黄芪总苷对氯化镉染毒大鼠肝肾损伤的保护作用

目的研究黄芪总苷对氯化镉染毒大鼠肝、肾损伤的保护作用。方法 36只Wistar大鼠随机均分为3组。染毒组和干预组均腹腔注射0.1%氯化镉,每周5次,共5周,染毒的同时干预组给予黄芪总苷(20 mg/kg·bw·d)灌胃治疗,1次/d,连续5周,末次给药24 h后股动脉采血处死大鼠,测定大鼠肝、肾组织的镉含量、SOD活性、LDH活性和MDA含量,观察肝、肾组织的Bcl-2和Bax的蛋白表达,测定大鼠肝组织AST活性、ALT和IL-2含量和TGF-β1的含量,测定大鼠肾组织GSH-Px活性。结果与空白组比较,染毒组肝肾组织镉含量、MDA含量、LDH活性、Bax蛋白表达均明显升高,SOD活性、Bcl-2蛋白表达明显下降(P0.05)。同时,染毒组肝组织AST活性、ALT活性、TGF-β1含量均明显升高,肝组织IL-2含量和肾组织GSH-Px的活性下降,差异有统计学意义(P0.05)。与染毒组比较,干预组大鼠肝肾组织、TGF-β1含量、MDA含量、LDH活性、Bax蛋白表达均明显降低,SOD活性、Bcl-2蛋白表达明显升高(P0.05)。同时,干预组大鼠肝组织AST活性、ALT活性、TGF-β1含量均明显降低,镉含量肾组织GSH-Px的活性明显增强,差异有统计学意义(P0.05)。结论黄芪总苷对镉所致大鼠的肝肾损伤具有保护作用,其机制可能与黄芪总苷抑制镉染毒大鼠体内氧化应激反应、调控酶活性和细胞周期蛋白有关。     

汉防己乙素抑制P38 MAPK和ERK1/2的磷酸化缓解心肌缺血再灌注大鼠心肌细胞凋亡和线粒体氧化损伤

目的探讨汉防己乙素(Fan)对心肌缺血再灌注(I/R)大鼠心肌细胞凋亡和线粒体损伤的影响。方法雄性SD大鼠分为假手术组、模型(I/R)组、I/R+Fan 1,3和10 mg·kg-1组,I/R+盐酸维拉帕米(VH)20 mg·kg-1组,每组9只。模型大鼠结扎左前降支冠状动脉30 min后,松开结扎线再灌注90 min。给药大鼠分别在造模前20 min ip给予Fan 1,3,10 mg·kg-1及VH 20 mg·kg-1。记录平均动脉血压(MAP),左心室收缩压(LVSP);ELISA法测定血清中肌红蛋白(Mb)和肌酸激酶同工酶(CK-MB)的含量;HE染色观察心肌组织病理损伤;TUNEL染色检测心肌细胞凋亡;试剂盒检测心肌组织超氧化物歧化酶(SOD)活性,丙二醛(MDA)和谷胱甘肽(GSH)含量;Western印迹法检测心肌组织Bcl-2、Bax、原癌基因(c-Myc)、活化胱天蛋白酶3蛋白表达水平和P38丝裂原活化蛋白激酶(P38 MAPK)及细胞外调节蛋白激酶1/2(ERK1/2)磷酸化水平。结果与假手术组比较,I/R组LVSP和MAP、GSH含量、SOD活性及c-Myc蛋白表达水平均显著降低(P<0.05);Mb,CK-MB和MDA含量、心肌细胞凋亡率、活化胱天蛋白酶3和Bax蛋白表达水平及P38MAPK和ERK1/2的磷酸化水平均显著升高(P<0.05)。与I/R组比较,I/R+Fan 3和10 mg·kg-1组LVSP和MAP、GSH含量、SOD活性及Bcl-2和c-Myc蛋白表达水平均显著升高(P<0.05),Mb,CK-MB和MDA含量显著降低(P<0.05),心肌细胞凋亡率显著降低(P<0.05),胱天蛋白酶3和Bax/Bcl-2蛋白表达水平显著降低(P<0.05),P38 MAPK和ERK1/2磷酸化水平显著降低(P<0.05)。结论 Fan能够抑制P38 MAPK和ERK1/2的磷酸化,缓解心肌I/R大鼠心肌细胞凋亡和线粒体损伤。     

TAL对慢支模型大鼠肺泡巨噬细胞凋亡的影响及部分机制研究

目的探讨枇杷叶三萜酸(TAL)对慢支模型(CB)大鼠肺泡巨噬细胞(AM)活性及凋亡的影响及其可能的作用机制。方法应用BCG联用LPS的方法复制大鼠CB模型,采用体内外给药的方法,观察TAL及MAPK3条通路对CB大鼠AM凋亡及活性的影响。MTT法检测细胞活性,电镜观察AM凋亡,流式细胞技术检测AM凋亡率及AM中凋亡相关基因Bcl-2、Bax的表达。Western blot法检测AM中ERK蛋白磷酸化水平。结果①与正常对照组比较,模型大鼠支气管肺泡灌洗液中AM数增加(P<0.01),而TAL灌胃给药可抑制模型大鼠异常增多的AM数量(P<0.01)。②慢支模型组AM活性较正常组相比明显增强(P<0.01),TAL可抑制CB模型组大鼠AM的活性(P<0.05)。③与正常组比较,模型大鼠AM凋亡率明显降低(P<0.01);TAL给药组及ERK通路抑制剂PD98059组AM凋亡率较模型组比较升高(P<0.05,P<0.01)。而JNK通路抑制剂Curcumin组AM凋亡率降低(P<0.05)。④模型大鼠AMERK磷酸化水平明显升高(P<0.01);TAL(5mg.L-1)体外给药可抑制慢支大鼠AM内ERKMAPK通路的磷酸化(P<0.05)。⑤模型大鼠AMBax表达明显降低而Bcl-2表达升高(P<0.01),TAL给药组可降低慢支大鼠AMBcl-2表达,升高Bax表达。结论慢支模型大鼠AM活性增强、凋亡减少,TAL可诱导AM凋亡,抑制AM活性,使AM内Bcl-2/Bax的表达趋于平衡。ERK、JNKMAPK信号传导通路参与慢支大鼠AM凋亡的调节,JNKMAPK信号通路促进AM凋亡而ERKMAPK信号通路抑制AM凋亡。TAL的促AM凋亡作用可能与其抑制慢支大鼠AMERKMAPK信号通路的磷酸化活化、调节Bcl-2/Bax的表达有关。     

N-乙酰半胱氨酸影响p38有丝分裂原活化蛋白激酶对顺铂诱导急性肾损伤的保护作用

目的研究N-乙酰半胱氨酸(N-acetylcysteine,NAC)对顺铂(cisplatin,CDDP)诱导大鼠急性肾损伤(acute kidney in-jury,AKI)后组织细胞凋亡的影响和与p38有丝分裂原活化蛋白激酶(p38 mitogen activated protein kinase,p38MAPK)的关系。方法静脉注射CDDP制备大鼠AKI模型。大鼠随机分为正常对照组、AKI模型对照组、NAC低剂量组(50 mg.kg-1)、NAC中剂量组(100 mg.kg-1)、NAC高剂量组(200 mg.kg-1)、特异性p38MAPK抑制剂SB203580组(10mg.kg-1)。大鼠预先连续给药3 d,给予CDDP,再继续给药5 d。TUNEL法进行细胞凋亡检查。试剂盒测定肾脏组织caspase-3。Western blot测定caspase-3、Bax、Bcl-2、磷酸化p38MAPK(phosphorylated p38MAPK,p-p38MAPK)表达。结果与正常对照组相比,CDDP诱导AKI模型组肾组织凋亡细胞增加,caspase-3、Bax、p-p38MAPK表达升高,Bcl-2表达降低(P<0.01)。与AKI模型组相比,NAC与SB203580减少凋亡细胞、降低肾脏组织caspase-3、Bax、p-p38MAPK表达和增加Bcl-2表达(P<0.01)。结论 NAC可有效防治CD-DP诱导大鼠AKI,并与p38MAPK相关。     

α-硫辛酸对百草枯中毒大鼠胸腺Bax、Bcl-2表达及SOD活力、MDA水平的影响

目的:研究α-硫辛酸(α-lipoic acid, LA)对百草枯(paraquat, PQ)中毒大鼠胸腺Bax、Bcl-2表达及SOD活力、MDA水平的影响。方法:SD雄性大鼠40只,随机分为4组,分为正常组、模型组、α-硫辛酸低剂量组和α-硫辛酸高剂量组。实验结束后,取大鼠胸腺组织进行HE染色,观察大鼠胸腺组织结构的变化。采用黄嘌呤氧化酶法(羟胺法)测定SOD活力、MDA水平,SABC免疫组化试剂盒检测胸腺组织Bcl-2相关X蛋白(Human Bcl-2 associated X protein, Bax)和重组人B细胞淋巴瘤因子2(B-Cell lymphoma-2, Bcl-2)的表达。结果:模型组胸腺皮质区淋巴细胞呈松散状分布,皮髓质分界较模糊。与正常组比较,模型组大鼠胸腺组织SOD活力显著下降(P<0.01),MDA水平显著升高(P<0.01); Bax和Bcl-2蛋白表达量有所增加(P<0.01)。与模型组比较,LA低剂量组和高剂量组大鼠胸腺组织SOD活力均明显升高(P<0.01),MDA水平明显下降(P<0.01);Bax和Bcl-2蛋白表达量明显减少,Bcl-2/Bax比值明显提高(P<0.01)。结论:LA可能通过增高Bcl-2/Bax比值而抑制胸腺淋巴细胞的凋亡,从而为LA抗氧化损伤治疗PQ中毒的实验方法提供依据。     

JAK2/STAT3信号通路在人参皂苷Re预处理预防异丙肾上腺素致急性心肌缺血损伤中的作用

目的观察人参皂苷Re预处理对异丙肾上腺素致急性心肌缺血大鼠心肌JAK2/STAT3通路的影响。方法应用异丙肾上腺素建立SD大鼠急性心肌缺血模型,将75只大鼠随机分为空白对照组(Control)、模型组(Model)、葛根素对照组(PUE)、Re高剂量组(Re-H,20 mg·kg^-1)、Re低剂量组(Re-L,10 mg·kg^-1)。Moor激光血流成像系统观测各组大鼠心脏表面血流值;ELISA法测定各组大鼠心肌中CK、LDH、SOD、MDA、GSH的含量;免疫组化法检测Bax、Bcl-2蛋白表达;Western blot方法检测各组大鼠心肌JAK、p-JAK、STAT3、p-STAT3蛋白的表达变化。结果与对照组比较,模型组大鼠心脏表面平均血流量明显下降,心肌CK、LDH、MDA含量升高,GSH、SOD含量下降,Bcl-2/Bax比值下降(P<0.05),JAK2/STAT3通路蛋白的表达有所增加;与模型组比较,Re-H组心肌表面平均血流有明显提升(P<0.05);CK、LDH、MDA含量降低,GSH-Px含量升高(P<0.05),Bcl-2/Bax比值上升(P<0.05),JAK2/STAT3通路蛋白的表达明显增强(P<0.05)。结论人参皂苷Re预处理对急性心肌缺血大鼠心肌有较好的保护作用,该作用可能与JAK2/STAT3通路的激活有关。     

黄芪多糖对镉染毒大鼠肾损伤的保护作用

目的探讨黄芪多糖在镉致肾损伤过程中发挥的作用。方法按照随机数字表法将大鼠分为3组,每组12只:空白组、模型组、实验组。模型组和实验组均腹腔注射1.5 mg·kg^-1氯化镉;染毒的同时,实验组给予黄芪多糖20mg·kg^-1,空白组和模型组灌胃等体积0.9%NaCl,干预和染毒每日1次,连续5周。染毒结束后,处死大鼠,摘取大鼠的肾组织,原子吸收分光光度法测定大鼠肾组织的镉(Cd)含量,比色分析法测定大鼠肾组织的超氧化物歧化酶(SOD)活性、乳酸脱氢酶(LDH)活性、谷胱甘肽过氧化物酶(GSH-Px)活性和丙二醛(MDA)含量,ELISA法检测大鼠血清白细胞介素-2(IL-2)含量和转化生长因子-β_1(TGF-β_1)的含量,同时免疫组化法观察肾组织Bcl-2和Bax的蛋白表达。结果空白组、模型组和实验组的IL-2含量分别为(117.38±10.89),(71.82±14.56),(102.46±13.82)pg·mL^-1;这3组的TGF-β_1含量分别为(4.88±0.38),(9.77±0.21),(6.35±0.41)pg·mL^-1;这3组的GSH-Px含量分别为(240.48±18.24),(159.26±21.06),(191.50±23.82)U·g^-1;这3组的LDH含量分别为(1125.25±37.91),(2089.46±35.87),(1159.61±28.86)U·g^-1;这3组的Cd含量分别为(0.02±0.01),(19.68±1.85),(12.99±2.11)mg·kg^-1;这3组的SOD含量分别为(71.55±3.56),(39.30±3.36),(67.25±2.68)U·mg^-1;这3组的MDA含量分别为(3.96±0.79),(7.47±0.78),(5.61±0.99)nmol·mg^-1;这3组的Bcl-2灰度值分别为37.54±3.23,68.43±5.21,38.25±6.17;这3组的Bax灰度值分别为57.87±8.93,27.54±5.45,48.23±3.54。模型组与空白组比较,以上指标差异有统计学意义(均P<0.01);实验组与模型组比较,以上指标差异均有统计学意义(P<0.05或P<0.01)。结论黄芪多糖预处理对镉致大鼠肾氧化损伤存在保护作用,其发挥保护作用是通过调控Bcl-2/Bax蛋白表达实现的。     

藏红花素预处理减轻大鼠胃缺血再灌注损伤作用 与PI3K/Akt信号通路的关系

目的 探讨藏红花素预处理对大鼠胃缺血再灌注(GI-R)损伤的保护作用及其与PI3K/Akt信号通路的关系。方法 采用分离并夹闭大鼠腹腔动脉30 min,去除动脉夹恢复血流1 h的方法制备GI-R模型。健康雄性SD大鼠30只,采用随机数字表法分为5组,每组6只:假手术组(Sham组)、胃缺血再灌注组(GI-R组)、溶剂对照组(Vehicle组)、藏红花素预处理组(crocin组)、藏红花素预处理联合PI3K/Akt信号通路抑制剂LY294002组(crocin+LY组)。记录各组大鼠胃黏膜损伤指数,并采用TUNEL法和免疫组化方法检测胃黏膜上皮细胞凋亡和增殖情况。测算大鼠胃黏膜组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性。蛋白质印迹法(Western Blot)法检测胃黏膜组织Bcl-2,Bax,p-Akt蛋白的表达。结果 成功制备大鼠GI-R损伤模型。与GI-R组相比,crocin组大鼠胃黏膜损伤指数、胃黏膜细胞凋亡率降低;胃黏膜组织MDA含量降低,SOD活性增强;p-Akt的蛋白表达水平增强,且Bcl-2蛋白表达增强,Bax蛋白表达减弱(P＜0.05)。而LY294002可减弱crocin的以上作用(P＜0.05)。结论 crocin对抗大鼠胃缺血再灌注损伤的保护作用机制可能与其上调PI3K/Akt信号通路活性,上调Bcl-2蛋白表达,下调Bax蛋白表达等作用有关。     

Bax/Bcl-2在淋巴回流障碍大鼠肾组织中的表达

目的：探讨阻断肾淋巴循环对大鼠肾脏细胞Bax、Bcl-2表达的影响及与大鼠肾脏功能的关系。方法选取雄性Wistar大鼠48只,将其随机分为模型组和对照组,各24只。各组大鼠分别于术后第1、7、14、28天各处死6只,留取肾组织标本提取组织蛋白、mRNA和制作石蜡切片。运用Real-time PCR、Western blot和免疫组织化学检测Bax、Bcl-2在肾组织中的表达,并测定24 h尿蛋白和血肌酐水平。结果模型组大鼠的肾功能逐渐减退,随着术后时间的延长,肾功能损害逐渐加重。模型组大鼠的Bax表达明显强于对照组,免疫组织化学显示,Bax的表达主要在肾小管及肾间质,远端小管的表达尤其明显,相反,模型组大鼠的Bcl-2的表达明显减弱。结论阻断肾淋巴循环可导致大鼠肾功能及肾小管间质的损害,并随时间延长而加重,肾细胞凋亡与此密切相关,其中Bax/Bcl-2途径发挥了积极作用。     

穴位注射黄芪对哮喘大鼠p38MAPK及Th1/Th2因子的影响

目的 观察哮喘大鼠肺组织p38蛋白激酶（p38 MAPK）和Th1/Th2类细胞因子（IFN-γ/IL-4）表达的变化,探讨穴位注射黄芪对其影响及可能机制.方法 SD大鼠随机分成4组（10只/组）,即正常对照组、哮喘模型组、地塞米松组和黄芪穴位注射组.应用卵蛋白（OVA）致敏激发法制备哮喘大鼠模型,分别采用酶联免疫吸附法（ELlSA）和蛋白质印迹检测血清中IL-4、IFN-γ含量和磷酸化p38 MAPK的变化,并观察肺组织病理学改变.结果 ①与正常对照组相比,哮喘模型组大鼠肺组织磷酸化p38 MAPK表达水平升高,血清IL-4含量升高、IFN-γ含量降低（P＜0.05）;②与哮喘模型组相比,黄芪穴位注射组大鼠血清IL-4含量、磷酸化p38 MAPK表达水平降低,血清IFN-γ含量升高（P＜0.05）;③黄芪穴位注射组与地塞米松组比较血清IL-4含量升高,IFN-γ含量降低,磷酸化p38 MAPK表达水平降低,差异有统计学意义（P＜0.05）;④在肺组织病理学方面,穴位注射黄芪注射液能明显改变哮喘大鼠病理变化;⑤肺组织磷酸化p38 MAPK的表达与IL-4比较呈显著正相关（r=0.596,P＜0.05）,与IFN-y比较呈显著负相关（r=-0.634,P＜0.05）.结论 p38 MAPK可能调控支气管哮喘的发病机制;穴位注射黄芪与糖皮质激素比较,对哮喘大鼠具有保护作用,偏重不一,其治疗作用与抑制p38 MAPK磷酸化、下调IL-4、上升IFN-γ表达水平有关.     

Effects on development

This chapter will review the effects produced on neural development by maternal consumption of cannabinoids during gestation and lactation, with emphasis in the maturation of several neurotransmitter systems (dopamine, serotonin, opioids, cannabinoids, etc.) and possible modifications in their functional expression at the behavioral or neuroendocrine levels. In addition, we have analyzed the possible existence of a sexual dimorphism in these ontogenic effects of cannabinoids, as well as the possible molecular mechanism underlying such effects. In general, the results discussed support the view that exposure to cannabinoids during critical periods of development produces marked modifications in the functional expression of diverse neuronal systems in adulthood. Furthermore, the functions of endocannabinoids in the brain are large not only in adulthood, but also in the period of prenatal and postnatal development. Thus, endocannabinoids have been reported to be present in early ages and to play a role in the process of brain development: neural proliferation and migration, axonal elongation, synaptogenesis and/or myelogenesis.     

美他多辛作用的研究

目的：因美他多辛对乙醇性肝病的生化杌理有积极作用,同时用于急性和慢性乙醇中毒、乙醇性肝病,但该药的致突变作用未见报道。本文在于检测关他多辛致突变性。方法：通过微生物回复突变试验、小鼠微核试验、哺乳动物培养细胞染色体试验证明。结果：美他多辛的三个试验结果均呈阴性。结论：美他多辛在用于治疗急性和慢性乙醇中毒、乙醇性肝病无致突变性。     

益母草治疗痛经机制探索

目的探讨益母草治疗痛经的药理作用及机制.方法经十二指肠给予益母草水提液,观察豚鼠在体子宫收缩频率及幅度的变化.分别采用由缩宫素及15甲基-PGF2α所致的子宫痉挛模型,观察小鼠口服益母草提取液后的作用.采用二甲苯致小鼠耳廓肿胀及实验性大鼠子宫炎症模型,分别观察小鼠、大鼠口服益母草提取液的抗炎作用.用放射免疫法及化学分析法分别检测大鼠口服益母草水提液后血液雌、孕激素及子宫平滑肌PGF2α及PGE2含量的变化.结果益母草水提液能增强未孕正常豚鼠在体子宫的收缩.益母草能在一定程度上缓解由15M-PGF2α及缩宫素所致的小鼠子宫痉挛,能减轻二甲苯所致的小鼠耳廓肿胀的程度,改善实验性子宫炎症状况,且能降低子宫炎症时其平滑肌上PGE2的含量,亦能降低大鼠子宫平滑肌上PGF2α的含量.益母草水提液能升高血液孕激素的水平,而对雌激素却无明显影响.结论益母草对子宫具有比较广泛的药理作用,可能通过抑制痉挛子宫的活动、抗炎、降低子宫平滑肌上PGF2α,PGE2的含量及升高体内孕激素水平等多种途径缓解痛经症状.     

黄芩苷元对炎症反应的影响

目的研究以黄芩苷元为主要成分的黄芩提取物SBM抗炎作用,并初步探讨其作用机制。方法观察SBM体外对PGE2合成、COX-2酶活性,COX-2蛋白表达、p38蛋白磷酸化的影响;观察给药后对角叉菜胶诱导大鼠足肿胀、醋酸诱导的小鼠扭体反应的影响。结果SBM可抑制LPS诱导腹腔巨噬细胞PGE2合成、COX-2酶活性及COX-2蛋白表达;抑制ConA诱导的小鼠脾淋巴细胞p38蛋白磷酸化;并可抑制角叉菜胶诱导的大鼠足肿胀及醋酸诱导的小鼠扭体反应。结论黄芩提取物SBM可通过抑制淋巴细胞功能、炎症介质产生发挥抗炎作用。     

奥氮平对脑电图的影响

目的 :观察奥氮平 (olanzapine)对脑电图的影响。方法 :开放性收集门诊和住院诊断为分裂样精神障碍及精神分裂症的首诊病人 98例 ,男性 65例、女性 3 3例 ,年龄为 (3 7±s1 5 )a,病程为 (3 .6±2 .4)mo,奥氮平 (2 .5～ 1 5mg·d-1)治疗前和治疗后 8wk末分别进行脑电描记术 (electroen cephalography,EEG)描记检查 ;疗效评定用简明精神病量表 (BPRS)。结果 :经 8wk治疗奥氮平对分裂样精神障碍 (2 1例 )、精神分裂症 (77例 )疗效肯定 ,脑电图轻度异常 1 5例 ,轻～中度异常 1 1例 ,异常发生率为 2 7% ,多以慢波增多θ活动散在各导为主 ,未发现有痫样活动。临床也未见病人有抽搐发作。结论 :奥氮平治疗后脑电图异常变化有一定的发生率 ,但异常的程度低 ,不影响其临床应用 ,但长期治疗的安全性需进一步研究     

Effects of caffeine on alertness

The alerting effects of caffeine were assessed using a standard physiological measure of daytime sleepiness/alertness, the Multiple Sleep Latency Test (MSLT). Healthy young men (n=24) were randomly assigned to receive caffeine 250 mg or placebo administered double blind, at 0900 and 1300 hours on each of 2 days. On the 3rd day both groups received placebo to test for conditioning to the alerting effects of caffeine. Each day sleep latency was measured at 1000, 1200, 1400, and 1600 hours and performance (divided attention at 1030 hours and auditory vigilance at 1430 hours) was assessed. Caffeine increased sleep latency (i.e., improved alertness) and auditory vigilance performance compared to placebo. Tolerance to the effects of caffeine on sleep latency developed over the four administrations. On the conditioning test (day 3) the group receiving caffeine the previous two days was more alert and performed better than the placebo group.     

Effects of cannabinoids on neurotransmission

The CB1 cannabinoid receptor is widely distributed in the central and peripheral nervous system. Within the neuron, the CB1 receptor is often localised in axon terminals, and its activation leads to inhibition of transmitter release. The consequence is inhibition of neurotransmission via a presynaptic mechanism. Inhibition of glutamatergic, GABAergic, glycinergic, cholinergic, noradrenergic and serotonergic neurotransmission has been observed in many regions of the central nervous system. In the peripheral nervous system, CB1 receptor-mediated inhibition of adrenergic, cholinergic and sensory neuroeffector transmission has been frequently observed. It is characteristic for the ubiquitous operation of CB1 receptor-mediated presynaptic inhibition that antagonistic components of functional systems (for example, the excitatory and inhibitory inputs of the same neuron) are simultaneously inhibited by cannabinoids. Inhibition of voltage-dependent calcium channels, activation of potassium channels and direct interference with the synaptic vesicle release mechanism are all implicated in the cannabinoid-evoked inhibition of transmitter release. Many presynaptic CB1 receptors are subject to an endogenous tone, i.e. they are constitutively active and/or are continuously activated by endocannabinoids. Compared with the abundant data on presynaptic inhibition by cannabinoids, there are only a few examples for cannabinoid action on the somadendritic parts of neurons in situ.     

Effects of Dexamethasone on Sleep

Abstract: The purpose of this study was to evaluate the effects of acute systemic corticosteroid administration on sleep structure in healthy individuals. We conducted a randomized, prospective, double-blind, placebo-controlled cross-over study of the effects of dexamethasone, 3 mg every eight hours for 48 hr on the sleep architecture of six normal volunteers (mean age 28 years, five males and one female). The subjects were participants blood pressure. Each subject was studied with a full polysomnogram on two successive nights when receiving either placebo or dexamethasone. Only the second night was used for analysis. Placebo and dexamethasone periods were separated by at least two weeks. There were significant increases in the REM latency, percent time spent awake and percent time spent in slow wave sleep in subjects taking dexamethasone when compared to their sleep while taking placebo. There were also significant decreases in the percent time spent in REM and the number of REM periods while on dexamethasone. We conclude that pharmacologic doseas of dexamethasone alter sleep architecture in healthy humans.     

Effects of gamichunggantang on hyperlipidemia

AIM: To evaluate the therapeutic effects of gamichunggantang (GCT) on hyperlipidemia through high cholesterol diet model. GCT is an Oriental herbal medication, which has been used for the treatment of fatty liver, hyperlipidemia or alcoholic liver disease in Daejeon University Oriental Hospital, Korea since 1999. METHODS: Rats were fed with high cholesterol diet for 4 weeks and GCT was administrated for 2 weeks from 2 weeks later in experimental days. The levels of serum total cholesterol, HDL-cholesterol, and triglyceride were analyzed every week. Absolute and relative liver weight to body, and histopathological changes were determined at last day. And, lipid metabolism-related gene expressions (ACAT and DGAT) in liver tissue were analyzed by using RT-PCR. RESULTS: In GCT group, TG levels were reduced at 3 and 4 weeks after GCT administration (39.4 %, P < 0.05 and 36.3 %, P < 0.01 respectively). Total cholesterol levels also were reduced at 3 weeks (20.5 %, P < 0.05) and 4 weeks (35.86 %, P < 0.01) after GCT administration, but HDL-cholesterol levels were increased significantly (P < 0.05) at 3 weeks (14.7 %) and 4 weeks (25.5 %) compared with hyperlipidemia-induced group without GCT. In the GCT treated group, liver weight was lower and lipid accumulation was decreased in histological finding. ACAT gene expression was suppressed compared with hyperlipidemia-induced group but not DGAT. CONCLUSION: GCT possesses preventive or therapeutic effects on diet-induced hyperlipidemia by inhibiting the intestinal absorption and storage of exogenous and endogenous cholesterol.