Objective To study the influences of dihydromyricetin ( DMY) on inflammatory reaction induced by fo-cal cerebral ischemia-reperfusion ( I/R) injury in mice.Methods Male Kunming mice were randomly divided into 3 groups:sham group,I/R group and DMY 500 mg/kg group.Mice model of middle cerebral artery occlusion (MCAO,3 h)/reperfusion (24 h) model was established by the improved intraluminal filament technique .Drugs were given orally 10 d (once a day ) before the surgery ,1 h before ischemia and 12 h after reperfusion .After reperfusion for 24 h,the expressions of ionized calcium binding adaptor molecule-1( Iba1) and 5-LOX in mice brain were assessed by immunohistochemistry;the contents of TNF-αand 5-LOX metabolites ( LTB4 and CysLTs ) in ischemic brain tissue were detected by ELISA .Results Compared with the I/R group,DMY at 500 mg/kg could obviously inhibit the activation of microglia ,lower the level of TNF-α,and reduce the expression of 5-LOX and the production of LTB4 and CysLTs (P<0.05或P<0.01).Con clusion DMY reduces inflammatory reaction induced by focal cerebral I /R injury,which might be associated with its inhibition on 5-LOX.

Objective To investigate the antioxidation effects of epigallocatechin gallate( EGCG) on daunorubicin( DNR)-induced myocardial injury in mice. Methods The Kunming mice were randomly divided into blank control group,model group,high dose EGCG group( 80 mg / kg),low dose EGCG group( 40 mg / kg). The mice in the blank control group and model group were given equal volume of saline by lavage. Seven days after treatment,the mice in each group were injected with DNR at a dose of 15 mg / kg except in blank control group. Forty-eight hours later,the superoxide dismutase( SOD) activity and malondialdehyde( MDA) content in serum and myocardium of mice were detected in each group. Results The serum MDA content of mice in the model group was significantly higher than that in the blank control group( P 0. 05),and the SOD activity of mice in the model group was significantly lower than that in the blank control group( P 0. 05). The serum MDA content of mice in the high and low dose EGCG groups was significantly lower than that in the model group( P 0. 05),and the serum SOD activity of mice in the high and low dose EGCG groups was significantly higher than that in the model group( P 0. 05). The myocardial MDA content of mice in the model group was significantly higher than that in the blank control group( P 0. 01),and the SOD activity decreased significantly in the model group( P 0. 05). The myocardial MDA content of mice in the high and low dose EGCG groups was significantly lower than that in the model group( P 0. 05),and the myocardial SOD activity of mice in the high dose EGCG group was significantly higher than that in the model group( P 0. 05). Conclusion EGCG plays an antioxidation role in the prevention of DNR-induced myocardial injury in mice.

Objective To investigate the protective effects of (-)-epigallocatechin gallate ( EGCG ) on daunorubicin ( DNR)-induced cardiotoxicity in mice. Methods The qualified mice were randomly divided into four groups:normal control group, myocardial injured model control group,high dose group (80 mg·kg-1 ) and low dose group (40 mg·kg-1 ) of EGCG. EGCG was administered intragastrically once daily for 7 days,followed by a single intraperitoneal injection of DNR (15 mg·kg-1 ) except in the normal control group. The electrocardiogram,myocardial enzymes and TNT-Hs in serum,cardiac ultrastructure of mice were detected after 48 h. Results In DNR model control group,the incidence of arrhythmia was 64. 7%. The activity of serum cardic enzymes including CK,CK-MB,LDH,α-HBDH and ALT,AST, level of TNT-Hs were significantly higher than those in the normal control group(P<0. 01),and myocardial ultrastructure was injured remarkably. The incidence of arrhythmia was 44. 4% in mice treated with high dose of EGCG and 31. 6% in mice with low dose of EGCG. Compared to the model control group, the activity of CK,CK-MB,LDH,α-HBDH and ALT,AST, level of TNT-Hs in serum decreased remarkably in EGCG groups( P<0. 05 or P<0. 01). Low can EGCG alleviated the injury to the ultrastructure of myocardium compared to the model control group. Conclusion EGCG can prevent the cardiac toxicity induced by DNR in mice.

通过大剂量给药,观察小鼠出现的毒性反应及死亡情况,考察鲜罗汉果素应用的安全性。方法：用昆明小白鼠进行急性毒性试验,鲜罗汉果素小鼠灌胃给药40mL/kg体重,24h内分3次灌胃给药,药后正常饲养,连续观察7d。结果：鲜罗汉果素小鼠灌胃给药剂量达到24g/kg,未见其它异常表现,亦无动物死亡。结论：鲜罗汉果素急性毒性较低,是一种基本无毒的物质,应用较安全。

Objective To study the effects of vitamin B_6(VitB_6) injection on small intestinal peristalsis in mice and its mechanisms.Methods The mice were divided into 12 groups:calcium chloride injection group(1 mg/10 g),neostigmine methylsulfate injection group(0.001 5 mg/10 g),atropine sulfate injection group(0.005 mg/10 g),their combination with VitB_6 injection and high/low dose treated groups,high dose VitB_6 injection group(5 mg/10 g),low dose VitB_6 injection group(0.5 mg/10 g) and physiologic saline group(0.1 mL/ 10 g ).After administration 30 minutes,mice were intragastric administration Indian ink(0.1 mL/g),and they were luxated and put to death 20 minutes later.The mice belly were cut open,the length of intestine and distance of Indian ink that had moved were measured,and then the ink progradation rate were calculated.Results Compared with control group,the high dose VitB_6 injection could inhibit normal intestinal peristalsis of mice markedly(P0.01).Both of high dose and low dose VitB_6 injection could inhibit the excited action of calcium chloride significantly( P_a 0.01),and high dose VitB_6 injection could enhance the inhibited action of atropine(P0.01).Both of high dose and low dose VitB_6 injection had antagonistic effect on the excited action of proserine methylsulfate,but it was not statistically significant(P_a0.05).Conclusions VitB_6 injection can inhibit hyperanakinesia of small intestine in mice,especially high dose.And this will be provided as theory foundation on enterospasm treatment.

目的:研究火麻油软胶囊的毒性作用,指导临床用药。方法:采用最大耐受量测定法及长期连续给药法分别观察其急性毒性和长期毒性。结果:最大耐受量为40ml/kg·d-1;长期毒性试验结果显示,大鼠的一般情况、体重、血常规、肝肾功能及病理学检查等与对照组比差异无统计学意义(P>0·05)。结论:火麻油软胶囊无毒性作用。

Objective To study the effects of Compound Di Gui Capsule (CDGC) on the levels of glucose and lipid in diabetic rats.Methods Rats models with diabetes mellitus were induced by intraperitoneal injection of streptozotocin (50mg·kg-1).Then the diabetic rats were divided into different groups at random.CDGC groups were given CDGC in the dosages of 2.4,1.2,0.6 g·kg-1·d-1 respectively by gastric gavage for 90 d.Levels of whole blood glucose,glycosylated hemoglobin,total cholesterol (TC),triglyceride (TG),low-density lipoprotein cholesterol (LDL-C),high-density lipoprotein cholesterol (HDL-C),nitric oxide (NO),total antioxidation capacity (T-AOC) were determined.The insulin level and the pathological changes of pancreatic tissues were also observed.Results The glucose level of diabetic rat was decreased 2h after administration.After administration of CDGC for 90d,the glycosylated hemoglobin,TG,LDL-C and NO were markedly decreased,islet βcells were protected and restored,and the insulin level and T-AOC were increased.Conclusion CDGC can regulate the metabolism of glucose and lipid in diabetic rats,and can protect and restore the pancreatic islet cells.

目的:分析复方鸡骨草胶囊对四氯化碳、D-半乳糖胺所致小鼠急性化学性肝损伤的保护作用。方法:实验于2006-01/03在广西医科大学药学院药理学教研室实验室完成。取健康成年昆明种系小鼠144只,按随机数字表法分为12组,每组12只。分为2个实验,四氯化碳和D-半乳糖胺肝损伤实验均设6个组,正常对照组、模型组、鸡骨草胶囊组、复方鸡骨草胶囊12.96g/kg,6.48g/kg,3.24g/kg组。鸡骨草胶囊组和复方鸡骨草胶囊12.96g/kg,6.48g/kg,3.24g/kg组分别灌胃给予鸡骨草胶囊14.47g/kg和复方鸡骨草胶囊（鸡骨草胶囊的升级产品,由鸡骨草、茵陈、栀子、三七、牛黄、白芍等多种中草药配伍组成）12.96,6.48,3.24g/kg,其余各组小鼠灌胃给予等量生理盐水,灌胃1次/d,连续5d。5d后除正常对照组外,其余各组腹腔注射1g/L的四氯化碳/花生油溶液10mL/kg或腹腔注射D-半乳糖胺800mg/kg,禁食,16h后测定血清谷丙转氨酶和谷草转氨酶活性,观察肝脏组织病理学改变。结果:144只小鼠全部进入结果分析,无脱失。四氯化碳和D-半乳糖胺肝损伤2个实验中,鸡骨草胶囊组和复方鸡骨草胶囊12.96g/kg,6.48g/kg组小鼠的血清谷丙转氨酶和谷草转氨酶活性显著低于模型组（P＜0.05～0.01）,鸡骨草胶囊和复方鸡骨草胶囊各剂量组肝组织受损程度显著轻于模型组（P＜0.05～0.01）,复方鸡骨草胶囊各剂量与鸡骨草胶囊的效应比较,差异无显著性意义（P＞0.05）。结论:复方鸡骨草胶囊对四氯化碳、D-半乳糖胺引起的小鼠急性化学性肝损伤均有明显的保护作用,保肝效应和鸡骨草胶囊相当。

Objective To explore the effects of extract of Gingko biloba leaves (EGb) on learning, memory and hippoeampal heine oxygenase-1 (HO-1) expression in diabetic rats.Methods The behaviors of streptozotoein-induced diabetic rats were observed by Morris water maze for learning and memory after 6 months of diabetes.The HO-1 mRNA expression and protein expression in hippocampus of diabetic rats were detected by RT- PCR and immunohistochemistry respectively.Results The escape latency time in Morris water maze of diabetic rats was prolonged markedly.HO-1 mRNA and HO-1 protein expressions in hippocampus of diabetic rats were increased (1.635±0.326 vs 0.978±0.214,7.2±1.7 vs 1.9±0.5,respectively,both P＜0.01).The escape latency times in EGb (100,50 mg/kg) treated groups were shortened.HO-1 mRNA and HO-1 protein expressions in hippocampus were decreased at the same time as compared with diabetic group (100 mg/kg:0.954±0.144,2.0±0.8;50 mg/kg:0.988±0.154,2.5±0.6,all P＜0.01).Conclusion EGb can significantly inhibit HO-1 expression in hippocampus and improve learning and memory dysfunction in diabetic rats.

Aim To study the protective effects of Xinnaoshenkang (XNSK) against focal cerebral injury caused by ischmia-reperfusion in rats and its mechanism. Methods The focal brain ischmia-reperfusion model in rats was made through by using an intraluminal monofilament to occlude the middle cerebral artery for 1.5 h and then reperfusing for 24h.Spectrophotometric assay was used to measure the contents of malondial-dehyde (MDA), lactic acid (LA),superoxide dismutase(SOD), reactive oxygen species(ROS), nitricoxide synthase(NOS) and several ATPase in cerebral cortex homogenates from rats. The effects on platelet aggregation were also observed. Results Compared with model and positive control groups,88,175,350 mg·kg-1 XNSK groups were found having significant inhibition of cerebral infarction,MDA,LA,ROS,NOS,platelet aggregation and significant increase of the activity of SOD,ATPase. Conclusion XNSK has protective effects against focal cerebral injury caused by ischmia-reperfusion in rats.

To investigate whether long term administration of Shenguangyuan granule to rats has toxicity. The Wistar rats were divided into three groups, and the dosage of 3.6g/kg, 7.2g/kg, and 14.48g/kg were perfused respectively to the three groups for 6 months. These dosages were 20,40 and 80 times more than the clinical dosages respectively. 6 months later after discontinuation, all the body weights, hematological or biochemical indexes, both relative weight and morphologies of heart, liver, spleen, lung, kidney, brain, testis and uterus were tested.No evident abnormal change of every index was observed in every group.[Conclusion]Long term administration of Shenguangyuan granule to rats was safe.

目的:探讨神曲胃痛片抗实验性胃溃疡的影响.方法:采用小鼠应激性胃溃疡、小鼠烧灼性胃溃疡、大鼠幽门结扎性胃溃疡和大鼠利血平性胃溃疡的模型,观察神曲胃痛片对溃疡的影响,同时在幽门结扎性胃溃疡模型中观察其对胃液量、胃蛋白酶活性、胃液游离酸酸度的影响.结果:神曲胃痛片可明显抑制应激性、幽门结扎性和利血平性胃溃疡的形成,且可促进烧灼性胃溃疡的愈合,对胃酸酸度和胃蛋白酶活性有明显的抑制作用.结论:神曲胃痛片具有明显的抗实验性胃溃疡作用.

目的:探讨心脑肾康对大鼠肾缺血再灌注损伤的保护作用.方法:通过结扎双肾动脉60 min后再灌注,建立大鼠肾缺血再灌注损伤的模型.化学法观察大鼠血清肌酐(Scr)、尿素氮(SUN)、丙二醛(MDA)含量,肾组织内MDA和超氧化物歧化酶(SOD)的变化.结果:与模型对照组比较,0.8 g/kg的心脑肾康高剂量可抑制由肾缺血再灌注引起的血清SUN、Scr、MDA含量和组织内MDA含量的变化,增强SOD的活性.结论:心脑肾康有保护大鼠肾缺血再灌注损伤的作用,其作用机制可能与抗自由基损伤有关.

目的:研究银杏叶提取物(EGb)对糖尿病大鼠行为学及大脑皮层和海马Na+-K+ATP酶活性的影响.方法:腹腔注射佐链霉素55 mg/kg建立糖尿病模型,以旷场分析法和Morris水迷宫法考察各组大鼠学习记忆能力,检测大脑皮层和海马的Na+-K+ATP酶活性.结果:大鼠糖尿病6个月后,旷场分析示中央格停留时间延长、探洞次数较少,Morris水迷宫实验示逃避潜伏时间延长、搜寻平台策略成绩降低,大脑皮层和海马的Na+-K+ATP酶活性明显下降.EGb可明显升高Na+-K+ATP酶活性(P＜0.05或P＜0.01),缩短中央格停留时间、水迷宫实验逃避潜伏期时间(P＜0.05或P＜0.01),提高探洞次数和搜寻平台策略成绩(P＜0.05或P＜0.01).结论:EGb可提高糖尿病大鼠大脑皮层和海马的Na+-K+ATP酶活性,改善学习记忆能力.

目的:探讨鹅掌藤浸膏口服给药的镇痛和抗炎作用.方法:选用甲醛致痛法、热板法观察鹅掌藤浸膏镇痛作用,选用角叉菜胶致炎法、巴豆油致炎法、棉球肉芽肿和弗氏完全佐剂性关节炎以及腹膜毛细血管通透性实验法观察其抗炎作用.结果:鹅掌藤浸膏能显著提高小鼠热痛阈值,减少甲醛所致大鼠痛反应分值;对角叉菜胶所致大鼠足肿胀有明显的抑制作用,能减轻巴豆油所致小鼠耳廓肿胀度,抑制小鼠棉球肉芽肿的形成,减轻弗氏完全佐剂所致的大鼠佐剂性关节炎肿胀度,对醋酸所致的小鼠毛细血管通透性增加也有明显的抑制作用.结论:鹅掌藤浸膏口服给药有明显的镇痛、抗炎作用.

目的:了解化瘤灵(HLL)胶囊抗小鼠移植性肿瘤的作用.方法:以小鼠S180肉瘤、小鼠肝癌(Hep A)为瘤株,观察化瘤灵胶囊对肿瘤的抑制作用.结果:化瘤灵对小鼠S180实体瘤和肝癌实体瘤均有明显的抑制作用,抑瘤率分别为49.3%、52.3%,并有延长Hep A腹水型荷瘤小鼠生命的作用,生命延长率为44.83%.小鼠急性毒性最大耐受量(MTD)为50g/kg.结论:化瘤灵在实验室条件下有一定抗肿瘤作用且毒性低.

目的:研究蛤蚧补肾丸(胶囊)的补肾壮阳作用.方法:采用去势大鼠制作肾虚模型,观察蛤蚧补肾丸(胶囊)补肾壮阳作用;观察蛤蚧补肾丸(胶囊)对氢化可的松诱发阳虚小鼠的保护作用及对大鼠交配能力的影响.结果:蛤蚧补肾丸(胶囊)可提高肾虚(去势大鼠)包皮腺的脏器指数,并可延长肾虚大鼠阴茎勃起的持续时间;蛤蚧补肾丸(胶囊)对正常大鼠的交配能力有一定的提高作用,对正常大鼠提肛肌的脏器指数有明显的提高作用,同时使血清睾丸酮的水平也比正常对照组提高17.99%-45.92%,并对于氢化可的松造成小鼠阳虚症状表现体温、自主活动和耐寒能力的下降以及生殖器官精囊腺+前列腺、提肛肌、包皮腺的脏器指数的下降,均有一定的保护作用.结论:蛤蚧补肾丸(胶囊)具有补肾壮阳作用.

目的:研究小麦非致病菌脂多糖(Pantoea agglomerans lipoplysaccharide,LPSp)对小鼠免疫功能的影响.方法:观察LPSp对小鼠免疫器官的重量、溶血素生成、碳粒廓清速率和2,4-二硝基氯苯迟发型超敏反应的影响.结果:LPSp可增加小鼠免疫器官脾和胸腺重量,促进溶血素生成,提高小鼠网状内皮系统吞噬功能,以及显著抑制2,4-二硝基氯苯诱发的迟发型超敏反应(P<0.05或P<0.01).结论:LPSp对小鼠的免疫功能具有明显的增强作用.

目的:探讨没食子儿茶素没食子酸脂(EGCG)对肾缺血再灌注时细胞凋亡的抑制作用.方法:建立大鼠肾缺血再灌注损伤的动物模型,对Cr、BUN、一氧化氮(NO)、Ca2+-ATP酶活性进行测定并对肾细胞凋亡及组织病理进行观察.结果:EGCG高剂量(40 mg/kg)Cr(17.89±8.48)μmol/L、BUN(4.91±2.71)μmol/L、NO(0.38±0.17)μmol/g prot比空白对照组明显降低(均P＜0.01),Ca2+-ATP酶(0.62±0.13)mmol/g prot*h-1比空白对照组明显升高(P＜0.01),并且能有效抑制细胞凋亡的产生,且较维生素C组作用更明显.结论:EGCG能减轻肾缺血再灌注损伤,减少细胞凋亡的发生,其作用机制可能与降低细胞内的 Ca2+和NO浓度有关.