首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 0 毫秒
1.
经络导平治疗海洛因戒断后期稽延性综合征   总被引:7,自引:0,他引:7  
舒荣  文秀英  茹立强  易君  吴耀  罗飚 《中国针灸》2003,23(6):325-328
目的 :评价经络导平仪治疗海洛因戒断后期稽延性综合征的疗效。方法 :90例经美沙酮治疗 8~ 1 0天后的患者 ,不干预戒断后期药物治疗的前提下 ,随机分为经络导平治疗组 78例和对照组 1 2例。对照观察治疗前后躯体不适症状及精神症状。结果 :治疗组患者临床症状均有明显改善(P <0 0 1 ) ,治疗组焦虑和抑郁等精神障碍性症状也得到显著改善 (P <0 0 0 1 ,P <0 0 1 ) ,与对照组比较差异有显著性意义 (P <0 0 1 ) ;对照组同期前后比较差异无显著性意义 (P >0 0 5 )。结论 :经络导平疗法具有临床应用价值  相似文献   

2.
目的:观察卵巢早衰大鼠子血清中丙二醛(MDA)、过氧化氢酶(CAT)、总超氧化物歧化酶(TSOD)的水平,探讨一贯煎制剂对卵巢早衰大鼠过氧化状态的拮抗作用。方法:实验设正常对照组、模型对照组、乙烯雌酚干预组、一贯煎干预组。灌胃给予雷公藤多苷50 mg/kg·d复制卵巢早衰大鼠模型,2周后灌胃给予各干预药,连续给药6周。第7周时检测各组大鼠的卵巢病理及卵巢指数,血清中MDA、Caspase-3、T-SOD、CAT水平。结果:比较四组卵巢病理HE染色、卵巢指数,说明造模成功,且一贯煎对卵巢早衰具有一定改善效果(P0.05)。与正常对照组比较,模型对照组的T-SOD、CAT水平明显降低(P0.05),MDA的水平显著升高(P0.05);与模型对照组比较,各干预药组上述指标均有不同程度的改变(P0.05)。结论:一贯煎制剂对卵巢早衰大鼠过氧化状态有拮抗作用,其作用机制与提高T-SOD、CAT水平;并降低MDA、Caspase-3的水平有关。  相似文献   

3.
AIM: Stress is recognized to precipitate anxiety and related psychological problems characterized by a wide range of biochemical and behavioral changes. The present study was carried out to investigate the protective effects of melatonin and buspirone, and their combination, against six hours immobilization stress-induced, anxiety-like behavioral and oxidative damage in mice. METHOD: Male Laca mice were pre-treated with melatonin(2.5, 5 mg·kg–1), buspirone(5, 10 mg·kg–1), and their combination for consecutive five days. On the 6th day, animals were immobilized for six hours, and thereafter various behavioral tests were performed followed by biochemical tests. RESULTS: Immobilization stress significantly impaired body weight, locomotor activity, and caused anxiety-like behavior, along with increased oxidative damage. Pretreatment with melatonin and buspirone significantly improved the loss in body weight and locomotor activity, attenuated anxiety-like behavior(in both the mirror chamber and plus maze performance tasks), further restored the levels of brain total proteins, and caused antioxidant-like effects, as evidenced by reduced lipid peroxidation, nitrite concentration, and restoration of reduced glutathione and catalase activity, as compared to control animals. In addition, combination of melatonin(2.5, 5 mg·kg–1) with buspirone(5 mg·kg–1) significantly potentiated their protective effects, as compared to their effects individually. CONCLUSION: The present study suggests that melatonin potentiates the beneficial effect of buspirone against immobilization stress-induced, anxiety-like behavioral and oxidative damage in mice possibly by involving a serotonergic mechanism.  相似文献   

4.
5.
目的:根据中医理论建立登革热湿热证动物模型,并对模型加以评价。方法:采用复合因素:高糖高脂饲料+高温仓+感染因子登革病毒(DEN),建立研制登革病毒感染的小鼠模型,观察小鼠一般生物学状态、临床表现及实验室检查指标,并给予中药方剂进行治疗。从病因、症状、体征、实验指标及中药治疗反证等方面评价模型。结果:动物模型符合登革热病的特点,未改变登革热模型的关键指标(湿热毒组病毒测定G值:32.70),同时模型小鼠出现明显湿热证客观指标的变化(P<0.01),经中药复方治疗后,上述指标得到明显的改善。结论:在中医理论指导下采用复合因素接种DEN,可建立小鼠感染模型,为研究中医药治疗登革热的效果和机制提供了较为合适的动物模型。  相似文献   

6.

Ethnopharmacological relevance

Myelophil is composed of Astragali Radix and Salviae Miltiorrhizae Radix, according to the long traditional pharmacological practices, and it has been used for patients with chronic fatigue-associated symptoms including concentration problem or memory loss.

Aim of the study

This study aimed to evaluate the clinical relevance of Myelophil on brain oxidative damage using a chronic cold stress mice model.

Material and methods

Balb/c mice were subjected to cold stress (4 °C for 4 h) six times per week for 2 weeks with or without oral administration of Myelophil (50, 100, or 200 mg/kg), or ascorbic acid (50 mg/kg).

Results

Chronic cold stress induced histopathological hippocampal apoptosis with drastically increased serum levels of total reactive oxygen species and nitric oxide, as well as brain lipid peroxidation levels, protein carbonyl, and caspase-3/7 activity. These alterations were significantly ameliorated by Myelophil treatment. Myelophil administration significantly recovered the depleted glutathione and its enzymes, superoxide dismutase activity, and catalase protein and gene expression levels. Serum levels of corticosterone, dopamine, and adrenaline were notably altered by chronic cold stress but were significantly ameliorated by Myelophil treatment. Myelophil also normalized alterations in tumor necrosis factor-α, interleukin (IL)-1β, and IL-10 gene expression and protein levels. Chronic cold stress up-regulated gene expression levels of phenylethanolamine N-methyltransferase and monoamine oxidase-B, and glucocorticoid receptors in the hypothalamus and hippocampus, respectively, whereas Myelophil treatment completely normalized these levels.

Conclusions

These results suggest that Myelophil has potent pharmaceutical effects against chronic cold-stress-induced brain damage by relieving oxidative stress and inflammation and regulating stress hormones in mice.  相似文献   

7.

Ethnopharmacological relevance

Lilium lancifolium Thunb. (Liliaceae) has long been used as a traditional medicine in Korea and China to treat bronchitis, pneumonia, and other pulmonary ailments.

Aim of the study

Cigarette smoke (CS) is a major risk factor for the development of pulmonary inflammatory response; it also triggers pulmonary alveoli enlargement. In the present study, we investigate the effects of Lilium lancifolium Thunb. root extract on pulmonary inflammatory responses in a CS-exposed mouse model.

Materials and methods

Water extract of Lilium lancifolium Thunb. root was fed to C57BL/6 mice prior CS exposure every day for 3 weeks. The numbers of macrophages and neutrophils in bronchoalveolar lavage fluid (BALF) were counted. The relative inflammatory factors, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), interleukin-1 beta (IL-1β), monocyte chemotactic protein-1 (MCP-1), and matrix metalloproteinase-12 (MMP-12) were measured by real-time PCR, ELISA, or Western blot analysis. The average alveoli size was determined by lung histology.

Results

Lilium lancifolium Thunb. root extract was found to significantly inhibit the numbers of macrophages and neutrophils in BALF due to CS exposure. Lilium lancifolium Thunb. root extract also reduced the protein secretion levels of TNF-α, IL-6, IL-1β, and MCP-1 in BALF and the RNA expression levels of TNF-α, IL-6, IL-1β, MCP-1, and MMP-12 in lung tissue compared with mice only exposed to CS. Moreover, MMP-12 in serum was down regulated in Lilium lancifolium Thunb. root extract treated mice compared with CS-exposed mice. Finally, a morphometric analysis of the lungs of Lilium lancifolium Thunb. root extract treated mice demonstrated a significant reduction in airspace size compared to mice only exposed to CS.

Conclusion

Our results show that Lilium lancifolium Thunb. root extract reduces lung inflammation and airspace enlargement in a CS-exposed mouse model. These data indicate that Lilium lancifolium Thunb. root extract is a therapeutic candidate for pulmonary inflammation and emphysema caused by CS.  相似文献   

8.

Aim of the study

To verify therapeutic effects of Gan-fu-kang (GFK), a traditional Chinese medicine compound, in a rat model and to investigate the underlying mechanisms.

Materials and methods

Liver fibrosis was established by 12 weeks of carbon tetrachloride (CCl4) treatment (0.5 mg/kg, twice per week) followed by 8 weeks of “recovery” in rats. Rats randomly received GFK (31.25, 312.5 and 3125 mg/kg/day, p.o.) or vehicle from weeks 9 to 20, and were sacrificed at the end of week 20 for histological, biochemical, and molecular biological examinations. In a separate set of experiments, rats received 12 weeks of CCl4 treatment, concomitant with GFK (312.5 mg/kg/day, p.o.) during the same period in some subjects, but were then sacrificed immediately. An additional group of rats receiving no CCl4 treatment served as normal controls.

Results and conclusions

(1) CCl4 treatment resulted in severe liver damage and fibrosis. (2) In the main block of the 20-week study, GFK attenuated liver damage and fibrosis. (3) In the 12-week study, GFK produced prevention effect against hepatic injury. (4) GFK suppressed the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), type I collagen, platelet-derived growth factor-BB (PDGF-BB)/PDGF receptor-β chains (PDGFRβ) and mitogen-activated protein kinases (MAPKs)/active protein-1 (AP-1) signal pathways. Taken together, these results indicated that GFK could attenuate liver injuries in both settings. Our findings also suggest that the AP-1 pathway is the likely molecular substrate for the observed GFK effects.  相似文献   

9.
OBJECTIVE:To investigate the inhibitory effect of Yiguanjian decoction(YD) on DNA damage in Concanavalin A(Con A)-induced liver injury mice model and to explain the possible mechanism.METHODS:Totally 120 male BALB/c mice were randomly divided into 6 groups,20 mice each:normal group,model group,Bifendate group,YD low dose group,YD middle dose group and YD high dose group.Except normal group,liver injury model induced by Con A was established.While modeling,each mouse in YD group was given YD(0.4 m L/20 g per day) by intragastric administration(0.13 g YD for YD low dose group;0.26 g for YD middle dose group;0.52 g for YD high dose group).Bifendate group was given Bifendate(0.2 gnd model·kg-1 grou·d-1) by gavage.Normal group ap were fed with same volume of physiological saline daily.After 8 weeks,the serum alanine transaminase(ALT)and aspartate transaminase(AST) were tested.The hematoxylin-eosin staining was used to evaluate the grade of liver inflammation and liver fibrosis stage.Hepatocellular DNA damage was detected by single cell gel electrophoresis technology.The protein expression of tumor necrosis factor-α(TNF-α),Bax and Mut T Homolog 1(MTH1) was detected by western blotting and enzyme linked immunosorbent assay.Bax m RNA and MTH1 m RNA were detected by Real-time Polymerase Chain Reaction(PCR).RESULTS:YD can improve the degree of liver inflammation and fibrosis in the liver of chronic hepatitis mice,the dose effect relationship is remarkable(P 0.05).YD can reduce liver cell DNA damage.The difference between YD middle dose group and model group was statistically significant(P 0.05).YD middle dose group had decreased the protein expression of TNF-α in the mice liver of immunological liver injury(P 0.05).YD can increase the protein expression of Bax(P 0.05).Compared with normal group,the protein expression of MTH1 was decreased(P 0.05),but there was no statistical significance between YD group and model group(P 0.05).YD can increase the m RNA expression of Bax and MTH1(both P 0.05).CONCLUSION:YD can effectively inhibit the DNA damage in immunological liver injury mice,the mechanism may be that it can decrease the TNF-αand increase the Bax and MTH1 expression.  相似文献   

10.
肝硬化是以一种或多种病因反复作用形成的以肝实质弥漫性纤维化、假小叶和再生结节形成,肝内外血管异常以致门静脉高压为特征的病理阶段,进展至失代偿期以肝功能严重损害为特征,出现腹水、胃食管静脉曲张破裂出血、肝性脑病等多种并发症,治疗上多为对症治疗,死亡率高,预后差。对于失代偿期肝硬化,中医药治疗不仅可以有效改善肝功能,且能显著提高患者的5年生存率,提示中医药在防治终末期肝病、促进肝硬化组织重构方面具有潜在优势。现代中医名家认为,肝硬化主要由气阴亏虚(肝、脾、肾)而湿热疫毒内侵,脉络瘀阻所致。肝肾阴虚是失代偿期肝硬化常见的主要证候。中医滋肾养肝方剂一贯煎是现代临床治疗慢性肝病肝肾阴虚证的代表方。由清代名医魏玉璞(魏之琇)所创,载于《续名医类案》。临床研究显示一贯煎可有效改善肝硬化患者的肝功能,促进腹水消退,减少肝性脑病等相关并发症的出现。实验研究提示一贯煎具有多途径、多层次、多靶点综合调节的特征,防治肝硬化的作用机制可能主要与抗氧化应激,改善肝脏炎症、提高肝细胞生物合成以及抑制肝星状细胞活化、减轻胶原沉积、改善肝窦血管化、促进肝细胞再生等有关。文章就近5年来关于一贯煎治疗肝硬化的临床及实验研究作一系统综述,为进一步拓展其临床应用价值提供参考。  相似文献   

11.
目的:建立HPLC法测定消肿止痛巴布膏中栀子苷的含量。方法:色谱柱采用Kromasil C18柱(250mm×4.6mm,5μm);流动相:甲醇-水(27:73),检测波长:240nm;流速:1.0ml·min^-1;柱温:30℃;结果:栀子苷进样量在0.06552~1.3104μg范围内线性关系良好(r=0.9999,n=6);平均回收率为98.5%,RSD=1.61%(n=6)。结论:所建立的方法准确、简便、快速,适用于消肿止痛巴布膏质量控制。  相似文献   

12.
目的:建立湿困脾胃证模型小鼠,观察藿香正气液对模型小鼠的胃肠道功能的作用影响。方法:30只KM种小鼠随机分为湿困脾胃证模型组、治疗组,正常组,每组10只。模型组每日灌服熟地混合液(0.5ml/只)并置于人工气候箱中饲养8h;治疗组除按模型组方法饲养外每日还需灌服藿香正气液(0.5ml/只);空白对照组置于常温环境下饲养并每日灌服蒸馏水(1ml/只)。建模6d后通过观察小鼠的一般体征、胃排空和肠推进能力、胃肠病理组织病变等方面来了解小鼠胃肠功能的改变。结果:与正常组相比,模型组小鼠胃排空和肠推进能力下降,胃肠组织炎症水肿,粘液分泌增多,经藿香正气液治疗后基本恢复到正常水平。结论:藿香正气液有改善湿困脾胃证小鼠胃肠功能失调的作用,这可能是其防治湿困脾胃证的作用机制之一。  相似文献   

13.
目的观察右美托咪定治疗ICU酒精戒断综合征患者的临床疗效及安全性。方法采用随机数字表法将出现震颤(抽搐)、焦虑、激惹等表现的96例ICU酒精戒断综合征患者分为3组,A组给予右美托咪定静脉泵注,负荷量为0.5~1.0μg/kg,10 min后减量至维持量0.2~0.6μg/(kg·h);B组给予异丙酚静脉泵注,负荷量为0.5~2.0 mg/kg,10 min后减量至维持量1~3 mg/(kg·h);C组给予地西泮肌肉注射镇静。观察3组镇静效果;记录用药前后患者的平均动脉压、心率、呼吸频率、脉搏血氧饱和度、动脉血氧分压、CIWA-Ar评分、APACHEⅡ评分,统计患者住ICU时间、不良反应发生情况及病死率。结果 A、B组镇静达标率明显高于C组(P均0.05),A组与B组比较差异无统计学意义(P0.05)。B组镇静起效时间最短,地西泮用量最少,3组间比较差异均有统计学意义(P均0.05)。A组用药后1 h的平均动脉压、心率明显低于B、C组(P均0.05),3组用药前后呼吸频率、脉搏血氧饱和度、动脉血氧分压均无明显变化(P均0.05)。3组用药后24 h CIWA-Ar评分及APACHEⅡ评分均较用药前明显下降(P均0.05),A组评分明显低于B、C组(P均0.05)。A组住ICU时间明显短于C组(P0.05)。结论右美托咪定可显著缓解酒精戒断综合征患者的躁动、谵妄等症状,改善预后,且不良反应少,可作为酒精戒断综合征患者镇静的临床推荐药物。  相似文献   

14.
目的:研究针刺对海洛因精神依赖小鼠核苷酸代谢及大脑和脾脏病理形态的影响,为针刺改善稽延性戒断症状提供理论依据.方法:将经行为学筛选后的昆明种小鼠随机分为空白组、空白针刺组、模型组、针刺组和药物对照组.按剂量逐日递增原则复制海洛因精神依赖小鼠模型,针刺"内关"、"三阴交"及"四神聪"进行治疗,观察黄嘌呤氧化酶(XOD)、腺苷脱氧酶(ADA)活性、及大脑和脾脏的病理形态变化.结果:针刺能降低海洛因精神依赖小鼠脾脏ADA及大脑XOD、ADA活性;针刺可减轻大脑、脾脏的病理损害.结论:针刺改善海洛因精神依赖小鼠的稽延性戒断症状与改善其核苷酸代谢、减轻大脑的病理损害有密切关系.  相似文献   

15.
本文主要讲述了阿片类物质依赖者康复的"毒损脑络"理论,证明其效果良好,值得临床推广应用。  相似文献   

16.
"劳倦过度、房室不节"肾阳虚小鼠模型脑基因芯片研究   总被引:1,自引:0,他引:1  
目的:应用基因芯片探讨"劳倦过度、房室不节"肾阳虚小鼠模型脑基因改变,试图说明传统中医建模方法及其肾阳虚表现,力求从基因水平上揭示肾阳虚的本质。方法:采用雄雌鼠比例1:6同笼喂养和雄鼠每日游泳4周,以诱导"劳倦过度、房室不节"肾阳虚鼠模型。用36K mouse genome array鼠脑芯片检测正常对照组和肾阳虚模型组鼠脑基因,并以二者荧光信号相对强度比值≥2和≤0.5筛选差异显著基因,并进一步查阅北京博奥生物分子注释系统,进行基因功能归类。结果:诱导成功"劳倦过度、房室不节"肾阳虚鼠模型,绘制了对照组与模型组基因表达谱比较的散点图。共筛选出186个差异表达基因,其中上调基因150个,下调基因36个。其中共有已知基因98个,上调已知基因71个,下调已知基因27个。下调基因中主要为生长激素、泌乳素、促性腺激素、黑色素和脑脂肪酸结合蛋白(B-FABP)相关基因;上调基因主要为炎症/免疫、促细胞凋亡相关基因以及影响多巴胺生成的限速酶、影响凝血纤溶机制和精子发育代谢的相关基因。结论:通过基因芯片对肾阳虚动物模型的检测,从基因水平上对肾阳虚证的本质做了一些诠释。  相似文献   

17.
响应面法优化一贯煎中多糖的提取工艺   总被引:1,自引:0,他引:1  
目的:利用响应面法对一贯煎总多糖的提取工艺进行优化。方法:在分析单因素的基础上,以一贯煎多糖得率为响应值,采用3因素3水平的响应面法(RSM)对其提取工艺进行研究。结果:最佳工艺参数为液固比11∶1,85%乙醇提取2次,每次1.8 h。结论:响应面法可在连续范围内进行分析,具有实验周期短、精密度高的优点。优化结果可为制剂生产提供参考依据。  相似文献   

18.
甘草酸对慢性哮喘小鼠骨代谢的影响   总被引:2,自引:0,他引:2  
目的 探讨甘草酸对慢性哮喘小鼠骨代谢的影响.方法 用卵蛋白致敏建立慢性哮喘小鼠模型,取右侧股骨测定骨干重、羟脯氨酸、骨钙、骨微量元素.结果 与正常组和哮喘组相比,甘草酸组股骨干重、骨羟脯氨酸、骨钙含量无明显改变;而泼尼松组股骨干重、骨羟脯氨酸和骨钙减少(P<0.05).结论 甘草酸不会导致慢性哮喘小鼠骨质丢失,而泼尼松抑制骨矿化和骨基质形成,最终造成慢性哮喘小鼠骨量的丢失.  相似文献   

19.
20.
针刺治疗海洛因戒断综合征的临床应用   总被引:10,自引:2,他引:10  
目的:规范针刺治疗海洛因戒断综合征手法操作技术.方法:对220例海洛因戒断综合征患者按随机数字表分为针刺治疗组111例和对照组109例.治疗组用针刺疗法;对照组口服盐酸洛非西定片,观察两组的临床疗效.结果:两组均有效戒除海洛因成瘾(急性期).治疗组前后自身比较戒断症状总分优于对照组(P<0.01),治疗组逐日戒断症状总分第4、第5天优于对照组(P<0.05),治疗组治疗失眠症状优于对照组(P<0.05),治疗组自身汉密尔顿焦虑量表(HAMA)计分优于对照组(P<0.001),治疗组HAMA计分第4天后优于对照组(P<0.05).结论:针刺治疗海洛因戒断综合征起效快,安全可靠,临床疗效满意.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号