆囊炎,胆石症的有效方法[1].但对第二掌骨侧穴位在治疗胆囊炎,胆石症中的作用的研究较少.笔者2001年在泉州市中医院针灸科实习期间观察了1例针刺第二掌骨侧穴位诱发"气至病所"的胆石症患者,报道如下.     

脱毛膏对家兔督脉及其两侧旁开皮肤组织热休克蛋白70合成影响的初步观察

目的探讨脱毛膏对后续皮肤相关应激实验的影响。方法免疫组织化学方法检测热休克蛋白70（HSP70），比较经脱毛膏脱毛处理后恢复期4h、16h皮肤HSP70表达的差异以及督脉线及其两侧旁开对照点HSP70表达的差异。结果脱毛后恢复期4h时皮肤高度表达HSP70．恢复期16h时HSP70袁达减少；督脉线与其两侧旁开非经对照点的HSP70表达在恢复期4h和16h时均未见明显差异。结论（1）脱毛膏会刺激皮肤应激合成HSP70．后续的其他实验宜在脱毛后16h进行。（2）脱毛膏脱毛法可用于针灸过程中经脉线上HSP70检测的皮肤处理。     

脑室注射反义寡核苷酸对大鼠Nogo-A mRNA及其蛋白表达的影响

目的研究侧脑室注射NogoA反义寡核苷酸对大鼠大脑皮质NogoAmRNA及其蛋白表达的影响。方法成年Wistar大鼠53只,分为A组(对照组)、B组及C组,后2组分别经侧脑室注射随机序列寡核苷酸及NogoA反义寡核苷酸,在注射后12、24、48及72h用逆转录聚合酶链反应(RTPCR)和免疫组织化学方法分别检测大脑皮质NogoAmRNA及其蛋白表达的变化。结果NogoAmRNA及其蛋白表达在脑室注射NogoA反义寡核苷酸后12h开始下降,24h降至最低,48h开始回升,72h恢复正常。结论脑室注射NogoA反义寡核苷酸能抑制NogoAmRNA及其蛋白的表达,且可能成为中枢神经损伤后再生的新措施。     

Nerve Growth Factor Inhibits Gd^3＋ -sensitive Calcium Influx and Reduces Chemical Anoxic Neuronal Death

To investigate whether glutamate and voltage-gated calcium channels-independent calcium influx exists during acute anoxic neuronal damage and its possible relationship to neuronal protective function of NGF. In in vitro model of acute anoxia, hippocampal cultures from newborn rats were exposed to 3 mmol/L KCN. Changes of intracellular Ca^2＋ concentration （[Ca^2＋]i） were monitored by con-focal imaging and cell viability was assayed by PI and cFDA staining. The results showed that after treatment with primary hippocampal cultures with 3 mmol/L KCN for 15 min, [Ca^2＋]i was significantly increased 6.27-fold compared to pre-anoxia level and 73.3% of the cells died. When combination of 20 μmol/L MK-801 （glutamate receptor antagonist）, 40 μmol/L CNQX （AMPA receptor antagonist） and 5 μmol/L nimodipine （voltage-gated calcium channel antagonist） （hereafter denoted as MCN） were administrated to hippocampal cultures, levels of [Ca^2＋]i and cell death rate induced by KCN were partially reduced by 35.9% and 47.5% respectively. However, Gd^3＋ （10 μmol/L） almost completely blocked KCN-mediated [Ca^2＋]i elevation by 81.9% and reduced neuronal death by 88.8% in the presence of MCN. It is noteworthy that NGF, used in combination with MCN, inhibited KCN-induced [Ca^2＋]i increase by 77.4% and reduced cell death by 87.1%. Only PLC in- hibitor U73122 （10 μmol/L） abolished NGF effects. It is concluded that Gd^3＋-sensitive calcium influx, which is NMDA （glutamate receptor） and voltage-gated calcium channels-independent, is responsible for acute anoxic neuronal death. NGF can inhibit Gd^3＋-sensitive calcium influx and reduce anoxic neuronal death through activating PLC pathway.