松果菊苷对脑缺血大鼠纹状体细胞外液中单胺类神经递质的影响

目的研究松果菊苷(ECH)对局灶型脑缺血大鼠纹状体细胞外液中单胺类递质的影响,以探讨ECH对脑神经保护作用的可能机制。方法 SD大鼠随机分为对照组、模型组、ECH高、低剂量组和川芎嗪(CXQ)组。各组大鼠给予相应的药物或生理盐水腹腔注射,每天1次,连续7 d。给药第3天,脑纹状体埋置探针套管,末次给药1 h后,制作大鼠局灶性脑缺血模型(MCAO),造模后立刻进行微透析,将透析液注入高效液相-电化学检测器(HPLC-ECD)测定各组纹状体细胞外液中去甲肾上腺素(NE)、多巴胺(DA)、5-羟色胺(5-HT)、3,4-二羟苯乙酸(DOPAC)、高香草酸(HVA)、5-羟吲哚乙酸(HIAA)的含量。结果与对照组相比,模型组NE、DA、5-HT水平升高,其酸性代谢产物DOPAC,HVA,HIAA也随之升高。与模型组比较,ECH高、低剂量组(30、15 mg.kg-1.d-1)和CXQ组的6种物质的含量均有所降低。结论 ECH的神经保护作用可能与对抗脑缺血后单胺类神经递质的升高有关。     

脑脉通注射液对全脑缺血及再灌流大鼠脑组织单胺类递质的影响

目的　脑脉通注射液对全脑缺血及再灌流大鼠的脑组织皮层、间脑及延髓的单胺类递质去甲肾上腺素(NE)、多巴胺 (DA)、5 -羟色胺 (5 HT)及 5 -羟吲哚乙酸 (5 -HIAA)的影响。方法　以 4血管法造成大鼠大脑缺血模型 ,应用脑脉通注射液高剂量 (6 .6 7g·kg-1)、中剂量 (3.33g·kg-1)和低剂量 (1.6 7g·kg-1)进行治疗 ,观测其对大鼠脑组织单胺类递质含量的影响及其量效关系。结果　脑脉通注射液能显著增加缺血脑组织NE和 5 -HT的含量 ,纠正DA含量异常 ,对其代谢产物 5 -HIAA有显著的下降作用 ,以中、高剂量总体疗效更佳。结论　脑脉通注射液能显著改善缺血及再灌流后脑组织单胺递质的紊乱状态 ,降低其代谢产物。     

松果菊苷对脑缺血大鼠纹状体细胞外液中氨基酸水平的影响

目的研究松果菊苷(ECH)对急性脑缺血大鼠纹状体细胞外液中4种氨基酸水平和脑梗死率的影响,以探讨ECH对脑神经保护作用的可能机制。方法 SD大鼠随机分为假手术对照组、模型组、阳性药川芎嗪组(CXQ,40 mg.kg-1)、ECH高剂量(ECH 40 mg.kg-1)组、ECH低剂量(ECH 20mg.kg-1)组和ECH配伍冰片(ECH 40 mg.kg-1,冰片400mg.kg-1)组。各组大鼠给予相应的药物或者生理盐水腹腔注射,每天1次,连续7 d。在给药d 3,脑纹状体埋置探针套管,末次给药1 h后,制作大鼠局灶性脑缺血模型(MCAO),模型成功后立刻进行微透析。将透析液注入高效液相-荧光检测器(HPLC-RF),此方法较氨基酸分析仪相比较,具有最低检测限低等特点,检测各组纹状体细胞外液中天门冬氨酸(Asp)、谷氨酸(Glu)、甘氨酸(Gly)、γ-氨基丁酸(GABA)的含量。结果与假手术对照组相比,模型组的Asp、Glu、Gly、GABA水平均明显升高;ECH给药组与模型组相比,ECH高剂量组能明显降低Asp、Glu的水平,而ECH低剂量组与ECH配伍冰片组Asp、Glu降低均不明显;ECH高、低组与配伍冰片组对Gly、GABA的影响均不明显;与模型组相比,ECH高、低剂量组能明显地缩小脑梗死面积。结论 ECH对脑神经的保护作用可能与对抗脑缺血后兴奋性氨基酸升高有关。     

硫酸软骨素对慢性酒精中毒模型大鼠脑组织神经递质的影响研究

目的:探讨硫酸软骨素(CS)对慢性酒精中毒模型大鼠脑组织神经递质的影响。方法:取大鼠随机分为正常对照组、模型组、纳洛酮组(腹腔注射纳洛酮注射液,0.08mg·kg-1·d-1)和CS低、中、高剂量组(灌胃CS,分别为50、100、150mg·kg-1·d-1),每组10只。除正常照组外,其余各组灌胃给于50%乙醇溶液8mL·kg-1·d-12周后,12mL·kg-1·d-16周,建立慢性酒精中毒模型,每天给予乙醇后给予相应药物。造模8周后苏木精-伊红染色法观察各组大鼠神经组织病理学变化,并以高效液相色谱法测定各组大鼠脑组织中单胺类神经递质去甲肾上腺素(NE)、5-羟色胺(5-HT)和多巴胺(DA)的含量。结果:与模型组比较,CS低、中、高剂量组大鼠神经组织病理学损伤程度均降低,NE、5-HT、DA含量均显著降低(P<0.05或P<0.01),且中剂量组最明显。结论:CS可能通过降低慢性酒精中毒模型大鼠脑组织中单胺类神经递质的含量来减轻脑损伤。     

松果菊苷对阿尔采末病大鼠海马、皮质内神经递质水平的影响

目的研究松果菊苷(ECH)对阿尔采末病(AD)模型大鼠海马、大脑皮质细胞外液中单胺类神经递质水平的影响,为ECH改善学习记忆力提供理论依据。方法 60只SD大鼠随机分为模型组、ECH低、中、高剂量组、阳性药石杉碱甲组以及假手术组。采用腹腔内注射D-半乳糖,并在右侧海马内注射Aβ25-35复制AD模型。Morris水迷宫评价各组大鼠学习记忆能力,应用脑双位点双通道同步微透析采样技术,联合运用高效液相-电化学法测定大鼠海马和皮质细胞外液中NA、DA、5-HT的含量。结果水迷宫结果显示,与假手术组相比,AD模型组大鼠逃避潜伏期明显延长(P<0.05),停留在原平台象限时间明显缩短(P<0.05);与模型组相比,ECH低、中、高剂量组均使大鼠学习记忆能力有不同程度的提高,ECH组逃避潜伏期明显缩短(P<0.05),停留在原平台象限时间明显延长(P<0.05)。同时,模型组较假手术组大脑皮质、海马中的NA、DA、5-HT明显降低(P<0.05);ECH组较模型组脑内单胺类神经递质水平恢复至接近正常水平。结论 ECH可以改善AD大鼠学习记忆力,并且明显升高海马、皮质细胞外液中单胺类神经递质的含量,具有一定的抗AD作用。并且ECH中、高剂量组、阳性药石杉碱甲组在提高学习记忆能力方面作用优于ECH低剂量组。     

巴戟天低聚糖对Aβ_(25-35)致拟痴呆模型大鼠学习记忆障碍的影响

目的观察巴戟天低聚糖(oligosaccharides of MorindaOfficinali,OMO)对Aβ25-35致拟痴呆模型大鼠学习记忆障碍的影响。方法采用SD大鼠双侧海马区注射Aβ25-35各10μg制备拟痴呆模型,实验设置空白对照组、假手术组、模型组、阳性药安理申(0.125 mg.kg-1.d-1)组、OMO高剂量(60 mg.kg.d-1)组和OMO低剂量(20 mg.kg.d-1)组。连续灌胃给药25 d后,采用Morris水迷宫进行行为学检测;采用HPLC-ECD法检测脑组织中单胺类神经递质水平;采用HE染色后检测脑组织中海马CA1区锥体细胞和神经元数量,以及大脑皮质和前脑基底核神经元数量等指标。结果水迷宫实验结果显示,Aβ25-35模型组定位航行潜伏期明显长于空白组,其定位航行总路程明显高于空白组,而各给药组潜伏期明显缩短。空间探索实验结果显示,空白组大鼠在第一象限(即平台原所在区域)游泳时间(27.36±3.38 s)长于其他象限,差异具有统计学意义(P<0.05);与空白组比较,模型组在第一象限游泳时间(20.77±5.63 s)明显缩短,OMO高剂量组(31.93±3.39 s)比空白组延长,差异具有统计学意义(P<0.01),其余各组差异没有统计学意义(P>0.05)。与模型组比较,给药组在第一象限游泳时间明显延长,且差异具有统计学意义(P<0.01)。与模型组比较,各给药组单胺类神经递质水平升高;与模型组比较,各给药组海马CA1区椎体细胞和神经元数量增加,以及大脑皮质和前脑基底核神经元计数增多。结论实验结果显示OMO可以明显提高Aβ25-35致拟痴呆大鼠学习记忆能力,其机制可能与提高单胺类神经递质水平和抑制大脑神经元凋亡有关。     

康脑液对脑缺血再灌注动物血管新生的影响

目的：观察康脑液对大鼠局灶脑缺血再灌注损伤后血管新生的影响。方法将雄性SD大鼠随机分为假手术组、模型组、尼莫地平组（1 mg· kg-1· d-1）及高、中、低剂量（24,12,6 g · kg-1· d-1） 康脑液组,线栓法制备大鼠脑缺血再灌注模型。于缺血后2 h再灌注0.5,3,7 d后,处死大鼠,用免疫组织化学法观察脑缺血区微血管密度（MVD）的变化及脑组织血管内皮生长因子（VECF）和肝细胞生长因子（HGF）的表达情况;同时分别于再灌注后2,24,48 h评价动物神经功能。结果与模型组相比,各剂量康脑液组与尼莫地平组的神经功能均明显改善,MVD显著升高,VEGF和HGF蛋白表达明显上调（ P＜0.05或P＜0.01） ,其中以中剂量康脑液组最为显著。结论康脑液增强大鼠局灶性脑缺血后VEGF及HGF的表达,是其抗脑缺血的可能作用机制之一。     

人参、银杏叶提取物对β-淀粉样蛋白_(1-40)毒性损伤大鼠全脑神经递质的影响

目的探讨给予人参、银杏叶提取物(脑维康)前后,β-淀粉样蛋白(β-amyloid peptide,Aβ)1-40毒性损伤大鼠全脑乙酰胆碱、单胺类递质及其代谢产物水平的变化和可能机制。方法以双侧海马CA1区注射Aβ1-40(每侧4 g.L-1)大鼠为模型,给药组大鼠每天灌胃给予脑维康(15.5、31、62mg.kg-1)4 wk。以改进的柱前、柱后双酶柱结合高效液相电化学方法检测大鼠全脑乙酰胆碱含量,以高效液相电化学方法检测大鼠全脑单胺类神经递质及其代谢产物的含量。结果双侧海马注射Aβ1-404 wk后,大鼠全脑乙酰胆碱、5-羟色胺含量明显降低(P<0.05~0.01),多巴胺、去甲肾上腺素表现下降趋势。给药4 wk后,脑维康各给药组大鼠全脑乙酰胆碱含量较模型组大鼠升高(P<0.05~0.01),多巴胺、5-羟色胺水平无变化,高香草酸、5-羟吲哚乙酸水平呈下降趋势,其中脑维康15.5 mg.kg-1组高香草酸含量下降(P<0.05)。结论脑维康可升高Aβ1-40毒性损伤大鼠脑内的乙酰胆碱水平,对单胺类递质代谢有一定的调节作用。该药改善大鼠学习记忆损伤的机制可能与其保护脑内胆碱能和单胺能系统或干预神经递质的合成、摄取和降解等作用有关。     

银杏内酯上调CGRP对大鼠脑缺血再灌注损伤产生保护作用

目的　研究银杏内酯对大鼠局灶性脑缺血再灌注损伤的保护作用与降钙素基因相关肽 (CGRP)的关系。方法　大脑中动脉线栓法 (MCAO)制作大鼠局灶性脑缺血再灌注损伤模型。 6 0只SD♂大鼠随机分为假手术组 (sham)、脑缺血再灌注模型组 (MCAO)、溶媒对照组 (MCAO +vehicle)、银杏内酯低剂量 (MCAO +ginkgolide 10mg·kg-1)、中剂量(MCAO +ginkgolide 2 0mg·kg-1)和高剂量 (MCAO +ginkgolide 4 0mg·kg-1)治疗组 ,每组 10只大鼠。术后对大鼠进行神经缺陷评分 ,并取脑组织测量梗死体积。另 6 0只大鼠 ,分组、实验方法及步骤同上 ,术后取梗死侧脑组织制成匀浆 ,放射免疫法测量脑组织降钙素基因相关肽和内皮素(ET)含量。结果　银杏内酯能明显改善缺血再灌注损伤大鼠神经缺陷症状 ,缩小脑梗死体积 ,剂量依赖性升高缺血脑组织中已降低的CGRP含量和CGRP/ET值。结论　银杏内酯升高缺血脑组织中CGRP含量 ,使缺血脑组织中比例失衡的CGRP/ET值向正常恢复 ,可能是银杏内酯对缺血脑组织产生保护作用的机制之一     

康脑液对脑缺血大鼠Fas、FasL蛋白表达的影响

目的观察康脑液对脑缺血再灌注损伤大鼠Fas、FasL蛋白表达的影响。方法线栓法制作大鼠脑缺血再灌注模型,将雄性SD大鼠随机分为假手术组、模型组、依达拉奉组(2.7 mg·kg-1)、康脑液高、中、低(24,12,6 g·kg-1.d-1)剂量组;于缺血后2 h再灌注3,6,12,24,48 h后处死,用免疫组化法观察Fas、FasL蛋白的表达。结果与模型组比较,康脑液高、中、低剂量组均能明显下调Fas、FasL蛋白的表达(P<0.05或P<0.01)。结论康脑液可通过抑制Fas、FasL蛋白的表达,减轻脑缺血后神经功能损伤,从而保护脑组织。     

脑缺血再灌注小鼠脑内不同神经核团单胺递质及其代谢产物的变化

目的　测定脑缺血再灌注后小鼠脑内不同神经核团单胺递质及其代谢产物的动态变化。方法　阻断小鼠双侧颈总动脉 (CCAO)进行缺血再灌 ,于术后当天 (d 0 )及d 1、3、5、2 0用HPLC ECD动态检测小鼠海马 ,纹状体 ,皮层的神经递质及其代谢产物的变化。结果　与假手术对照组相比 ,脑缺血再灌注小鼠术后上述神经核团去甲肾上腺素 (NE) ,多巴胺 (DA) ,5 羟色胺 (5 HT)等神经递质及其代谢产物含量降低 ,其中海马表现尤为明显。结论　脑内多个神经系统参与了脑缺血再灌注小鼠的病理过程 ,小鼠海马对缺血损伤最为敏感。提示脑缺血再灌注后海马神经递质异常是其后期行为表现的物质基础 ,是临床治疗中应予以重视的靶点     

阿米替林对局灶性脑缺血/再灌注损伤脑内单胺类神经递质的影响

目的研究阿米替林对大鼠局灶性脑缺血/再灌注损伤的作用。方法用线栓法建立大鼠局灶性脑缺血/再灌注损伤模型,用TTC染色和图像分析系统测梗死体积;神经功能缺损采用0～5级评分;荧光分光光度法测定大脑皮层和纹状体多巴胺(DA)、去甲肾上腺素(NE)、5-羟色胺(5-HT)及5-羟吲哚乙酸(5-HIAA)。观察阿米替林对大鼠局灶性脑缺血1h/再灌注2h时脑梗死体积、神经功能及大脑皮层和纹状体单胺类神经递质的影响。结果缺血1h/再灌注2h时,阿米替林可使脑梗死体积变小、神经功能缺损评分分值明显降低、单胺递质含量明显提高,与模型组相比差异有显著性。结论阿米替林对大鼠局灶性脑缺血/再灌注引起的神经损伤有保护作用。其机制可能与其减少缺血/再灌注期间单胺类神经递质的释放有关。     

对氨基水杨酸钠对氯化锰染毒大鼠脑单胺递质的影响

本文报道了对氨基水杨酸钠(PAS-Na)对氯化锰腹腔注射染毒大鼠脑单胺递质水平的影响。PAS-Na能使锰染毒所降低了的脑多巴胺(DA)水平逆转;锰使脑去甲肾上腺素(NE)含量增加,染毒后以PAS-Na治疗则使之进一步升高;锰染毒和染毒后治疗组的5-羟色胺(5-HT)及5-羟吲哚醋酸(5-HIAA)的变化与DA相似,但PAS-Na使5-HT、5-HIAA水平升高的幅度大都较NE和DA的要小,提示5-HT能神经元对PAS-Na治疗作用的敏感性低于儿茶酚胺(CA)能神经元。     

Effects of prenatal and postnatal exposure to amitraz on norepinephrine, serotonin and dopamine levels in brain regions of male and female rats

The effects of maternal exposure to amitraz on brain region monoamine levels of male and female offspring rats at 60 days of age were observed. Maternal and offspring body weight, physical and general activity development were unaffected by the exposure of dams to amitraz (20mg/kgbw, orally on days 6-21 of pregnancy and 1-10 of lactation). Male and female offspring were sacrificed at 60 days of age and possible alterations in the content and metabolism of NE, DA and 5-HT were determined in brain regions by HPLC. The results showed that all these neurotransmitter systems were altered in a brain regional-related manner. In male and female offspring, amitraz induced a significant decrease in the prefrontal cortex 5-HT and its metabolite 5-HIAA and DA and its metabolites DOPAC and HVA levels with interaction of sex. Nevertheless, we verified that striatum DA and 5-HT and corresponding metabolite contents decreased in male and female offspring without statistical distinction of sex. In contrast, amitraz did not modify 5-HT content, but caused an increase in 5-HIAA content in the medulla oblongata and hippocampus in male and female offspring. Alterations in the hippocampus DA, DOPAC and HVA levels after amitraz exposure were also observed displaying a sex interaction. NE levels also showed a decrease after amitraz treatment in the prefrontal cortex and striatum without statistical sex interaction, but MHPG levels decreased in both regions with a sex interaction. Amitraz evoked increases in 5-HT turnover in the prefrontal cortex as well as in DA turnover in the striatum and hippocampus but decreases in NE turnover in the hypothalamus, prefrontal cortex and striatum. The present findings indicated that maternal exposure to amitraz altered noradrenergic, serotonergic and dopaminergic neurochemistry in their offspring in the prefrontal cortex, striatum and hippocampus, and those variations could be related to several alterations in the functions in which these brain regions are involved.     

Kainic acid-induced changes of serotonin and dopamine metabolism in the striatum and substantia nigra of the rat

Levels of the putative neurotransmitters serotonin (5-HT) and dopamine (DA) and their respective metabolites 5-hydroxyindoleacetic acid (5-HIAA) and dihydroxyphenylacetic acid (DOPAC) was determined in the rat striatum after unilateral intrastriatal injection of the convulsive neurotoxin kainic acid. Two days after intrastriatal kainic acid injection, levels of the 5-HT metabolite 5-HIAA were increased by abut 200% in the injected striatum and by about 150% in the contralateral striatum. An elevated striatal 5-HIAA content was still detectable 10 days after the kainate lesion, but approached normal values 10 weeks after the injection of the neurotoxin. Two days after the lesion, but not at the other time intervals, a moderate increase of 5-HIAA also occurred bilaterally in other brain areas such as the substantia nigra, frontal cortex and hypothalamus. Levels of 5-HT were decreased significantly in the injected striatum 2 days after the intrastriatal application of kainic acid and increased by about 40% after 10 weeks. The 5-HT concentration in the contralateral striatum or in the three other brain areas examined was unchanged at all time intervals. Levels of the DA metabolite DOPAC and DA turnover were increased in the lesioned striatum 2 days after kainic acid injection; concomitantly the DOPAC level was increased in the substantia nigra of the contralateral side. DOPAC levels of the contralateral striatum were unchanged or slightly reduced 2 days after the injection. Ten days as well as 10 weeks after the lesion there was a slightly increased DOPAC concentration in both striata. The levels of DA were not altered at any time interval after the injection of kainic acid.     

Effects of Panax ginseng root on the vertical and horizontal motor activities and on brain monoamine-related substances in mice

Effects of the Panax ginseng root (PGR) on spontaneous motor activity (vertical and horizontal motor activities), and on monoamine-related substances (tyrosine, DA, DOPAC, 3-MT, HVA, NE, MHPG, tryptophan, 5-HT, and 5-HIAA) in discrete brain areas (cerebral cortex, hippocampus, hypothalamus, corpus striatum, limbic lobe, midbrain, cerebellum, and medulla oblongata) of ddY male mice (weighing 18-22 g) were examined using an infrared photo-cell counter and HPLC with electrochemical detection. PGR (100 mg/kg) was orally administered, twice a day, for 2 successive weeks (2W-group) or 7 successive weeks (7W-group). Vertical and horizontal motor activities increased significantly in the 7W-group but not in the 2W-group when compared to those of the control group. As to brain monoamine-related substances, the metabolism of DA and NE in the cerebral cortex and of 5-HT in the corpus striatum and cerebellum in the 2W-group were facilitated, while metabolism of DA in the corpus striatum and of 5-HT in the hypothalamus and midbrain were inhibited. In the 7W-group, except for a facilitated metabolism of 5-HT in the cerebellum, metabolism of DA, NE and 5-HT in all discrete brain areas were inhibited. These results show that PGR exerts an influence on the CNS.     

Cocaine and regional brain monoamines in mice.

Cocaine HCl (0, 10, or 50 mg/kg) was injected into adult male ICR mice IP. Thirty minutes later, brains were removed and nine regions were isolated: olfactory bulbs (OB), olfactory tubercles (OT), prefrontal cortex (PC), septum (SP), striatum (ST), amygdala (AMY), hypothalamus (HT), hippocampus (HC), and thalamus (TH). Using high-performance liquid chromatography, concentrations of norepinephrine (NE), dopamine (DA), serotonin (5-HT), and their major metabolites were determined. At 10 mg/kg cocaine, NE levels were increased in the AMY and its metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), was decreased in the PC, AMY, and HT. DA levels were also increased in the AMY, while its intracellular metabolite, dihydroxyphenylacetic acid (DOPAC), was decreased in the ST and its extracellular metabolite, homovanillic acid (HVA), was decreased in the PC. 3-Methoxytyramine (3-MT) levels were not altered in any tissue. 5-HT levels were increased in the AMY, HT, and TH, while its metabolite 5-hydroxyindoleacetic acid (5-HIAA) was decreased in the OB and ST. MHPG/NE ratios were decreased in the PC, AMY, and HT as were those for HVA/DA. DOPAC/DA ratios were decreased in the ST and AMY and increased in the SP while those for 3-MT/DA were decreased in the TH and increased in the PC. 5-HIAA/5-HT ratios were decreased in the AMY, HC and TH. At 50 mg/kg cocaine, there was an increase in DA in the TH. There was a decrease in DOPAC, HVA, and 3-MT, as well as the DOPAC/DA ratio in the ST. In the OT, there was a decrease in DOPAC, the DOPAC/DA ratio, 3-MT, and the 3-MT/DA ratio.(ABSTRACT TRUNCATED AT 250 WORDS)     

Anti-emetic mechanisms of Xiaobanxia Tang decoction on the chemotherapy-induced pica model in rats

OBJECTIVE To investigate the mechanisms of Xiaobanxia Tang(XBXT)in the prevention and treatment of chemotherapy-induced nausea and vomiting.METHODS The chemotherapy-induced rat pica model was established by intraperitoneal injection of cisplatin 6mg·kg-1.Kaolin consumption was used as an indicator of nausea and vomiting.Wistar male rats were randomly divided into normal control,XBXT normal control,model,ondansetron treating,XBXT decoction high and low dose groups.The rats in ondansetron group,XBXT normal control group,XBXT high and low dose groups were gavaged ondansetron 2.6mg·kg-1·d-1,XBXT 1.6,3.2and 1.6g·kg-1·d-1,respectively 1hbefore cisplatin injection,and the administration were given every 12 h.Kaolin consumptions were weighed every 12 h.After 24 hand 72hof cisplatin injection,animals were sacrificed respectively.The contents of 5-HT,5-HIAA,dopamine(DA),DOPAC,substance P(SP),TPH,MAO and TH were measured by ELISA.The mRNA expression of 5-HT transporter(SERT),5-HT3 Areceptor,SP precursor(PPTA),NK1 and D2receptors in rat ileum and medulla oblongata were measured by RT-PCR,the protein expression were measured by Western blotting.RESULTS The high and low dosages of XBXT could significantly inhibit kaolin consumptions in cisplatin-treated rats,and reduce5-HT,increase 5-HIAA contents and reduce 5-HT3 Areceptor mRNA and protein expression,above effects are related to the reduction of TPH and the enhancement of MAOA levels.The two dosages of XBXT could significantly reduce SP and NK1 mRNA and protein expression,which was related to the reduction of PPTA mRNA expression.XBXT could also significantly reduce DA contents and D2 receptor mRNA and protein expression,which was related to the reduction of TH.CONCLUSION XBXT has significant antiemetic effect in chemotherapy-induced nausea and vomiting,the underlying mechanisms are related to the inhibition of 5-HT and5-HT3 Areceptor,SP and NK1 receptor,DA and D2 receptor.