肉苁蓉苯乙醇苷对大鼠高原脑水肿的防治作用

目的观察肉苁蓉苯乙醇苷预防给药对高原脑水肿模型大鼠的作用及可能的作用机制。方法大鼠随机分为正常对照组,模型组,大花红景天口服液组[1.78 mL/(kg·d)],肉苁蓉苯乙醇苷低、中、高剂量组[75、150、300 mg/(kg·d)],每组12只,灌胃预防给药10 d,第8日起除正常对照组外其余各组置于模拟海拔5 000 m高原环境72 h建立高原脑水肿模型,观察各组大鼠脑组织病理改变,检测脑组织含水量、脑组织匀浆中白介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、丙二醛(MDA)含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)酶活力。结果与正常对照组相比,模型组大鼠出现明显的脑水肿,脑组织含水量显著升高,脑匀浆液中IL-6、TNF-α、MDA含量增高,SOD和GSH-Px酶活力显著降低。肉苁蓉苯乙醇苷能够改善高原脑水肿大鼠脑水肿病理改变,降低脑组织含水量,降低脑匀浆中IL-6、TNF-α、MDA含量,且能提高SOD和GSH-Px的酶活力。结论肉苁蓉苯乙醇苷能够预防高原脑水肿的发生,可能与其抗炎、抗氧化应激有关。     

肉苁蓉苯乙醇总苷对脂多糖致大鼠急性肺损伤的抑制作用

目的探讨肉苁蓉苯乙醇总苷(CPhG)对脂多糖(LPS)致大鼠急性肺损伤的保护作用及可能的作用机制。方法 SD大鼠60只,随机分为6组:正常对照组、模型组(LPS 3 mg·kg~(-1))、模型+地塞米松(Dex)2 mg·kg~(-1)(阳性药对照组)、模型+CPhG 125,250和500 mg·kg~(-1)组,每组10只,CPhG各剂量组每天按设定剂量ig给予受试物,其余3组均给予相同体积的蒸馏水,连续30 d;第31天,除正常对照组外,其余各组大鼠均经口气管插管后,采用雾化注射器喷入LPS建立大鼠急性肺损伤模型,模型+Dex 2 mg·kg~(-1)组在造模前1 h给予Dex 2 mg·kg~(-1);造模3 h后,经腹主动脉采血处死大鼠。检测全血中性粒细胞百分比,血清超氧化物歧化酶(SOD)和谷胱甘肽(GSH)活性,丙二醛(MDA)和一氧化氮(NO)含量;检测肺泡灌洗液中的肿瘤坏死因子α(TNF-α)、白细胞介素1β(IL-1β)和IL-6含量;计算右肺中叶湿/干重比值(W/D),HE染色观察右肺后叶病理组织变化。结果与正常对照组相比,模型组大鼠全血中性粒细胞百分比、右肺中叶W/D升高(P<0.05),血清MDA和NO含量升高(P<0.05),SOD活性降低(P<0.05),TNF-α和IL-6含量升高(P<0.05);与模型组相比,模型+CPhG 500 mg·kg~(-1)组大鼠全血中性粒细胞百分比和右肺中叶W/D降低(P<0.05),大鼠肺泡灌洗液中TNF-α和IL-6含量明显下降(P<0.05),右肺后叶组织炎症反应程度均有不同程地的减轻(P<0.05),血清中SOD和GSH活性显著升高(P<0.05),MDA和NO含量明显降低(P<0.05)。结论CPhG对LPS致大鼠急性肺损伤具有抑制作用,其作用机制可能与其抗氧化作用、减轻肺水肿和减少炎症因子的释放有关。     

塞来昔布通过MAPK/ERK信号通路抑制炎症反应改善急性脑出血大鼠神经功能的机制研究

目的 探究塞来昔布对大鼠急性脑出血神经功能的影响。方法 采用随机数字表法将SD大鼠分为假手术组、模型组、抑制剂组和塞来昔布组。除假手术组外各组采用自体血注入法制作脑出血模型。抑制剂组大鼠在模型组基础上在前侧脑室注射细胞外调解蛋白激酶(ERK)抑制剂(DCZ19931),塞来昔布组大鼠腹腔注射100 mg·kg^-1·d^-1的塞来昔布,连续两周。采用Longa五级评分法比较大鼠神经功能损伤程度;检测各组大鼠脑组织含水量,同时采用免疫印迹法检测各组大鼠脑组织中水通道蛋白4(AQP4)表达水平;采用酶联免疫吸附法检测各组大鼠脑组织中白细胞介素-1β(IL-1β)、肿瘤坏死因子-α(TNF-α)、超氧化物歧化酶(SOD)和丙二醛(MDA)含量;采用免疫印迹法检测各组大鼠丝裂原活化蛋白激酶(MAPK)/ERK信号通路蛋白表达情况。结果 与假手术组相比,模型组大鼠神经功能评分、脑组织含水量、脑组织中AQP4蛋白相对表达水平、IL-1β、TNF-α、MDA含量、p-ERK1、p-ERK2、MAPK蛋白相对表达水平显著升高,SOD含量显著降低(P <0....     

炎症介质在重症急性胰腺炎大鼠并发脑损伤中的作用

目的 探讨炎症介质在大鼠重症急性胰腺炎(SAP)并发脑损伤中的作用.方法 60只雄性SD大鼠随机均分为两组:SAP模型组以0.1 ml/min匀速逆行胰管注入3.5％牛磺胆酸钠0.1 ml/100 g;假手术组作为对照.每组又均分为3个亚组,分别于建模后3、6和12h应用放射免疫法测定血清TNF-α和IL-1β水平,采用化学比色法检测脑组织丙二醛(MDA)及超氧化物歧化酶(SOD)含量,RT-PCR法检测脑组织TNF-αmRNA和IL-1β mRNA含量,免疫组织化学法检测脑组织核因子κB(NF-κB) p65活性.结果 与假手术组比较,SAP组血清TNF-α及IL-1β水平、脑组织NF-κB p65活性、脑组织MDA含量、脑组织TNF-α mRNA及IL-1βmRNA含量均随着时间的延长逐步升高,而脑组织SOD含量逐步降低(P＜0.01).结论 炎症介质在SAP相关性脑损伤的发生、发展中发挥重要作用.     

参茸益精片对急性高原缺氧脑损伤的保护作用研究

目的观察参茸益精片对急性高原缺氧脑损伤的保护作用,并探讨其分子机制。方法将SD大鼠随机分为空白对照组(对照组)、高原急性缺氧模型组(模型组)和参茸益精片治疗组(治疗组),每组6只。建立急性高原缺氧脑损伤大鼠动物模型,治疗组灌胃参茸益精片。观察大鼠脑组织SOD活性和MDA水平的变化,Western blot和RT-PCR检测胆碱乙酰转移酶(Choline acetyltransferase,ChAT)和蛋白激酶C(Protein kinase C,PKC)表达水平的变化。结果与对照组比较,模型组大鼠脑组织SOD活性显著降低(P<0.01),MDA水平显著增加(P<0.01);治疗组大鼠脑组织SOD活性显著增加(P<0.01),MDA水平显著降低(P<0.01)。模型组大鼠脑组织ChAT和PKC表达水平显著降低(P<0.05),治疗组ChAT和PKC表达水平显著升高(P<0.05)。结论参茸益精片可以保护急性高原缺氧引起的脑损伤,可能与其调节ChAT和PKC的表达水平有关。     

藏药复方多血康胶囊对脂多糖诱导急性肺损伤小鼠的保护作用

目的:考察藏药复方多血康胶囊对脂多糖诱导急性肺损伤小鼠的保护作用。方法:将60只KM小鼠随机分为空白组、模型组、地塞米松组(阳性对照,1 mg/kg)和复方多血康胶囊高、中、低剂量组(3.6、1.8、0.9 g/kg,以生药计),每组10只。ig给药,空白组和模型组小鼠ig等体积生理盐水,每天1次。连续给药7 d后,除空白组外,其余各组小鼠均ip脂多糖诱导急性肺损伤。造模6h后,观察小鼠肺组织病理改变,测量肺组织含水量,检测肺组织中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、丙二醛(MDA)水平以及血清中白细胞介素6(IL-6)、肿瘤坏死因子α(TNF-α)水平。结果:与空白组比较,模型组小鼠肺组织发生充血水肿、炎症细胞浸润、肺泡间隔及肺泡壁明显增宽等病理变化,肺组织含水量和肺组织中MDA水平以及血清中IL-6、TNF-α水平均显著升高(P<0.01),肺组织中SOD、GSH-Px水平显著降低(P<0.05)。与模型组比较,各给药组小鼠肺组织损伤程度均不同程度降低;除复方多血康胶囊低剂量组大鼠肺组织含水量、肺组织中MDA水平以及血清中TNF-α水平变化不明显外,其余各给药组小鼠上述指标均显著改善(P<0.05或P<0.01)。结论:藏药复方多血康胶囊可明显减轻小鼠氧化应激和炎症反应,对脂多糖诱导的急性肺损伤小鼠有一定保护作用。     

虎杖苷对模拟高原低氧环境所致小鼠脑、肺损伤的保护作用

目的探讨中药提取物虎杖苷对模拟高原低氧环境下小鼠脑、肺组织损伤的保护作用及其可能机制。方法 50只昆明小鼠随机分为平原对照组、高原低氧模型组及虎杖苷低、中、高剂量组[25、50、100 mg/(kg·d)],每组10只。给药组灌胃虎杖苷溶液,对照组及模型组灌胃等体积溶媒,连续给药7 d后,放置于复合环境模拟实验舱内,模拟海拔6 000 m高度72 h。出舱后处死动物,取肺叶及脑HE染色观察组织病理学变化;干湿重法测定肺组织湿干比值及脑含水量;化学法测定超氧化物歧化酶(SOD)活性、丙二醛(MDA)含量;ELISA法测定肺组织肿瘤坏死因子(TNF-α)及白细胞介素6(IL-6)含量;免疫组化法检测肺组织Toll样受体2/4(TLR2/4)蛋白表达。结果与平原对照组相比,高原低氧模型组小鼠肺组织出现明显炎性渗出、水肿,神经元细胞核固缩、浓染等病理改变,肺湿干质量比(W/D)和脑含水量明显升高(P<0.05),组织匀浆中MDA、TNF-α及IL-6含量明显升高(P<0.05),SOD活性明显降低(P<0.05);与高原低氧模型组相比,虎杖苷连续给药7 d,能改善脑、肺组织的病理性变化,明显提高小鼠肺、脑组织SOD活性,降低MDA水平,抑制肺组织炎性因子TNF-α、IL-6的升高(P<0.05或P<0.01);免疫组化结果显示,高原低氧模型组小鼠肺组织出现明显TLR2/4蛋白阳性表达,而虎杖苷中、高剂量组表达均降低(P<0.01)。结论虎杖苷可以降低脑含水量、肺W/D及MDA含量,提高SOD活性,抑制肺组织中TNF-α及IL-6水平,从而减轻小鼠在高原缺氧环境下脑、肺组织损伤,虎杖苷抑制炎症反应的作用机制可能与其调节TLR2/4的表达有关。     

芪蛭通络胶囊及其9味活血化瘀药拆方对脑缺血再灌注损伤模型大鼠的保护作用

目的:研究芪蛭通络胶囊及其9味活血化瘀药拆方对大鼠脑缺血再灌注损伤的保护作用,为通过拆方的方法研究芪蛭通络胶囊活性成分奠定基础。方法:将60只SD大鼠随机分为假手术组(0.5%羧甲基纤维素钠)、模型组(0.5%羧甲基纤维素钠)、芪蛭通络胶囊缺活血化瘀药味组[0.389 g/(kg·d)]、芪蛭通络胶囊活血化瘀药味组[0.253 g/(kg·d)]和芪蛭通络胶囊成品组[0.500 g/(kg·d)],每组12只;各组大鼠均灌胃给药,每天1次,连续14 d;末次给药2 h后,除假手术组外,其余各组大鼠均采用线栓法复制脑缺血再灌注损伤模型。缺血2 h再灌注24 h后,依据Bederson评分法对各组大鼠进行神经功能评分,氯化三苯基四氮唑(TTC)染色法计算其脑梗死面积,生化法测定大鼠脑组织中一氧化氮(NO)、丙二醛(MDA)、乳酸脱氢酶(LDH)、超氧化物歧化酶(SOD)的含量,酶联免疫吸附法检测大鼠脑组织中白细胞介素1β(IL-1β)、肿瘤坏死因子α(TNF-α)的含量。结果:与假手术组比较,模型组大鼠的神经功能评分显著升高(P<0.05),脑梗死面积和脑组织中NO、MDA、LDH、IL-1β、TNF-α含量均显著增加(P<0.05),脑组织中SOD含量显著减少(P<0.05)。与模型组比较,各给药组大鼠神经功能评分均显著降低(P<0.05),脑梗死面积和脑组织中NO、MDA、LDH、IL-1β、TNF-α含量均显著减少(P<0.05),脑组织中SOD含量显著增加(P<0.05)。与芪蛭通络胶囊成品组比较,芪蛭通络胶囊活血化瘀药味组和芪蛭通络胶囊缺活血化瘀药味组大鼠脑梗死面积和脑组织中NO、MDA、LDH、IL-1β、TNF-α含量均显著增加(P<0.05),SOD含量均显著减少(P<0.05)。结论:芪蛭通络胶囊的全方及其9味活血化瘀药(或不含9味活血化瘀药)的拆方对大鼠脑缺血再灌注损伤均具有一定的保护作用,活血化瘀药味拆方的保护作用虽不及全方,但全方缺活血化瘀药味后其保护作用也明显下降,表明活血化瘀药在全方发挥保护脑缺血再灌注损伤功能中具有重要作用,将活血化瘀药物拆分出来研究对阐明芪蛭通络胶囊全方的作用具有一定的意义。     

α-细辛脑防治青霉素诱导大鼠癫痫发作实验研究

目的 观察α-细辛脑对青霉素诱导大鼠癫痫急性发作的作用并分析其抗癫痫的作用机制.方法 将wistar大鼠随机分成正常对照组、模型对照组和药物实验组,正常对照组和模型对照组大鼠腹腔注射生理盐水,药物实验组腹腔注射α-细辛脑,20min后模型对照组和药物实验组注射青霉素(480万U/kg)诱导大鼠癫痫发作.观察并比较3组大鼠的行为变化情况,比色法检测大鼠脑组织中超氧化物歧化酶(SOD)、丙二醛(MDA)含量,ELISA方法 检测白细胞介素1β(IL-1β)与肿瘤坏死因子(TNF-α)含量. 结果 α-细辛脑可使癫痫大鼠发作程度减轻和发作潜伏期延长;使癫痫大鼠脑内MDA、TNF-α和IL-1β含量明显降低,SOD活性明显升高.结论 α-细辛脑可有效地防治癫痫的发作并有效地改善癫痫大鼠的预后情况.其抗癫痫作用与调节脑组织的相关因子、提高其脑组织清除自由基、增强抗氧化作用有着密切关系.     

阿尔泰金莲花总黄酮对PM_(2.5)致人支气管上皮BEAS-2B细胞急性损伤保护作用的研究

目的探讨阿尔泰金莲花总黄酮对PM_(2.5)致人支气管上皮BEAS-2B细胞急性损伤的保护作用及其可能的作用机制。方法将细胞分为正常对照组,PM_(2.5)模型组,PM_(2.5)+阿尔泰金莲花总黄酮高、中和低剂量(28.19、14.10和7.05 mg/L)组,PM_(2.5)+地塞米松阳性对照(1 mmol/L)组;实验开始时,各组根据所设药物剂量分别干预细胞24 h;24 h后除正常对照组外,其余各组均用浓度为100 mg/L PM_(2.5)溶液作用于BEAS-2B细胞24 h,构建急性肺损伤(ALI)模型;24 h后收集细胞与培养上清液,酶联免疫吸附法(ELISA)测定细胞培养上清液IL-6、IL-8、IL-1β和TNF-α含量,比色法细胞内超氧化物歧化酶(SOD)含量、丙二醛(MDA)含量、还原型谷胱甘肽(GSH)含量和培养上清液中乳酸脱氢酶(LDH)漏出量;qRT-PCR检测各组细胞内IL-6、IL-8、IL-1β和TNF-αmRNA含量。结果与PM_(2.5)模型组相比,PM_(2.5)+阿尔泰金莲花总黄酮各剂量组细胞培养上清液中IL-1β、IL-6、IL-8和TNF-α含量与细胞内IL-1β、IL-6、IL-8和TNF-αmRNA的表达水平均降低均降低(P0.05);PM_(2.5)+阿尔泰金莲花总黄酮各剂量组细胞内SOD和GSH含量均升高,细胞内MDA和细胞培养上清中LDH含量均降低(P0.05);相比于PM_(2.5)+地塞米松阳性对照组,PM_(2.5)+阿尔泰金莲花总黄酮高和中剂量组细胞培养上清液中IL-1β、IL-6、IL-8和TNF-α含量与细胞内IL-1β、IL-6、IL-8和TNF-αmRNA的表达水平均降低(P0.05);细胞内SOD和GSH含量均升高,细胞内MDA和细胞培养上清中LDH含量均降低(P0.05)。结论阿尔泰金莲花总黄酮提取物对PM_(2.5)诱导的BEAS-2B细胞急性损伤具有一定的保护作用,其作用机制可能与其抑制炎症反应、抗氧化损伤有关。     

Efficacy of gut lavage,hemodialysis, and hemoperfusion in the therapy of paraquat or diquat intoxication

Clinical and in vitro investigations were carried out to test the efficacy of gut lavage, hemodialysis, and hemoperfusion in the treatment of poisoning with paraquat or diquat. In a patient suffering from diquat intoxication 130 times more diquat was removed by gut lavage 30 h after ingestion than was removed by complete aspiration of the gastric contents.Determination of in vitro clearances for paraquat and diquat by hemodialysis showed that, at serum concentrations of 1–2 ppm, such as are frequently encountered in poisoning in man, toxicologically relevant quantities of herbicide cannot be removed from the body. At a concentration of 20 ppm, on the other hand, hemodialysis proved to be effective, the clearance being 70 ml/min at a blood flow rate of 100 ml/min. The efficacy of hemoperfusion with coated activated charcoal was on the whole better. Especially at concentrations around 1–2 ppm, the clearance values for hemoperfusion were some 5–7 times higher than those for hemodialysis.In a patient suffering from paraquat poisoning, both hemodialysis as well as hemoperfusion were carried out. The in vitro results could be confirmed: At serum concentrations of paraquat less than 1 ppm no clearance could be obtained by hemodialysis while by hemoperfusion with activated charcoal quite high clearance values were measured and the serum level dropped down to zero.

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Zusammenfassung Klinische Untersuchungen und Laboratoriumsversuche wurden durchgeführt, um die Wirksamkeit von Darmspülung, Hämodialyse und Hämoperfusion bei Paraquat- und Deiquat-Vergiftungen zu prüfen.Bei einem Patienten wurde 30 Std nach Deiquat-Aufnahme durch Darmspülung 130mal mehr Deiquat entfernt als durch vollständige Aspiration des Mageninhaltes. In vitro-Versuche ergaben, daß bei Blutserumkonzentrationen von 1–2 ppm, die bei Vergiftungen oft gemessen werden, durch Hämodialyse keine toxikologisch relevanten Paraquat- oder Deiquat-Mengen entfernt werden können. Dagegen erwies sich die Hämodialyse bei 20 ppm und einer Blutumlaufgeschwindigkeit von 100 ml/min mit einer Clearance von 70 ml/min als wirksam. Die Hämoperfusion mit beschicheter Aktivkohle war in diesen Versuchen aber eindeutig überlegen, denn insbesondere bei Konzentrationen um 1–2 ppm waren die Clearance-Werte 5–7mal höher als bei der Hämodialyse.Die in vitro-Ergebnisse wurden bei einem Patienten mit einer Paraquat-Vergiftung bestätigt: Bei Konzentrationen unter 1 ppm war die Hämodialyse wirkungslos, während durch Hämoperfusion relativ hohe Clearance-Werte erreicht wurden, so daß der Serumspiegel rasch unter die Nachweisgrenze abfiel.

     

In vitro studies on sterically stabilized liposomes (SL) as enzyme carriers in organophosphorus (OP) antagonism

This study describes a new approach for organophosphorous (OP) antidotal treatment by encapsulating an OP hydrolyzing enzyme, OPA anhydrolase (OPAA), within sterically stabilized liposomes. The recombinant OPAA enzyme was derived from Alteromonas strain JD6. It has broad substrate specificity to a wide range of OP compounds: DFP and the nerve agents, soman and sarin. Liposomes encapsulating OPAA (SL)* were made by mechanical dispersion method. Hydrolysis of DFP by (SL)* was measured by following an increase of fluoride ion concentration using a fluoride ion selective electrode. OPAA entrapped in the carrier liposomes rapidly hydrolyze DFP, with the rate of DFP hydrolysis directly proportional to the amount of (SL)* added to the solution. Liposomal carriers containing no enzyme did not hydrolyze DFP. The reaction was linear and the rate of hydrolysis was first order in the substrate. This enzyme carrier system serves as a biodegradable protective environment for the recombinant OP-metabolizing enzyme, OPAA, resulting in prolongation of enzymatic concentration in the body. These studies suggest that the protection of OP intoxication can be strikingly enhanced by adding OPAA encapsulated within (SL)* to pralidoxime and atropine.     

Aquatic Insects and Trace Metals: Bioavailability,Bioaccumulation, and Toxicity

Abstract

The uptake of metals from food and water sources by insects is thought to be additive. For a given metal, the proportions taken up from water and food will depend both on the bioavailable concentration of the metal associated with each source and the mechanism and rate by which the metal enters the insect. Attempts to correlate insect trace metal concentrations with the trophic level of insects should be made with a knowledge of the feeding relationships of the individual taxa concerned. Pathways for the uptake of essential metals, such as copper and zinc, exist at the cellular level, and other nonessential metals, such as cadmium, also appear to enter via these routes. Within cells, trace metals can be bound to proteins or stored in granules. The internal distribution of metals among body tissues is very heterogeneous, and distribution patterns tend to be both metal and taxon specific. Trace metals associated with insects can be both bound on the surface of their chitinous exoskeleton and incorporated into body tissues. The quantities of trace meals accumulated by an individual reflect the net balance between the rate of metal influx from both dissolved and particulate sources and the rate of metal efflux from the organism. The toxicity of metals has been demonstrated at all levels of biological organization: cell, tissue, individual, population, and community. Much of the literature pertaining to the toxic effects of metals on aquatic insects is based on laboratory observations and, as such, it is difficult to extrapolate the data to insects in nature. The few experimental studies in nature suggest that trace metal contaminants can affect both the distribution and the abundance of aquatic insects. Insects have a largely unexploited potential as biomonitors of metal contamination in nature. A better understanding of the physico-chemical and biological mechanisms mediating trace metal bioavailability and exchange will facilitate the development of general predictive models relating trace metal concentrations in insects to those in their environment. Such models will facilitate the use of insects as contaminant biomonitors.     

Pharmacological treatment of COVID-19: an opinion paper

The precocity and efficacy of the vaccines developed so far against COVID-19 has been the most significant and saving advance against the pandemic. The development of vaccines has not prevented, during the whole period of the pandemic, the constant search for therapeutic medicines, both among existing drugs with different indications and in the development of new drugs. The Scientific Committee of the COVID-19 of the Illustrious College of Physicians of Madrid wanted to offer an early, simplified and critical approach to these new drugs, to new developments in immunotherapy and to what has been learned from the immune response modulators already known and which have proven effective against the virus, in order to help understand the current situation.     

Alzheimer’s disease – current trends in basic and clinical research. Highlights from the 16th ECNP

Advances in the molecular biological knowledge of neuronal nicotinic acetylcholine receptors (nAChRs) have led to a growing interest by the pharmaceutical industry in the development of novel compounds that selectively modulate nAChR function. The ability of (-)-nicotine, an activator of nAChRs, to enhance attentional aspects of cognition in animals and humans, to exert neuroprotective and anxiolytic-like effects, and presumably to mediate the negative correlation between smoking and Alzheimer's (and Parkinson's) Disease, has focused interest on the potential therapeutic utility of modulators of nAChR function for treatment of some of the deficits associated with these progressive, neurodegenerative conditions. Numerous compounds are known which activate nAChRs and which might serve as lead compounds toward the development of such agents. The pharmacologic diversity of neuronal nAChR subtypes suggests the possibility of developing selective compounds which would have more favourable side-effect profiles than existing agents. This broader class of agents, collectively called cholinergic channel modulators (ChCMs), is anticipated to encompass compounds which would have more favourable side-effect profiles than existing agents, which generally exhibit low selectivity. This selectivity may be achieved by preferentially activating some subtypes of nAChRs (i.e., Cholinergic Channel Activators, ChCAs) or inhibiting the function of other subtypes (Cholinergic Channel Inhibitors, ChCIs). An overview of the biology of nAChRs and the rationale for the use of ChCMs for the treatment of dementia related to neurodegenerative diseases are presented, followed by a discussion of lead compounds and compounds under consideration for clinical evaluation.     

Steroidal sapogenin contents in some domestic plants

In order to find out the values of the steroid resources for the future use. the compositions and contents of steroidal sapogenins from 13 domestic plants have been investigated. As a result,Dioscorea nipponica, D. quinqueloba andSmilax china were found to have large amount of diosgenin. And pennogenin inTrillium kamtschaticum andParis verticillata, yuccagenin inAllium fistulosum, hecogenin inAgave americana and neochlorogenin inSolanum nigum were appeared to be major steroidal sapogenins.