脑缺血/中药疗法

摘要： [目的]探讨补阳还五汤对脑缺血再灌注大鼠糖原合成酶激酶-3β(GSK3β)mRNA表达与CD63的影响.[方法]将SPF级雄性SD大鼠60只随机分为假手术组,模型组,氢氯吡格雷组,补阳还五汤高、低剂量组,每组12只.氢氯吡格雷组灌胃给予氢氯吡格雷水溶液6.8 mg· kg-1· d-1,补阳还五汤高、低剂量组分别给予补阳还五汤水溶液26、6.5 g·kg-1·d-1,其余各组给予生理盐水;连续给药14 d后,采用右侧大脑中动脉线栓法复制大鼠急性局灶性脑缺血再灌注模型;测定各组大鼠血浆CD63含量与海马组织GSK3β mRNA表达情况.[结果]与假手术组比较,模型组大鼠脑梗死体积显著增加(P＜0.05),.与模型组比较,补阳还五汤组与氢氯吡格雷组均能显著减少脑梗死体积(P＜0.05);与假手术组比较,模型组海马组织GSK3β mRNA表达与血浆中CD63表达均显著升高(P＜0.05);与模型组比较,补阳还五汤高、低剂量组与氢氯吡格雷组均能显著抑制海马组织GSK3β mRNA表达与血浆中CD63表达(P＜0.05),而补阳还五汤高剂量组抑制作用更明显.[结论]补阳还五汤对脑缺血再灌注大鼠的保护作用可能与下调GSK3β mRNA过表达及抑制CD63表达有关.

摘要： [目的]观察补阳还五汤含药血清对体外缺氧缺糖后星形胶质细胞谷氨酸转运体1 (GLT-1)及谷氨酰胺合成酶(GS)蛋白表达的影响.[方法]体外培养新生SD乳鼠大脑星形胶质细胞,采用抗神经胶质纤维酸性蛋白(GFAP)单克隆抗体确认星形胶质细胞.缺氧缺糖2h后,应用Western blot法检测各组星形胶质细胞复氧复糖后各个时间点(12、24、48 h)GLT-1、GS蛋白表达的变化情况,采用谷氨酸试剂盒测定细胞外液谷氨酸浓度.[结果]与正常组比较,缺氧缺糖对照组各时间点星形胶质细胞GLT-1、GS蛋白表达均显著下降(P＜0.05);补阳还五汤含药血清组于复氧复糖24 h后GLT-1、GS蛋白表达均显著上调达到最高水平,与缺氧缺糖对照血清组比较,差异均有统计学意义(P＜0.05);与此一致的是补阳还五汤含药血清组显著降低了24 h后细胞培养液中谷氨酸的浓度(P＜0.05).[结论]补阳还五汤可通过上调星形胶质细胞GLT-1、GS表达促进缺氧缺糖后谷氨酸的转运,进而降低谷氨酸的毒性作用.

摘要： 【目的】观察补阳还五汤对缺氧缺糖（oxygen-glucose deprivation， OGD）损伤PC12细胞凋亡的影响，筛选补阳还五汤中抑制OGD损伤PC12细胞凋亡的主要药味。【方法】将补阳还五汤中7种单味药即黄芪、赤芍、当归尾、地龙、川芎、桃仁、红花作为实验因素，每个因素选取有或无2个水平，按L8（27）正交试验表安排试验。采用OGD细胞模型，运用中药血清药理学方法和流式细胞术技术，以细胞凋亡率为评价指标，利用直观分析和方差分析法，比较空白血清组（有氧+含糖培养基+空白血清）、模型组（缺氧+无糖培养基+空白血清）和补阳还五汤（缺氧+无糖培养基+含药血清）以及各拆方对OGD损伤PC12细胞凋亡的影响。【结果】与空白血清组比较，模型组PC12细胞凋亡率显著增加，差异有统计学意义(P0．05)，含赤芍的拆方细胞凋亡率低于不含赤芍的拆方。【结论】补阳还五汤具有抑制OGD损伤PC12细胞凋亡的作用，其中发挥作用的主要药味为赤芍。%Objective To investigate the protective effect of Buyang Huanwu Decoction ( BYHWD) on PC12 cell apoptosis induced by oxygen-glucose deprivation ( OGD) and to screen out the main ingredients of BYHWD on protecting PC12 cell from injury induced by OGD. Methods Seven herbs of BYHWD were selected as the influencing factors, and they were Radix Astragali, Radix Paeoniae Rubra, the carda part of Radix Angelicae Sinensis, Pheretima Asiatica, Rhizoma Chuanxiong, Semen Persicae, and Flos carthami. Two levels were designed for each factor, and the experiment was arranged according to L8 ( 27) orthogonal test table. Apoptosis of PC12 cells induced by OGD was detected by serum pharmacology method and flow cytometry techniques. With apoptotic rate as the evaluation index, visual analysis and variance analysis were used for the comparison of apoptosis of PC12 cells in the blank control group ( oxygen + sugary medium + blank serum) , model group (oxygen-glucose-free medium + blank serum) and drug groups (oxygen-glucose-free medium +serum containing BYHWD or the separate recipe of BYHWD ) . Results Compared with the blank control group, apoptotic rate was increased in PC12 cells of the model group, the difference was statistically significant ( P<0.01) . Compared with the model group, the apoptotic rate was decreased in BYHWD group, and the differences was statistically significant (P<0.01) . The results of orthogonal analysis showed that Semen Persicae, Flos carthami and Radix Paeoniae Rubra were the main active ingredients of BYHWD on depressing apoptosis of PC12 cell induced by OGD ( P<0.01). The apoptotic rate of serum containing the prescription with Radix Paeoniae Rubra was lower than that of the prescription without Radix Paeoniae Rubra. Conclusion BYHWD could inhibit OGD-induced PC12 cell apoptosis, and Radix Paeoniae Rubra is the main active herb on depressing apoptosis in BYHWD.

摘要： Objective To compare the effect of the decoction and capsule of Buyang Huanwu Recipe ( BHR) on protecting and repairing the neurons with global cerebral ischemia-reperfusion injury, and to explore the anti-oxidization mechanism. Methods Sprague-Dawley male rats were randomized into pseudo-operation group, model group, BHR decoction group (in the dosage of 10 g o kg-1 o d-1 ), and high-, moderate- and low-dosage BHR capsule groups (in the dosage of 7. 56, 3. 78, and 1. 89 g o kg-1 o d-1). Four-vessel occlusion method was used to establish the rat model of global cerebral ischemia-reperfusion injury. The effect of the decoction and capsule of BHR on the repair of pathological morphological structure of the hippocampal CA1 was observed. Meanwhile, serum and cerebral superoxide dismutase (SOD) activity and malondialdehyde content as well as the cerebral water content were measured. Results The decoction and capsule of BHR improved the pathological morphological structure of the hippocampal CA1 , and the effect of the capsule was better. Serum and cerebral SOD activity was increased and MDA content was decreased in the decoction group and the capsule groups (P <0. 01 compared with the model group), and the effect was better in moderate-dose BHR capsule group. Cerebral water content was decreased in the decoction and capsule of BHR groups (P<0. 01) , and the decrease was obvious in high-dosage BHR capsule group. Conclusion The decoction and capsule of BHR can protect the neurons from global cerebral ischemia-reperfusion injury, and the capsule has more reliable effect.%[目的]比较补阳还五汤复方胶囊与原方汤剂保护和修复大鼠全脑缺血再灌注损伤神经细胞的作用,并从抗氧化角度探讨其作用机制.[方法]选用SD雄性大鼠,随机分为假手术组,模型组,补阳还五汤原方汤剂组(剂量为10 g·kg-1·d-1),复方胶囊高、中、低剂量组(剂量分别为7.56、3.78、1.89 g· kg-1·d-1)；采用4血管闭塞法复制全脑缺血再灌注模型,比较补阳还五汤复方胶囊和原方汤剂对海马CA1区病理形态结构的修复程度,并对血清及脑组织超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量及脑组织含水量进行测定.[结果]原方汤剂组及复方胶囊各剂量组对海马CA1区神经元细胞病理形态变化均有康复改善作用,且复方胶囊中剂量组作用最为显著；在血清和脑组织中,原方汤剂组及复方胶囊组均可使SOD活性显著升高,MDA含量显著下降(P＜0.01),且以复方胶囊中剂量组作用最为明显；原方汤剂组及复方胶囊各剂量组均可显著降低脑组织含水量(P＜0.01),其中复方胶囊高剂量组作用最明显.[结论]补阳还五汤原方汤剂及复方胶囊对大鼠全脑缺血再灌注损伤均有保护作用,但复方胶囊疗效更为确切.

摘要： 目的 探讨血塞通( XST)干预治疗SD大鼠全脑缺血/再灌注(I/R)后大脑海马回核因子-κappaB p65( NF-κBp65)的表达,阐明其在全脑I/R损伤后的保护作用.方法 72只健康SD大鼠,随机分为假手术组( SO)24只,全脑I/R组24只,XST治疗组24只.采用简化的Pulsinelli等的四血管阻塞法建立急性全脑I/R损伤及XST对其作用的模型；用HE染色检测海马CA1区存活锥体细胞数目；用TUNEL原位末端标记法检测锥体细胞凋亡率；用免疫组织化学SABC法检测海马CA1区锥体细胞中NF-κB p65的表达.结果 XST组在再灌注后存活锥体细胞数持续增加,且在用药后3、12、24、48 h均明显多于I/R组[(99.23 ±4.22)个/mm vs (75.83±7.17)个/mm,( 80.93±5.36)个/mm vs (51.50 ±8.26)个/mm,(103.24 ±5.48)个/mm vs(35.67±13.17)个/mm,( 126.22±7.54)个/mm vs (9.83 ±4.71)个/mm],差异均有统计学意义(P＜0.01)；XST组各时间点锥体细胞凋亡率与I/R组比较均明显降低[(8.82±2.71)％ vs (22.58±4.68)％,(19.15±6.23)％vs(42.68±3.04)％,(11.82±2.87)％ vs(55.51±6.81)％,(8.44±3.23)％ vs(71.69±7.71)％],差异均有统计学意义(P＜0 01)；XST组各时间点NF-κB p65表达阳性的细胞数均明显少于I/R组[(13.20±2.50) vs(18.00±1.87),( 8.20±5.31)vs(41.60±3.65),(6.70±3.36)vs(55.30±5.10),(7.10 ±3.57) vs (72.80±4.71)],差异均有统计学意义(P＜0.05,P＜0.01).结论 在全脑I/R损伤后,XST可抑制NF-κB p65的表达,抗细胞凋亡,增加存活神经元的数目而起到脑保护作用,从而为XST在脑复苏应用中提供有力的理论依据.%Objective To investigate the expression of NF-κBp65 in hippocampus after the XST intervention therapy in the SD rats with global cerebral I/R injury and testify the protective effect of XST after global cerebral I/R injury.Methods 72 healthy SD rats were randomly divided into 3 groups,sham operation(SO) group ( n =24),I/R group( n =24) and XST group( n =24).The model of acute global cerebral ischemia/reperfusion (including:I/R and XST group) injury was produced by means of simple Pulsinelli- brierley's four arteries occlusion method.H.E.staining was performed to detect the number of surviving neurons and TUNEL was used to detect the rate of neurons apoptosis.The expression activation of NF-κB p65 in hippocampus comu-ammonis ( CA1 ) region were examined by immunohistochemical method (SABC).Results The survival pyramidal neurons in the XST group continued to increase,and it was significantly more than the I/R group at each time-point after reperfusion[ (99.23 ±4.22)/mm vs (75.83 ±7.17 )/mm,(80.93 ± 5.36)/mm vs (51.50 ± 8.26 )/mm,(103.24 ± 5.48 )/mm vs (35.67 ± 13.17 )/mm,( 126.22 ± 7.54 )/mm vs (9.83 ± 4.71 )/mm ],the differences were statistically significant ( P ＜0.01 ).The apoptosis rate of pyramidal cell in the XST group at each time-point were more significantly reduced than the I/R group [ ( 8.82 ± 2.71 ) ％ vs ( 22.58 ± 4.68 ) ％.( 19.15 ± 6.23 ) ％ vs (42.68 ± 3.04 ) ％,( 11.82 ± 2.87 ) ％ vs ( 55.51 ± 6.81 ) ％,( 8.44 ± 3.23 ) ％ vs ( 71.69 ± 7.71 ) ％ ],the differences were statistically significant ( P ＜0.01 ).The positive neurons of NF-κBp65 expression in the XST group at different time-points were significantly less than the L/R group[ ( 13.20 ±2.50) vs ( 18.00 ± 1.87),(8.20 ±5.31) vs (41.60±3.65),(6.70±3.36) vs (55.30±5.10),(7.10±3.57) vs (72.80 ±4.71)],the differences were statistically significant ( P ＜ 0.05,P ＜ 0.01 ).Conclusions After global cerebral ischemia/reperfusion,XST could protect the brain from global cerebral ischemia/reperfusion injury by holding up the expression of NF- kappaB p65,and inhibiting neuronal apoptosis,and increasing the number of surviving neurons.Thus,the results of this experiment could provide a powerful and weighty objective indication for XST being used during cerebral resuscitation.

摘要： Objective To investigate the influence of Naolisu Capsules (NC) on hypoxia inducible factor alpha ( HIF-a) expression in the hippocampus of rats with vascular dementia (VD) induced by chronic ischemia, and to explore the mechanism of NC on improving cognitive disorder in VD rats. Methods SD rats were randomized into sham-operation group, model group, dihydroergotoxine group (in the dosage of 0. 6 mg ? Kg"1 ? D"' ) , and high-and low-dosage NC groups (in the dosage of 2. 50 and 1. 25 g ? Kg"1 ? D~', respectively). VD rats models were established by ligation of bilateral common carotid artery. Morris water maze was used for the examination of learning and memory of VD rats. Immunohistochemical method was applied for the detection of the number of cells with positive expression of HIF-a. Results Learning and memory were obviously improved, and the number of cells with positive expression of HIF-a in the hippocampus was decreased in NC groups (P < 0. 01 compared with those in the model group). Conclusion The therapeutic mechanism of NC for VD is related with the decrease of hippocampal HIF-a expression and with the increase of cellular oxygen concentration in ischemic brain tissue.%[目的]通过观察中药复方脑力苏胶囊对血管性痴呆(VD)大鼠海马低氧诱导因子-1α (HIF-1α)阳性细胞表达的影响,探讨其改善VD大鼠认知障碍的作用机制.[方法]选用雄性SD大鼠90只,随机分为假手术组,模型组,脑力苏高、低剂量组(剂量分别为2.5、1.25g· kg-1·d-1),喜得镇组(剂量为0.6mg·kg-1·d-1)；采用双侧颈总动脉结扎法复制VD大鼠模型,采用Morris水迷宫测试法检测VD大鼠学习、记忆改善状况,免疫组化法检测大鼠海马(CA1区)HIF-1α阳性细胞数.[结果]脑力苏高、低剂量组大鼠学习记忆能力显著改善(P＜0.01),海马HIF-1α阳性细胞表达较模型组显著降低(P＜0.01).[结论]脑力苏胶囊治疗VD的作用与其能降低海马HIF-1α表达,提高缺血脑组织细胞内氧浓度有关.

摘要： 目的:观察黄连解毒汤对小鼠脑缺血慢性神经损伤的保护作用.方法:以大脑中动脉阻塞(MCAO)15 min诱导小鼠短暂性局灶性脑缺血.从术前7 d开始,用药组灌服黄连解毒汤2 g/kg和4 g/kg,实验对照组和假手术组灌服生理盐水,均连续给药21 d,一日一次.缺血后35 d(5周)内进行神经症状评分、斜板试验,并记录小鼠的最终生存率.实验结束后,测定脑损伤体积和神经元数量.结果:黄连解毒汤4 g/kg能显著提高小鼠MCAO术后35 d的最终生存率,2 g/kg和4 g/kg均明显改善术后的神经症状,降低脑梗死体积、减轻脑萎缩.黄连解毒汤4 g/kg可明显增加缺血侧海马CA1区、纹状体和皮层的神经元密度,2 g/kg明显增加缺血侧海马CA1区的神经元密度.结论:黄连解毒汤对小鼠局灶性脑缺血慢性神经损伤有保护作用,能提高小鼠的最终生存率并促进神经功能的恢复.

摘要： Objective To investigate the mechanisms of Chinese traditional medicine mixture protection of vascular endothelial cell from apoptosis in cerebral ischemia-reperfusion injury. Methods Healthy, clean SD rats were randomly divided into 4 groups: Sham opera-tion group (SOG), cerebral ischemia reperfusion injury group (IRG), cerebral ischemia preconditioning group (IPG) and Chinese tradi-tional medicine mixture preconditioning group (CPG). Furthermore, IRG, IPG and NPC were divided into 4 sub-groups: 1 d, 7d, 14d, 21d subgroup, according to the different time point since ischemia-reperfusion took place. And in CPG, Naotai formula extract was used. Cere-bral vascular endothelial cells of rats were removed and Hoechst 33258 staining and the DNA gradient bands were used to detect the apoptosis of these cells. Then the influence of Naotai formula extract on caspase-3, 8 and 9 activation, and Bid lysis was examined by Western-blot, and the mechanisms of Chinese traditional medicine mixture protection of vascular endothelial cell were investigated from apoptosis signal pathway. Result Naotai formula extract can inhibit the apoptosis of endothelial cells in ischemia-reperfusion injury, and it also can inhibit the activation of caspase-3, 8 and 9, thus inhibit the lysis of Bid into tBid. Conclusion Naomi formula extract inhibit the apoptosis of endo-thelial ceils in ischemia-reperfusion injury via apoptosis signal pathway.%目的 从凋亡信号通路探讨中药保护脑缺血再灌注损伤中血管内皮细胞凋亡机制.方法 将64只清洁级SD大鼠随机分为4组(每组16只):假手术对照组、脑缺血再灌注组、脑缺血预处理组和中药预处理组;再将脑缺血再灌注组、脑缺血预处理组和中药预处理组按不同时相分为1、7、14及21 d的4个亚组,中药预处理组应用中药脑泰方提取物进行干预.取大鼠大脑中静脉血管内皮细胞,分别行Hoechst 33258染色后计数以及DNA"梯状"条带检测内皮细胞凋亡情况,再应用Western-blot分析中药脑泰方对Caspase-3,8,9活化和Bid裂解的影响情况;从凋亡信号通路探讨中药保护脑缺血再灌注损伤中血管内皮细胞凋亡机制.结果 中药脑泰方提取物可抑制脑缺血再灌注损伤中血管内皮细胞凋亡,能明显抑制缺血再灌注损伤所致的Caspase-3,8,9活化,也抑制了Bid裂解成tBid.结论 中药脑泰方提取物从凋亡信号通路抑制了脑缺血再灌注损伤中血管内皮细胞凋亡.

摘要： [目的]观察复方海带胶囊(主要由海带、黄芪、川芎等中药组成)对实验性脑缺血的保护作用.[方法]取NIH小鼠40只,随机分为模型组、复方海带胶囊组(剂量为0.38 g·kg-1·d-1)、复方丹参滴丸组(剂量为0.12 g·kg-1·d-1)和尼莫地平组(0.018 g·kg-1·d-1),采用结扎右侧颈总动脉及迷走神经法复制小鼠脑缺血模型,观察复方海带胶囊对模型小鼠脑卒中指数的影响;取SD大鼠70只,随机分为假手术组、模型组、复方海带胶囊低、中、高剂量组(剂量分别为0.095、0.190、0.380g·kg-1)、复方丹参滴丸组(剂量为0.086g·kg-1)和尼莫地平组(剂量为0.013 g·kg-1),采用线栓法复制大鼠大脑中动脉栓塞模型(MCAO),观察复方海带胶囊对模型大鼠神经功能和脑组织含水量的影响.[结果]复方海带胶囊能显著性降低脑缺血模型小鼠的脑卒中指数,降低MCAO模型大鼠的神经功能评分和脑组织含水量(P＜0.05或P＜0.01).[结论]复方海带胶囊治疗脑缺血的机制可能与其改善脑缺血及神经症状,减轻脑水肿的作用有关.

摘要： [目的]观察补阳还五汤预干预对全脑缺血大鼠皮层神经元L型Ca2+通道的影响,探讨Ca2+信号异常参与缺血性神经元损伤的机制及补阳还五汤抗脑缺血的分子机制.[方法]72只SD大鼠随机分为12组,即假手术组(2组)、模型组和补阳还五汤组(此2组各分为缺血再灌注后2、12、24、48、72 h5个时间点组);补阳还五汤各组按0.64 g/kg剂量灌胃,每天2次,连续5 d.除假手术组外,各组均参照改良的Pulsinelli4血管闭塞法复制全脑缺血大鼠模型,缺血后的大鼠分别在存活2、12、24、48、72 h后进行皮层神经细胞急性分离,单通道电流经EPC-9膜片钳放大器放大,采用Pulse&Pulsefit采集入计算机,检测各组大鼠血流再灌注后不同时间点的L型Ca2+通道的平均开放时间和开放概率.[结果]模型大鼠皮层神经元L型Ca2+通道因缺血激活而开放,其开放时间在再灌后各时间点均比假手术组延长,开放概率分别在再灌注2 h和24h时出现高峰;而补阳还五汤组的皮层神经元L型Ca2+通道的开放时间在再灌72 h时比模型组降低(P＜0.01),其开放概率在模型组出现第1个高峰时(再灌2 h)被显著性地降低至与假手术组相仿水平(与模型组比较P＜0.01,与假手术组比较P＞0.05).[结论]补阳还五汤在缺血再灌早期(再灌2 h),主要通过降低L型Ca2+通道开放概率,即影响L型Ca2+通道的可利用性以减少Ca2+内流.而在缺血再灌后期(再灌72 h),主要通过降低L型Ca2+通道开放时间,即影响L型Ca2+通道开放特性以减少Ca2+内流.

摘要： 一种健脾行气中药疗法对术后促进肠内营养的方法，手术后24h，采用口服或经术中放置的胃空肠造瘘置管或经胃肠鼻饲管注入瑞素肠内营养乳剂治疗，同时给予健脾行气中药(药物组成：太子参、山药、麦芽、陈皮、三七)治疗，连续治疗1周。在术后第1天和第8天(即营养疗法前和营养疗法后1d)，观察患者血液中的血红蛋白含量(Hb)、总淋巴细胞计数(TLC)、血清白蛋白(ALB)、血清总蛋白(TP)以及血清白蛋白和球蛋白比值(ρA/ρG)的变化情况。

摘要： 本发明公开了一种猪胃肠燥热津液不足型厌食症的中药疗法，其用以下组方药物进行治疗：郁金5-10份、青皮4-8份、枳实3-5份、橘皮4-6份、丝瓜络3-5份、蒲蒻2-3份、地锦4-5份、丁香4-5份、大黄1-3份、菜菔子3-4份、肉苁蓉3-5份。本发明使用的药物中的各原料通过科学配伍，具有疏肝破气，消积散滞，健胃消食，通便顺气等功效，对治疗猪胃肠燥热津液不足型厌食症有很好的疗效。

摘要： 本发明公开了一种猪脾胃不和型厌食症的中药疗法，其用以下组方药物进行治疗：神曲8-10份、半夏4-5份、芡实3-4份、鸡内金6-8份、生姜3-4份、吴茱萸2-3份、香砂2-3份、炒麦芽4-5份、仙灵脾1-2份、土茯苓3-5份、白术3-5份、桂枝5-7份。本发明使用的药物中的各原料通过科学配伍，具有清热去湿，健脾和胃，止泻和润肠通便等功效，对治疗猪脾胃不和型厌食症有很好的疗效。

摘要： 本发明公开了一种猪脾虚湿困型厌食症的中药疗法，其用以下组方药物进行治疗：当归4‑6份、丹参7‑10份、柴胡10‑12份、藿香7‑9份、白头翁8‑12份、黄连3‑5份、荷叶10‑12份、黄柏5‑10份、地瓜藤12‑14份、鬼针草6‑8份、厚朴6‑8份、紫苏7‑9份。本发明使用的药物中的各原料通过科学配伍，具有健脾利湿、理气散瘀的功效，对治疗猪脾虚湿困型厌食症有很好的疗效。

摘要： 本发明公开了一种猪脾胃虚弱型厌食症的中药疗法，其用以下组方药物进行治疗：白术68份、炙甘草79份、党参24份、白茅根79份、猪苓24份、鱼腥草35份、龙骨24份、甜叶菊79份、陈皮68份、蝉蜕24份、太子参35份、黄芪57份。本发明使用的药物中的各原料通过科学配伍，具有补中益气、养血生津、理气化淤和滋肝健脾等功效，对治疗猪脾胃虚弱型厌食症有很好的疗效。

摘要： 本发明提供了一种治疗热毒血瘀型脑缺血中风的中药注射液，其原料药包括丹参、当归、川芎、赤芍、三七、灯盏细辛、川牛膝、水蛭、地龙、全蝎、郁金、红花、桃仁、姜黄、毛冬青、凌霄花、柿叶、青黛、石菖蒲、连翘、虎杖、牛黄粉、人工熊胆、冰片、麝香、黄连、葛根、栀子、牡丹皮、茵陈、穿心莲、野菊花、金银花、山楂、生大黄和芦荟。该注射液可以直接入血，直达全身，更快，更直接的起效，迅速改善脑缺血灶供血情况，挽救患者生命，提高患者预后质量，通过实验研究，临床研究以及注射剂安全性评估，本发明中药注射液适合于临床推广使用。

摘要： 本发明涉及用于治疗流感病毒疾病的给药疗法，涉及对流感A病毒给药具有中和活性的单克隆抗体的混合组合物而治疗流感病毒相关疾病的方法。本发明的治疗方法通过对流感A病毒将具有中和活性的单克隆抗体的混合组合物进行静脉内给药而能够治疗流感A病毒相关疾病。此外，本发明的治疗方法能够满足针对流感病毒相关疾病的生物治疗剂的尚未满足的医疗需求(unmet medical need)。

摘要： 本发明涉及通过提供药学上有效量的药物化合物的组合来治疗肺结核的方法。

摘要： 一、膏药治疗骨质增生主化骨刺。二、药物组成：地丁、凤仙子、盐肤木根、乳香、没药、祖师麻、草乌、毛茛、洋金花子、芒消。皂角刺、黄丹、透骨草、柳树菌耳、榆耳、研粉。三、生产方法：水煮地丁，过滤再浓缩，先用武火后用文火，用听、看，用筷子挑起清稀如细线时加入众药粉搅拌均匀，此种制法改变了（用油炸温度过高，破坏了中药内的有效成份）此膏药突破了骨质增生。四、方便百姓：讲卫生，不会到处流，减少了患者痛苦，也减少经济负担。五、改进功能：中医界治疗骨质增生，按痹症，祛风散寒，除湿温阳。我用中西医结合，分析骨质增生是缺乏钙类，另外是肾虚，热入骨内，采用补泻兼施，清热化痰，软坚解毒，去骨槽风劳，状骨解表。

摘要： 本实用新型公开一种基于睡药疗法的动物睡药槽装置，包括一槽型睡药槽(1)，睡药槽(1)底部上层为动物固定平台(11)，在动物固定平台(11)上分别设有腹部固定绑带(111)和四肢固定绑带(112)，睡药槽(1)底部下层内设有温度感应器(2)、电源装置(3)以及温度显示控制电路；睡药槽(1)的一垂直侧面上还开设有动物头部固定孔(12)，另一垂直侧面上设有温度显示面板(13)，其中温度感应器(2)通过睡药槽(1)底部内下层的温度显示控制电路与温度显示面板(13)连接。该装置结构简单，易于操作，可实时显示睡药温度，避免睡药污染实验台，有利于药物计量和药效发挥。