Xinlk对吗啡依赖大鼠和小鼠催促戒断症状及耐受性的影响

目的:观察中药xinlk对动物的镇痛作用及其戒毒治疗作用。方法:采用热板法试验观察xinlk对小鼠的镇痛作用和小鼠扭体法计算镇痛作用的ED50,观察动物连续多次给药后痛阈值的变化,检测动物是否对药物产生耐受性单次或连续给药是否表现竖尾反应,检测动物是否对药物产生依赖性,结果:试验证实xinlk(260mg.kg-1、130mg.kg-1、65mg.kg-1)呈剂量依赖性均有较好的镇痛作用,且能明显抑制吗啡依赖小鼠纳洛酮催促后跳跃反应、竖尾反应和体重下降,且可明显抑制吗啡依赖大鼠纳洛酮催促戒断的大部分阳性戒断症状包括体重下降。结论:xinlk对物理化学等伤害性…     

气功戒毒的实验研究

本文采用ｓｃ吗啡,剂量递增法制作吗啡依赖小鼠模型,经纳洛酮催促,观察小鼠的戒断症状。采用盘古神功给成瘾小鼠发功后,小鼠戒断后的跳跃个数及跳跃反应次数均明显减少,体重下降减轻。小鼠条件性位置偏爱实验结果表明,盘古神经功能缩短小鼠在拌药盒中逗留的时间。此外,盘古和神功可明显增加小鼠戊巴比妥钠阈下睡眠的个数及延长戊巴比妥钠诱导的睡眠时间。这些结果表明,盘古神功能显著缓解吗啡准依赖小鼠纲洛酮催促的戒断症状     

吗啡依赖小鼠海马神经元c-fos的表达

目的:探讨吗啡依赖小鼠海马不同亚区神经元c-fos表达的差异。方法:以剂量递增法皮下注射吗啡建立吗啡依赖小鼠模型,腹腔注射纳洛酮诱发戒断症状。根据小鼠戒断反应中出现的跳跃次数、体重下降等指标评定戒断反应强度。采用免疫组织化学法显示吗啡依赖小鼠和正常对照组小鼠海马神经元c-fos的表达。结果:吗啡依赖组海马CA1区和齿状回Fos阳性神经元数目明显增加(P<0.05),CA3区无明显改变(P>0.05)。纳洛酮催促戒断组海马CA1和CA3区Fos阳性神经元数目明显增加(P<0.05),齿状回Fos阳性神经元数目增加更为明显(P<0.01)。吗啡依赖组与纳洛酮催促戒断组CA3区阳性神经元数目有显著性差异(P<0.05)。结论:海马神经元c-fos的表达增强可能与吗啡依赖对神经元的损伤有关。     

多巴胺受体阻滞剂协调吗啡镇痛及其镇痛机制分析

目的:观察低剂量多巴胺受体阻滞剂氟哌啶醇与阈下镇痛剂量吗啡合用对抗热刺激和醋酸致小鼠痛反应的作用,并初步分析其协同镇痛作用的主导机制。方法:采用热板法测试给予氟哌啶醇(0.3125mg/kg,0.625mg/kg,1.25mg/kg)、吗啡(3.125mg/kg,6.25mg/kg,12.5mg/kg)和氟哌啶醇(0.3125mg/kg)与吗啡(3.125mg/kg)合用,对热刺激致小鼠痛反应的变化及苯丙胺(10mg/kg)和纳洛酮(5.0mg/kg)对其合用小鼠痛反应的影响。采用扭体法测试给予氟哌啶醇(0.625mg/kg,1.25mg/kg,2.5mg/kg)、吗啡(1.25mg/kg,2.5mg/kg,5.0mg/kg)及氟哌啶醇(0.625mg/kg)与吗啡(1.25mg/kg)合用,对醋酸(0.7%,0.1mL/10g,ip)诱致小鼠扭体出现潜伏期、20min内扭体反应次数的影响。结果:氟哌啶醇与吗啡合用明显提高小鼠对热刺激致痛的痛阈,显著延长醋酸致小鼠扭体反应潜伏期和抑制扭体反应次数;纳洛酮可取消两者合用的协同镇痛效应,而苯丙胺无明显影响。结论:多巴胺受体阻滞剂氟哌啶醇与吗啡合用可产生协同镇痛作用,而吗啡在协同镇痛中起主导作用。     

吗啡依赖对小鼠睾丸组织的影响及其相关机制分析

为了解吗啡依赖对小鼠睾丸发育及其功能的影响 ,研究了吗啡依赖对睾丸生精细胞凋亡的影响及其可能机制。以剂量递增法皮下注射吗啡建立吗啡成瘾小鼠模型 ,用纳洛酮催促戒断 ,观察戒断症状 ,采用原子吸收、放射免疫分析和原位缺口平移 (ISNT)技术观察睾丸细胞锌和钙调素 (CaM)含量、睾丸超氧歧化酶 (SOD)、还原型谷胱甘肽过氧化物酶 (GSH Px)活性和睾丸组织中凋亡细胞数目。结果表明 ,与对照组相比 ,吗啡依赖组和纳洛酮催促戒断组躯体运动神经功能和植物神经功能亢进 ,睾丸锌和CaM含量减少 ,睾丸SOD、GSH Px活性降低 ,睾丸组织中生精细胞凋亡数目明显增多 (P <0 0 5或P <0 0 1)。吗啡依赖小鼠可诱导睾丸组织中细胞凋亡 ,这种变化可能与睾丸组织中锌和CaM含量减少、睾丸SOD和GSH Px活性降低有关。     

西地那非对小鼠吗啡戒断反应和血浆中NO含量的影响

目的 :观察磷酸二酯酶 5 (phosphodiesterasePDE5 )抑制剂西地那非 (Sildenafil)对小鼠吗啡戒断反应的影响。方法 :用皮下递增注射吗啡法建立吗啡依赖模型 ,腹腔注射纳洛酮催瘾 ,根据小鼠戒断反应中出现的跳跃潜伏期 (min)及 15min内跳跃次数 ,以及体重丢失克数评定吗啡戒断反应强度。观察皮下注射不同剂量 (l5mg·kg- 1 、 30mg·kg- 1 、 6 0mg·kg- 1 )的西地那非对吗啡戒断反应的影响 ,同时用硝酸还原酶法检测血浆和脑组织中NO含量。结果 :三种不同剂量的西地那非可加重小鼠吗啡戒断反应 ,并呈很好的量效关系。 30mg·kg- 1 的西地那非可增加吗啡戒断小鼠血浆中的NO含量 ,但对脑内NO无显著影响。结论 :西地那非可加重小鼠吗啡戒断症状并增加吗啡戒断小鼠血浆中NO含量 ,但对脑组织中NO无明显影响。     

CCK-8及其受体拮抗剂对吗啡戒断大鼠额叶皮质及海马CREB与pCREB表达的影响

 目的：观察八肽胆囊收缩素（CCK-8）及其受体拮抗剂对吗啡戒断大鼠额叶皮质和海马cAMP反应元件结合蛋白（CREB）表达及其磷酸化（pCREB）的影响,初步探讨CCK-8调节吗啡戒断大鼠的受体后机制。方法：建立大鼠吗啡慢性依赖及纳络酮催促戒断模型,并给予CCK-8、CCK1受体拮抗剂L-364718和CCK2受体拮抗剂LY-288513慢性干预,应用Western blotting和免疫组织化学技术观察额叶皮质和海马CREB与pCREB 表达的变化。结果：（1） 正常组大鼠额叶皮质神经元胞浆、胞核均表达CREB蛋白,pCREB蛋白则仅在胞核中高表达;海马CA1区锥体细胞层神经元中,CREB蛋白在胞浆中高表达,胞核低表达,pCREB蛋白则仅在胞核中表达。（2） 慢性吗啡作用后CREB无明显变化,pCREB增加;急性纳洛酮催促戒断后CREB仍无明显变化,pCREB进一步升高。（3） 与戒断组相比,CCK-8、L-364718和LY-288513慢性干预对吗啡依赖戒断大鼠额叶皮质CREB蛋白表达无明显影响,pCREB蛋白表达均明显降低;L-364718和LY-288513慢性干预后,海马CREB与pCREB表达均明显降低,而CCK-8慢性干预对CREB蛋白表达无明显影响,仅pCREB蛋白表达明显降低。结论：CCK-8及其受体拮抗剂可能通过调节核转录因子CREB减轻吗啡戒断症状,并具有脑区特异性。     

两种吗啡依赖小鼠模型的行为学及相关指标的对比研究

目的 :比较两种吗啡依赖小鼠模型的戒断行为及相关指标的相互关系。方法 :以剂量递增法建立两种吗啡依赖小鼠模型 ,纳洛酮催促戒断。之后 ,比较两种吗啡依赖小鼠的戒断症状及心、肝、肾、肺、肾上腺和睾丸重量。结果 :两种方法均成功建立了小鼠吗啡依赖 ,7日法模型小鼠平均跳跃次数、“湿狗”样抖动次数及上睑下垂和前爪震颤的动物数均明显多于 5日法 ,尤其是平均跳跃次数和“湿狗”样抖动次数与 5日法有极显著性差异 (P <0 0 0 1) ,且 7日法模型小鼠心、肾和睾丸重量明显小于 5日法。但 5日法建立模型时间短 ,吗啡累积总剂量小 ,且可观察到跳跃和体重降低这两项反映吗啡依赖的客观指标。结论 :两种方法均可观察吗啡依赖和评价药物依赖性潜力 ,但 7日法比 5日法更全面、准确、客观。     

654-2对吗啡戒断大鼠肠系膜微循环的影响

目的观察654-2对吗啡戒断大鼠肠系膜微循环的影响。方法采用递增皮下注射吗啡6天后，经纳络酮催瘾（0．5mg／kg），建立吗啡戒断模型，在戒断前给654-2组大鼠腹腔注射654-2（10mg／kg），然后用BI-2000医学图像分析系统分别观测正常大鼠、吗啡戒断大鼠和654-2治疗组大鼠肠系膜微血管管径、血流速度及有无渗出、出血。结果与吗啡戒断组比较，654-2组大鼠肠系膜微血管口径，血流速度以及血液渗出等情况均有不同程度的改善（P〈0．05）。结论654-2能明显改善吗啡戒断大鼠肠系膜微循环，可能是通过654-2解除微血管痉挛、抑制血小板聚集、增加红细胞的变形性而起作用。     

吗啡依赖大鼠的行为与VTA单胺释放改变研究

本文研究了大鼠在吗啡依赖和戒断状态下的行为以及活体上被盖腹侧区（VTA）单胺释放的改变，结果发现，在吗啡依赖状态，大鼠在无躯体戒断反应出现时仍表现出对吗啡地点的偏好；其躯体戒断反应减轻后地点偏好无明显改变。其吗啡依赖状态下单胺释放受抑制，于躯体戒断反应最严重时NE释放达最高峰，显著高于正常对照，DA释放于戒断吗啡后逐渐回升，但于戒药1周时仍然显著低于正常对照水平。     

Evidence on Possible Mycoplasma Etiology of Aster Yellows Disease II. Suppression of Aster Yellows in Insect Vectors

Chlortetracycline or chloramphenicol (but not kanamycin, penicillin, or erythromycin), when administered in hydroponic solution to diseased aster, reduced the availability of the aster yellows (AY) agent to nymphs of Macrosteles fascifrons (Stål). Insects exposed to healthy plants whose roots were immersed in chlortetracycline were able to acquire AY agent from diseased plants the day after removal from the antibiotic-treated plants, but the latent period of the ensuing disease in the insects was prolonged. Chlortetracycline or tylosin tartrate blocked AY infection in nymphs injected with a mixture of antibiotic and the AY agent, but polymyxin, neomycin, vancomycin, penicillin, carbomycin, or chloramphenicol did not. All tetracyclines tested, methacycline, oxytetracycline, and chlortetracycline, produced a dramatic reduction in the ability of infected vectors to transmit AY agent. Tylosin tartrate also reduced transmission when injected into AY-transmitting vectors, but carbomycin, spectinomycin, cycloserine, penicillin, erythromycin, or kanamycin had no such effect. During the first 10 days after injection of tylosin tartrate or oxytetracycline into transmitting vectors, ability of the insects to transmit AY decayed rapidly. Transmission by insects injected with buffer alone, after decreasing the first day after injection, gradually returned to its normal level in less than 1 week. By 2 to 3 weeks after injection with tylosin or oxytetracycline, ability to transmit AY was regained by vectors. The results suggest that tetracycline antibiotics and tylosin tartrate inhibit multiplication of AY agent in the insect. The spectrum of antibiotic activity in the insect is consistent with the hypothesis that AY and other plant yellows diseases are caused by mycoplasma-like organisms.     

四组复方中药对模拟失重大鼠血液流变性的影响

目的:观察中药在对抗失重或模拟失重导致的血液循环状态紊乱中的作用。方法:采用大鼠头低位30°尾吊模型模拟失重对机体的影响,用四组(丹黄刺组、参川熟组、参山杜组、参银生组)复方中药对抗模拟失重大鼠血液流变学变化。结果:单纯尾吊导致大鼠体重明显降低(P<0.01),中、低切血粘度、纤维蛋白原含量、异形红细胞比例明显增高(P<0.01);红细胞最大变形指数、积分变形指数和血细胞压积明显降低(P<0.01)。中药组与单纯尾吊组相比,各指标均有不同程度地改善。结论:复方中药可有效改善尾吊导致的大鼠血液流变学异常。     

A preliminary study of the use of human adipose tissue-derived stem cells for the treatment of streptozotocin-induced diabetes mellitus in a rat model

The purpose of this study is to determine if intraventricular injection of human adipose tissue-derived stem cells (hADSC) are effective in treating streptozotocin (STZ)-induced diabetes mellitus (DM) in nude rats. Twenty-two adult, male nude rats (strain Crl:NIH-Fox1^RNU) were used to induce diabetes using streptozotocin. A single, 150 mg/kg STZ was injected intraperitoneally. Severity of the induced diabetic state was assessed by daily monitoring of body weight, clinical signs, and blood glucose levels. C-peptide was assessed before ADSC injection (T0) and at 3, 5, and 21 days after ADSC injection. Eight rats (40%) developed DM within 24 h after STZ injection. Of the eight rats that developed DM, five were given 2 million freshly prepared ADSC intraventricularly under echocardiography guidance 10 days after STZ injection and three were only given sterile saline for comparison. Surviving rats were humanly sacrificed 21 days after ADSC injection. The average weight of diabetic rats decreased significantly after STZ injection. ADSC injection had no effect on the body weight of rats. Non-fasting serum glucose levels increased significantly in both groups. In diabetic rats, C-peptide decreased significantly before ADSC injection and seemed to return to normal 21 days after ADSC administration. Results of this preliminary study might suggest a beneficial effect of using hADSC for the treatment of STZ-induced diabetes in adult nude rats.     

不同浓度淫羊藿含药血清干预骨髓基质干细胞的成脂分化

背景：如何抑制骨髓基质干细胞成脂分化,促进其成骨分化将是防治骨质疏松的新途径之一。 目的：观察不同浓度淫羊藿含药血清对骨质疏松大鼠骨髓基质干细胞成脂分化的干预作用。 方法：全骨髓培养法培养SD大鼠骨髓间充质干细胞,12只SPF级SD雌性大鼠按体表面积的方法给予淫羊藿水提液,药物以蒸馏水定容至所需浓度,相当于临床剂量的20倍、10倍、5倍灌胃,连续灌胃7 d后眼眶取血,观察各组干预后7 d成脂分化情况。 结果与结论：中药低、中剂量含药血清组的成脂率低于空白组 (P < 0.01、0.05),说明中药淫羊藿含药血清发挥了抑制骨质疏松骨髓基质干细胞向脂肪细胞分化的作用。中药各剂量组的组间比较差异无显著性意义(P  > 0.05),但3组成脂率数值方面以中剂量组最佳。     

加味补中益气汤治疗大鼠肺孢子虫肺炎的疗效观察

目的探讨加味补中益气汤治疗大鼠肺孢子虫肺炎（PCP）的疗效。方法按国内公认的PCP造模方法，建立大鼠PCP动物模型。设中药治疗组和预防组，同时建立西药对照组、PCP模型对照组及正常对照组。通过观察各组大鼠存活率、体重、肺内肺孢子虫包囊的数量和肺组织病理学变化考核药物疗效。结果中药组大鼠存活率高于PCP模型组，但低于正常组；中药治疗组和预防组大鼠平均体重高于PCP模型组，包囊数低于PCP模型对照组；中药治疗组和预防组大鼠肺组织炎症反应明显轻于PCP模型对照组。结论加味补中益气汤对大鼠肺孢子虫肺炎，有一定的疗效。     

The effect of physical restraint on IL-1 beta- and LPS-induced fever.

The stress of physical restraint has been shown to cause an elevation in the body temperature of rats. In this study, we compared the febrile responses of restrained and unrestrained animals to the injection of interleukin-1 beta (IL-1 beta) and lipopolysaccharide (LPS). We found that, prior to injection, the body temperature of the restrained animals was about 1 degree C higher than that of the unrestrained rats. The restrained rats showed significantly smaller increases in body temperature in response to the injection of either pyrogen than did the unrestrained animals.     

Ⅱ型胶原注射液对大鼠骨性关节炎的治疗研究

目的评价Ⅱ型胶原注射液对大鼠骨性关节炎的治疗作用。方法采用酸溶法提取高纯度的Ⅱ型胶原注射液（创尔关节腔注射液,纯度98．5％以上）。雄性SD大鼠64只,无特定病原体动物即SPF级．体质量110～150g（合格证号0083113）。采用改良的Hulth法制作大鼠膝关节骨性关节炎模型,按体质量随机分组为正常对照组、模型对照组、天节腔注射液组、透明质酸钠组．每组16只。于术后l、3、5、7、9、11周关节腔注射液组、透明质酸钠组关节腔分别注射Ⅱ型胶原注射液、透明质酸钠凝胶,正常对照组和模型对照组注射等量的0．9％氯化纳溶液进行治疗。于治疗时间第7周和第13周．各取动物眼眶静脉丛采血．测定血清C反应蛋白（CRP）、类风湿因子（RF）含量．取右侧膝关节进行病理组织观察并通过wilhelmin关节软骨损伤分级及关节软骨组织学Mankin’s评分评价Ⅱ型胶原注射液对大鼠骨性关节炎的疗效,结果各组大鼠血清中CRP的含量差异均无统计学意义（P〉0．05）。关节腔注射液组和透明质酸钠组中大鼠血清中的RF含量降低,炎症反应得到改善;与正常对照组[第7、13周分别为（89．56±6．10）IU／L、（83．86±15．32）[U／L]相比．模型对照组术后第13周的血清中RF含量无统计学意义（P〉0．05）,关节腔注射液组血清中RF含量也无统计学意义（P〉0．05）．而透明质酸钠组血清中RF含量[第7、13周分别为（85．95±7．68）IU／L、（81．64±11．45）IU／L]显著下降（P〈0．05）;与模型对照组相比。关节腔注射液组和透明质酸钠组第13周的Wilhelmin分级具有一定的改善．Mankin’s评分均较同时期模型对照组有减少的趋势。结论Ⅱ型胶原注射液能够缓解大鼠骨性关节炎的病理过程．     

健脾补肾药对脾虚大鼠细胞因子水平的影响

目的 :观察健脾补肾方药对实验性脾虚证大鼠细胞因子的影响 ,探讨脾虚证与细胞因子的关系及脏腑相关的意义。方法 :选用SD雄性大鼠 ,随机分为 :正常对照组 ,脾虚模型组 ,健脾补肾方高、低剂量组 ,通过大黄复制脾虚证动物模型 ,并用健脾补肾方药进行防治。采用放射免疫分析观察各组动物血清肿瘤坏死因子(TNF)、白细胞介素 - 6 (IL - 6 )、白细胞介素 - 2 (IL - 2 )水平的变化。结果 :脾虚模型组大鼠血清TNF、IL - 6、IL - 2含量均比正常对照组显著降低 (p <0 0 1) ,而健脾补肾方药能明显升高TNF、IL - 6、IL - 2含量 ,使体重增加 ,脾脏和胸腺组织的重量增加。结论 :脾虚证的发生与细胞因子网络调节系统的失衡有关 ,而健脾补肾中药对实验性脾虚证有较好的防治作用 ,脾肾相关理论对实践有指导意义。     

Dissociation of epinephrine's hyperglycemic and anorectic effect

The contributions of alpha- and beta-adrenergic receptor mechanisms to epinephrine-induced hyperglycemia, to prandial hepatic glycogenolysis, and to epinephrine-induced inhibition of feeding were investigated in rats, because epinephrine's hyperglycemic and anorectic effect might be related to each other. Intraperitoneal injection of the selective alpha-adrenergic receptor antagonist phentolamine (0.5 mg/kg body weight) but not of the selective beta-adrenergic receptor antagonist propranolol (0.5 mg/kg body weight) reduced the hyperglycemic effect of a subsequent epinephrine injection (0.05 mg/kg body weight). In addition, injection of phentolamine (0.5 mg/kg b.w.) or injection of phentolamine plus propranolol (0.5 mg/kg b.w. each) similarly inhibited epinephrine-induced hepatic glycogenolysis. In contrast, phentolamine injection did not affect prandial hepatic glycogenolysis. Neither phentolamine nor propranolol injection was sufficient to affect the inhibition of feeding induced by subsequent epinephrine injection, but the combination of both receptor blockers completely abolished epinephrine's effect on food intake. These findings are not consistent with the idea that epinephrine-induced hypophagia is related to epinephrine's effect on hepatic carbohydrate metabolism. In addition, the data suggest that catecholamines are not the main contributors to prandial hepatic glycogenolysis in rats.     

Dissociation between peripheral and central heat loss mechanisms induced by neonatal capsaicin

Fifty-eight 4-day-old male rats were studied. Peripheral desensitization was induced in 36 rats by sc administration of capsaicin in increasing doses (350, 700, 1,400, 2,100, and 2,800 micrograms) on 5 consecutive days. When adult, 9 treated and 5 control rats were chronically implanted with a lateral intracerebroventricular (icv) guide cannula. This tube was used for icv capsaicin injection. Eleven treated rats and 6 controls were implanted with a hypothalamic thermode. Hypothalamic heating was activated with the aid of this water-perfused thermode. Twenty-eight rats, 12 control and 16 treated, were injected ip and sc with capsaicin. Results showed that in control rats, icv, ip, and sc capsaicin injections produced a fall in body (core) temperature and an increase in cutaneous temperature. These changes are attributed to cutaneous vasodilation. In capsaicin-treated rats, sc and ip injections had no effect on body temperature. However, neonatal treatment did not inhibit the effect of capsaicin on body temperature. Furthermore, in these rats thermoregulatory behavior for fresh air was identical to that of controls at all ambient temperatures before and during hypothalamic heating. These results suggest that the central heat receptors responsible for autonomic and behavioral thermoregulation in the treated rats function normally when icv capsaicin is injected or when the hypothalamus is heated. In contrast, neonatal injection of capsaicin produced an inhibition of the heat loss mechanisms induced by ip or sc capsaicin, i.e., by stimulation of the peripheral nervous system.