枸杞多糖对衰老小鼠脑NO、NOS的影响

目的研究枸杞多糖对衰老小鼠NO、NOS的影响.方法采用老年小鼠和D-半乳糖致衰老小鼠,分别连续灌服枸杞多糖20mg/kg*d两个月和一个月,应用Griess法检测脑NO含量,双波长分光光度计测定NOS活性.结果老年小鼠和D-半乳糖致衰老小鼠脑NO含量、NOS活性明显低于青年小鼠和正常对照小鼠,给药后则可明显提高之.结论枸杞多糖能明显提高衰老小鼠脑NO含量和NOS活性.     

甘肃党参水提物对D-半乳糖所致衰老小鼠脑组织SOD、MDA影响的实验研究

目的：研究甘肃党参水提物对衰老模型小鼠的影响,初步探讨其延缓衰老的作用机制。方法：采用D-半乳糖致亚急性衰老小鼠模型,测定小鼠脑组织中超氧化物歧化酶（SOD）、丙二醛（MDA）的含量及胸腺指数和脾脏指数。结果：甘肃党参水提取物可明显使D-半乳糖所致衰老小鼠胸腺、脾脏指数升高;提高其脑组织抗氧化酶SOD活性,降低MDA含量。结论：甘肃党参水提物可能通过提高机体免疫功能,清除衰老机体产生的过多的自由基,增强抗脂质过氧化过程而起到延缓衰老的作用。     

仙人掌抗衰老作用的实验研究

目的：探讨仙人掌的抗衰老作用及其机制。方法：以D－半乳糖衰老模型小鼠为实验对象，以其体重、免疫器官重量，肝、脑丙二醛（MDA）、全血、脑谷胱甘肽过氧化物酶（GSH－PX）及血清、脑中超氧化物歧化酶（SOD）的活力为观察指标，观察仙人掌的抗衰老作用。结果：仙人掌大、小剂量均能降低小鼠肝、脑组织MDA含量（P＜0．01），提高全血、脑GSH－PX及血清、脑中SOD活力，并阻抗小鼠体重及胸腺指数下降。结论：仙人掌能有效地防止D－半乳糖所致的小鼠多项衰老体征的出现，改善小鼠的机能状态。     

树舌多糖GF对HepA癌细胞c-Myc mRNA丰度的影响

目的:探明树舌多糖(GAPS)GF对HepA瘤细胞c-Myc mRNA丰度的影响.方法:接种HepA瘤后的小鼠随机分为3组:模型组、树舌多糖组和猪苓多糖组,树舌多糖组和猪苓多糖组小鼠分别注射树舌多糖GF和猪苓多糖.应用原位杂交技术检测各组小鼠HepA癌细胞中c-Myc mRNA的丰度.结果:树舌多糖组、猪苓多糖组中c-Myc表达量均显著低于模型组(P＜0.01),树舌多糖组与猪苓多糖组间无显著性差异.结论:树舌多糖GF抑制c-Myc基因的转录可能是其抗肿瘤的作用机制之一.     

竹节参多糖抗脑衰老作用的实验研究

目的 研究竹节参多糖的抗氧化和延缓衰老作用.方法 颈背部皮下注射D-半乳糖建立小鼠衰老模型,用自制的竹节参多糖分为低、中、高剂量的灌胃药物组,并用生理盐水灌胃作正常对照组,香菇菌多糖作阳性对照组, 连续用药60 d.结果 中、高剂量竹节参多糖能明显提高脑组织中过氧化氢酶(CAT)的活性 (P＜0.01)、降低丙二醛(MDA)含量 (P＜0.01),同时能明显提高血液中超氧化物歧化酶(SOD)的活性.结论 竹节参多糖具有较好的消除自由基、延缓脑衰老的作用.     

紫花地丁总黄酮和多糖对D-半乳糖致衰小鼠血清中过氧化氢酶活性的影响

[目的]研究紫花地丁总黄酮和多糖对D-半乳糖致衰小鼠血清中过氧化氢酶(CAT)活性的影响。[方法]采用D-半乳糖致亚急性衰老法制备小鼠衰老模型,随机分组,分别灌胃给予不同剂量的紫花地丁总黄酮和多糖,测定小鼠血清中CAT的活性。[结果]正常对照组与各治疗组的CAT活力明显高于模型对照组,差异有统计学意义(P<0.05,P<0.01)。紫花地丁总黄酮中、低剂量组提高小鼠血清CAT的活力的作用强于紫花地丁多糖中、低剂量组,差异有统计学意义(P<0.05),紫花地丁总黄酮和多糖高剂量组之间差异无统计学意义。[结论]紫花地丁总黄酮和多糖对D-半乳糖致衰小鼠血清中过氧化氢酶(CAT)的活性具有提高的作用。     

巴戟天多糖的降血糖和抗氧化作用研究

目的:研究巴戟天多糖的降血糖和抗氧化作用.方法:采用肾上腺素所致高血糖小鼠模型及四氧嘧啶所致高血糖小鼠模型,观察巴戟天多糖对实验性高血糖小鼠的降血糖作用;采用D-半乳糖致小鼠衰老模型,观察巴戟天多糖对小鼠血浆、肝、心和脑中SOD活性及MDA含量的影响.结果:巴戟天多糖能降低肾上腺素和四氧嘧啶所致高血糖小鼠的血糖,能提高D-半乳糖衰老型小鼠血浆、肝、心和脑中SOD的活性并降低MDA的含量.结论:巴戟天多糖具有降血糖及抗氧化作用.     

肾阳虚小鼠睾丸NO、NOS、MDA、SOD变化的实验研究

目的:以"劳倦过度、房事不节"肾阳虚小鼠为模型,观察该模型小鼠睾丸NO、NOS和MDA、SOD的变化.方法:用强迫小鼠游泳法造成劳倦过度,以Colldege效应诱导雄性小鼠房事不节,建立肾阳虚小鼠模型.造模4周后,检测睾丸组织匀浆中NO和MDA含量以及NOS和SOD活力.结果:造模组睾丸中NO含量和NOS活力显著增强(P＜0.01),MDA含量上升(P＜0.05),SOD活力下降(P＜0.05);肾气丸干预组NOS活力显著降低(P＜0.01),NO和MDA含量明显减少(P＜0.05),SOD活力升高(P＜0.05).结论:肾阳虚小鼠睾丸组织内自由基生成增多,自由基清除能力下降.     

制何首乌多糖对衰老模型小鼠抗氧化作用的研究

目的 :观察制何首乌多糖的抗氧化作用。方法 :应用D 半乳糖复制小鼠衰老模型。结果 :制何首乌多糖能显著提高D 半乳糖衰老模型小鼠血SOD、CAT及GSH Px活力 ,降低血浆、脑匀浆及肝匀浆LPO水平。结论 :制何首乌多糖有抗氧化作用。     

大枣多糖对小鼠腹腔巨噬细胞吞噬功能的影响

目的:观察大枣多糖对正常及免疫抑制小鼠腹腔巨噬细胞吞噬功能的影响.方法:选择40只正常小鼠,随机分成4组,分别口服自来水和16、8、4g·kg-1大枣多糖;另外30只小鼠,随机分成3组,即空白组,环磷酰胺(CY)免疫抑制组和免疫抑制多糖组,4周后,计算小鼠腹腔巨噬细胞的吞噬百分率和吞噬指数.结果:不同剂量大枣多糖可显著提高小鼠腹腔巨噬细胞的吞噬率,免疫抑制组小鼠各指标显著低于正常对照组,大枣多糖可明显改善免疫抑制小鼠腹腔巨噬细胞的吞噬功能.结论:大枣多糖能增强小鼠腹腔巨噬细胞的吞噬功能并对CY所致的免疫抑制具有明显的拮抗作用.     

实验性肝损伤模型建立的初步探讨

目的建立四氯化碳(CCl4)所致大鼠急性肝损伤、小鼠四氯化碳反复给予造成肝中毒及酒精性肝病小鼠模型,筛选最佳给药剂量和次数。方法①SD大鼠每隔2天给予CCl41次,连续4次(10天),采用灌胃(ig)和腹腔注射(ip)的两种途径,测定谷丙转氨酶(ALT)及谷草转氨酶(AST),并测体重和肝脏重、胸腺重,求脏器系数。②给小鼠CCl4灌胃给药,观察CCl4给药后24-96h(1-4d)的血清ALT变化。③给小鼠不同剂量、次数和时间的酒精,测定血清ALT。结果①CCl4所致大鼠急性肝损伤模型给药途径以腹腔注射为好,CCl4浓度以10%为好。②小鼠四氯化碳反复给予造成肝中毒,以20%CCl40.05ml/10g,三天1次灌胃给药的方法为好。③关于酒精所致小鼠急性肝损伤模型,以二锅头酒原液0.1ml/10g一天1次,5-7天的酒量为好。结论本试验筛选了实验性肝损伤模型的CCl4浓度、剂量及给药途径和酒精剂量、次数和时间,但为更好地建立模型,有待进一步探讨。     

Studies on pharmacological junctions of hairy root of Astragalus membranaceus]

OBJECTIVE: To investigate the effect of hairy root of Astragalus membranaceus(HRA). METHOD: HRA were given 10 g/kg per day for 50 days to aged mice treated with D-galactose, and the effect on memory and antioxidant functions were estimated. After administration of HRA 10 g/kg for four days, anti-ischemia-reperfusion kidney model of rat was prepared. The kidney function, activity of superoxide dismutase (SOD) and content of malondialdehyde(MDA) in kidney were examined. Mice with immunosuppression induced by cyclophosphamide were given orally HRA 10 g/kg for 12 days. The activity of natural killer (NK) cells was measured. RESULT: HRA improved the memory, raised SOD activity in brain and liver, decreased the MDA content in the liver of aged mice, reduced the MDA content in ischemia-reperfusion kidney, decreased the creatinine level in blood of rats, and promoted the activity of NK cells in immunosuppressed mice. CONCLUSION: Similar to the natural A. membranaceus, HRA has senility-preventing, antioxidizing and immunomodulating functions.     

养寿丹延缓衰老作用的实验研究

养寿丹延缓衰老作用的实验研究结果发现,养寿丹可使小鼠红细胞超氧化物岐化酶(SOD)的活性明显增强,使小鼠血清和肝组织中的过氧化脂质(LPO)的含量降低,并能降低小鼠心肌脂褐质含量,可延长果蝇的平均寿命及半数致死天数和置高寿命。说明养寿丹具有一定程度的延缓衰老作用。     

猪苓多糖对肝损伤小鼠单核巨噬细胞的影响

本实验抽取小鼠腹腔渗出细胞,体外培养,用荧光测定法检测腹腔巨噬细胞释放的 H_2O_2量。结果表明 CCl_4所致肝损伤小鼠腹腔单核巨噬细胞数和释放 H_2O_2能力明显下降,猪苓多糖能增加和回升正常及肝损伤小鼠的腹腔巨噬细胞数量和释放 H_2O_2能力。该药能提高机体的细胞免疫功能,是治疗慢性肝炎的重要机理之一。     

Yang-gan-wan protects mice against apoptosis induced by anti-Fas antibody (Jo2)

We investigated the protective effect of yang-gan-wan (YGW, Pro-Liver pill), a Chinese herbal remedy, against liver apoptosis (programmed cell death) induced by anti-Fas antibody (Jo2). Mice were pretreated daily with 200 mg/kg YGW for 14 days before treatment with 10 microg/20 kg body weight Jo2. YGW significantly reduced the elevated activity of alanine aminotransferase (ALT) and also reduced the elevated activity of sorbitol dehydrogenase (SDH) produced 4 hrs after treatment with Jo2. YGW also increased the survival of mice treated with Jo2 by about 1 hr in 11 out of 16 mice (69%). Most of the mice died 9 hrs after Jo2 injection. This study demonstrates that YGW has protective effects against liver apoptosis induced by Jo2.     

Prevention of hepatic injury by a traditional Chinese formulation, BJ-JN, in mice treated with Bacille-Calmette-Guérin and lipopolysaccharide

The hepatoprotective effects of BJ-JN (a traditional Chinese formulation) were evaluated in Bacille-Calmette-Guérin and lipopolysaccharide (BCG/LPS)-induced immunological liver injury (ILI) in mice. BJ-JN (0.75, 1.5, 3 g/kg) was administered via gavage daily for 10 days. Liver index (liver weight/body weight), serum levels of alanine aminotransferase (ALT), hepatic nitric oxide (NO), malondialdehyde (MDA) content, superoxide dismutase (SOD) activity, splenocyte proliferation, production of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) by peritoneal macrophages, and histopathologic changes of the liver were evaluated following the 10 days treatment. BJ-JN (0.75, 1.5, 3 g/kg) effectively reduced the BCG/LPS-induced elevated liver index, serum ALT levels, hepatic NO and MDA content, and restored hepatic SOD activity in ILI mice. BJ-JN treatment also alleviated diminished splenocyte proliferation induced by concanavalin A (ConA) and repressed abnormally high levels of TNF-alpha and IL-1 from peritoneal macrophages. The histopathological analysis suggested that BJ-JN reduced the degree of liver injury of ILI mice. These results suggest that BJ-JN has a protective and therapeutic effect on ILI mice, which might be associated with its antioxidant properties, ability to reduce NO production and immunoregulatory function.     

淫羊藿黄酮对抗小鼠D-半乳糖衰老模型的研究

雄性小白鼠隔日皮下注射D-半乳糖40mg/kg68天可造成亚急性衰老模型,在注射D-半乳糖的同时PO淫羊藿黄酮0.70g/kg能显著恢复D-半乳糖衰老模型小鼠T和B淋巴细胞增殖反应的功能,明显提高小鼠肝脏总SOD的活性,减少肝组织过氧化脂质的形成,减少心、肝等组织的脂褐素形成,但对脑的脂褐素减少不明显。     

Peucedanum japonicum Thunb inhibits high-fat diet induced obesity in mice

This study examined the antiobese activity of Peucedanum japonicum Thunb (PJT) in mice. In the first experiment, 4-week-old C57BL/6 mice were fed seven different diets containing 15% corn oil and 0-20% PJT powder for 4 weeks. Feeding the 10% and 20% PJT diet suppressed the body weight gain and the accumulation of abdominal and subcutaneous fats. PJT reduced serum and liver levels of triglyceride and serum levels of leptin in a dose-dependent manner. PJT intake decreased the proportion of saturated fatty acids and increased polyunsaturated and n-3 fatty acids in the liver. To obtain more insight into the antiobese activity of PJT, its effect on lipid absorption and enzyme activities related to lipid metabolism was studied in the second experiment. There was an increased faecal excretion of triglyceride in mice fed 5% and 10% PJT diets. Fatty acid synthase activity was decreased while carnitine palmitoyltransferase activity was increased by 10% PJT intake. These findings pointed to the usefulness of PJT for the development of a safe natural agent to reduce obesity or body weight for the first time. The rationale for the lipid lowering mechanism of PJT and the candidate compound responsible for the observations have also been discussed.     

肿节风注射液抗小鼠前胃癌FC的作用及毒性

目的 研究肿节风注射液(zJF)抗小鼠前胃癌FC的作用及毒性。方法 建立小鼠体内荷小鼠前胃癌FC模型，测定zJF的抑制率和体重、胸腺指数和脾指数以及给药前后外周血白细胞的变化，同时研究zJF对小鼠前胃癌FC细胞株生长的抑制作用。结果 zJF具有明显的抗肿瘤作用，ipZJF0.2g/kg、1g/kg、0.2g/kg的抑瘤率分别为39．83％、64．41％、53．39％，又能明显升高荷瘤小鼠的脾指数和胸腺指数，升高外周血白细胞，增加荷瘤小鼠的体重。zJFl00mg／mL、50mg／mL、25mg／mL、12．5mg／mL、6．25mg／mL对小鼠前胃癌FC细胞增殖的抑制率分别为65％、63％、57％、55％、44％。结论 zJF体内、外对小鼠前胃癌FC均具有抗肿瘤作用，并可增加荷瘤鼠免疫器官指数及外周血白细胞数。     

次黄嘌呤－内源性单胺氧化酶（MAO）抑制剂样活性的研究

体外实验证明，嘌呤类化合物对Ｂ－型ＭＡＯ活性有不同程度的抑制作用，其抑制强度为：次黄嘌呤＞鸟便嘌呤＞腺嘌呤＞嘌呤＞黄嘌呤＞尿酸。老龄小鼠（１８月龄）的血、脑及肝组织ＭＡＯ活性较年青小鼠（１月龄）显著升高，而上述组织中嘌呤类化合物的含量却随年龄增加而降低。老龄小鼠肝线粒体外膜ＭＡＯ提取物中次黄嘌呤含量明显低于年青小鼠，但两组ＭＡＯ中腺嘌呤含量却无明显差异。离体温孵实验证明［３Ｈ］次黄嘌呤与老龄小鼠脑和肝ＭＡＯ结合量明显高于年青小鼠。体内结合实验结果亦表明［３Ｈ］次黄嘌呤与老龄小鼠肝ＭＡＯ结合量高于年青小鼠外，并证明［３Ｈ］次黄嘌呤的结合部位是在ＭＡＯ酶蛋白上，而非在辅基上。此外，多次灌服次黄嘌呤２００ｍｇ／ｋｇ可明显抑制老龄小鼠脑ＭＡＯ－Ｂ活性，并使单胺类物质（５－ＨＴ、ＤＡ）含量明显增加。