左归丸对低钾大鼠小脑颗粒神经元凋亡的保护作用

目的：探讨补益方左归丸体外抗凋亡作用及其分子机制。方法：应用体外培养的大鼠小脑颗粒神经元去极化诱导凋亡模型，观察不同浓度左归丸水提液对神经元存活率、DNA断裂特性、胞核形态学变化的影响。结果：左归丸水提液浓度依赖性地逆转低钾所致的大鼠小脑颗粒神经元凋亡，这种逆转作用不能被ERK抑制剂PD98059所阻断，但可被PI3K抑制剂LY294002阻断。结论：左归丸水提液对低钾所致的大鼠小脑颗粒神经元凋亡有保护作用，PI3K／Akt信号传导通路参与其作用。     

左归丸对低钾大鼠小脑颗粒神经元凋亡的保护作用

目的 :探讨补益方左归丸体外抗凋亡作用及其分子机制。方法 :应用体外培养的大鼠小脑颗粒神经元去极化诱导凋亡模型 ,观察不同浓度左归丸水提液对神经元存活率、DNA断裂特性、胞核形态学变化的影响。结果 :左归丸水提液浓度依赖性地逆转低钾所致的大鼠小脑颗粒神经元凋亡 ,这种逆转作用不能被ERK抑制剂PD980 5 9所阻断 ,但可被PI3K抑制剂LY2 94 0 0 2阻断。结论 :左归丸水提液对低钾所致的大鼠小脑颗粒神经元凋亡有保护作用 ,PI3K/Akt信号传导通路参与其作用。     

钙调素拮抗剂E6对缺血性损伤神经细胞的保护作用

 目的:观察具有较强钙调素拮抗活性的双苄基异喹啉类化合物E6对缺血性神经细胞损伤的保护作用?方法:采用NaCN加缺糖引起肾上腺髓质瘤细胞(PC12细胞株)损伤和谷氨酸(glutamate,Glu)引起乳大鼠脑皮质神经细胞损伤模型?结果:E6对NaCN加缺糖损伤的PC12细胞保护作用较弱,而对Glu损伤的原代皮质细胞有较强的保护作用,并降低培养液中一氧化氮(NO)的含量?NO合成前体L-精氨酸(L-arginine,L-Arg)可减弱E6的保护作用?E6对硝普钠(sodium nitroprusside,SNP)损伤的原代神经细胞无保护作用?结论:E6可能是作用于Glu引起神经元损伤途径中NO生成之前的环节,从而表现出对缺血样损伤神经细胞的保护作用?     

白芸豆中α-淀粉酶抑制剂的研究

α-淀粉酶抑制剂(α-amylase inhibitor,简称α-AI)是一种天然生物活性物质,属于糖苷水解酶的一种,国外称之为"starch blocker".α-AI能抑制肠胃道内唾液、胰淀粉酶的活性,阻碍或延缓人体对食物中主要的碳水化合物的水解和消化,降低食物中淀粉糖类物质的分解吸收,从而起到降低血糖、血脂的作用,抑制血糖浓度的升高,从而有利于糖尿病患者的饮食治疗.     

三黄颗粒对α-萘异硫氰酸酯诱导胆汁淤积大鼠肝损伤保护作用的研究

目的:探究三黄颗粒对α-萘异硫氰酸酯诱导胆汁淤积性大鼠肝损伤的保护作用。方法:将72只SD大鼠随机分为6组,正常对照组、模型组、阳性对照组和三黄颗粒低、中、高剂量组,每组12只,隔日1次ANIT灌胃造模,各组连续灌胃给药4周,取血并采集肝脏标本。放射免疫法检测LA、HA、PC-Ⅲ、IV-C值;全自动生化分析仪检测大鼠血清肝功能生化指标;切取大鼠肝中叶,制作病理组织切片,光学显微镜下观察。结果:三黄颗粒组大鼠肝功能指标较模型组均不同程度的降低;肝脏纤维化指标有明显的改善;大鼠肝HE染色切片得出,高、中、低剂量组之间存在差异,肝脏形态改善明显。结论:三黄颗粒可减轻α-萘异硫氰酸酯诱导胆汁淤积性大鼠肝损伤病理变化,改善肝功能,减轻肝脏纤维化,中等剂量疗效较好。     

肾炎2号对IgA肾病大鼠α-平滑肌肌动蛋白表达的实验研究

目的:探讨肾炎2号对IgA肾病大鼠肾小球内α-平滑肌肌动蛋白(α-SMA)表达的影响。方法:使用口服和尾静脉注射牛血清白蛋白(BSA)的方法进行IgA肾病模型的制作,治疗组、对照组造模同时分别给予肾炎2号(15g/kg)和福辛普利(4.17mg/kg)至12周末。观察尿常规、24h尿蛋白定量、肾组织的病理改变及肾小球内α-平滑肌肌动蛋白(α-SMA)的表达。结果:①第7~12周末模型组的24h尿蛋白定量明显高于正常组、治疗组与对照组(P<0.01)。②与模型组比较,治疗组大鼠肾小球内α-SMA的表达减弱(P<0.01),但治疗组、对照组相比无明显统计学上的差异(P>0.05)。结论:肾炎2号具有减轻肾小球内α-SMA的表达的作用。     

越鞠丸合甘麦大枣汤加减对谷氨酸诱导的HT22细胞损伤模型的神经保护作用

目的:探讨越鞠丸合甘麦大枣汤加减(YJGZ)对谷氨酸诱导的小鼠海马神经元细胞系(HT22)细胞损伤的神经保护作用。方法:HT22细胞系无菌培养,以高浓度谷氨酸建立细胞损伤模型,并制备YJGZ水提液和含药血清,分为正常组,模型组,YJGZ含药血清组(1%,5%,10%),YJGZ水提液组(166 mg·L~(-1)),尼莫地平组(100μmol·L~(-1))。噻唑蓝(MTT)比色法检测各组细胞存活率;酶联免疫吸附测定(ELISA)检测乳酸脱氢酶(LDH)释放率及细胞内活性氧自由基(ROS)的含量;蛋白免疫印迹法(Western blot)检测海马N-甲基-D-天冬氨酸受体亚单位2B蛋白(NR2B),环磷腺苷效应元件结合蛋白(CREB),磷酸化CREB(p-CREB),细胞外调节蛋白激酶(ERK),磷酸化ERK(p-ERK)的蛋白表达水平。结果:与正常组比较,模型组细胞存活率显著下降(P 0. 01),乳酸脱氢酶(LDH)释放率明显增加(P 0. 05),细胞内活性氧(ROS)水平明显增加(P 0. 05),NR2B蛋白的表达明显升高(P 0. 05),CREB,p-CREB,ERK,p-ERK蛋白表达水平明显降低(P 0. 05);与模型组比较,YJGZ水提液组和尼莫地平组均能显著提高谷氨酸模型条件下HT22细胞的存活率(P 0. 01),减少细胞损伤,减少LDH的释放率,降低细胞内ROS水平(P 0. 05,P 0. 01),降低NR2B蛋白的表达水平(P 0. 05),增加CREB,p-CREB,ERK,p-ERK蛋白的表达(P 0. 05); YJGZ含药血清组与模型组比较,HT22细胞存活率并没有提高。结论:YJGZ水提液对谷氨酸诱导的HT22细胞损伤具有显著的保护作用。     

灯盏花素对大鼠脑微血管内皮细胞损伤的保护作用

目的观察灯盏花素对谷氨酸致原代培养的大鼠脑微血管内皮细胞(rBMECs)损伤的保护作用。方法灯盏花素(200、100、50μmol/L)作用于rBMECs 24 h后,加入谷氨酸(终浓度为1 mmol/L)培养18 h,MTT法检测rBMECs细胞活性,并按试剂盒方法检测细胞上清液中乳酸脱氢酶(LDH)水平、细胞中丙二醛(MDA)水平和超氧化物歧化酶(SOD)活性。结果谷氨酸(l mmol/L)使原代培养的rBMECs明显受到损伤,灯盏花素高、中浓度(200、100μmol/L)可显著对抗谷氨酸造成的rBMECs损伤,抑制LDH释放,降低MDA水平,增强SOD活性。结论灯盏花素对谷氨酸所致原代培养的rBMECs损伤具有明显的保护作用,其机制与增强细胞抗氧化能力有关。     

β-细辛醚对谷氨酸所致脑皮层神经元损伤的保护作用

目的:研究β-细辛醚对谷氨酸所诱导的离体培养皮层神经细胞损伤的保护作用。方法:运用新生乳鼠皮层神经细胞体外原代培养技术建立神经细胞谷氨酸损伤模型,观察β-细辛醚对其细胞形态、损伤程度、存活力、细胞内钙离子浓度和细胞凋亡的影响。结果:40 mmol/L谷氨酸作用皮层神经细胞16h,出现明显损伤,凋亡率和死亡率升高,培养上清液中LDH含量增加;7.5、15、30μg/mlβ-细辛醚可有效改善谷氨酸损伤引起的神经细胞形态改变,提高细胞存活力、减少LDH渗漏、降低细胞凋亡率;15、30μg/mlβ-细辛醚能降低由谷氨酸引起的细胞内钙离子含量。结论:β-细辛醚对谷氨酸所致的皮层神经细胞损伤具有保护作用,其作用机制可能与钙拮抗作用有关。     

痛风泰颗粒对急性痛风大鼠IL-1、IL-6及TNF-α含量的影响

目的:观察痛风泰颗粒对急性痛风大鼠炎症因子白细胞介素-1(IL-1)、白细胞介素-6(IL-6)及肿瘤坏死因子-α(TNF-α)含量的影响,探讨痛风泰颗粒治疗痛风的可能作用机理。方法:将36只SD大鼠随机分为空白组、模型组、痛风泰颗粒组、戴芬组,除空白组外,其他三组建立急性痛风性关节炎的病理模型。造模成功后,分别药物干预7天,观察各组实验大鼠造模前后关节肤色、肤温、肿胀等情况,应用酶联免疫法(ELISA)检测大鼠右内踝关节液中的IL-1、IL-6的含量和血清中TNF-α含量。结果:与空白组比较,模型组IL-1、IL-6、TNF-α的含量显著升高(P0.05),提示急性痛风模型造模成功。与模型组比较,痛风泰颗粒组和戴芬组IL-1、IL-6、TNF-α的含量显著下降,差异均有统计学意义(P0.05)。痛风泰颗粒组与戴芬组比较,差异无统计学意义。结论:痛风泰颗粒可能是通过抑制炎症因子IL-1、IL-6、TNF-α的释放来治疗痛风。     

小檗碱对铝过负荷致小鼠慢性脑损伤的保护作用及机制

目的观察小檗碱对铝过负荷致大鼠慢性脑损伤的保护作用及机制。方法采用AlCl3(Al3 ,400mg/kg)ig大鼠,建立铝过负荷致大鼠慢性脑损伤的动物模型,并在每次铝给予4h后,小檗碱(100mg/kg)ig大鼠;观察大鼠行为学、组织病理学、生化酶学、单胺氧化酶-B(MAO-B)mRNA及蛋白表达水平变化。结果铝过负荷能明显导致大鼠被动回避性学习记忆能力和空间识别能力障碍、海马神经元损伤,使其脑组织乙酰胆碱转移酶(ChAT)活性显著降低,而胆碱脂酶(AchE)活性显著升高,超氧化物歧化酶(SOD)活性显著降低,而丙二醛(MDA)水平显著升高,MAO-B活性与MAO-BmRNA及蛋白表达水平显著增加;小檗碱能明显改善铝过负荷大鼠的学习记忆能力障碍,明显减轻铝过负荷大鼠海马神经细胞的损伤,明显阻遏铝过负荷大鼠海马组织ChAT与SOD活性的降低、AchE活性与MDA水平的增高、MAO-B活性及其mRNA与蛋白表达的增加。结论小檗碱对铝过负荷致大鼠慢性脑损伤有明显的保护作用,其作用机制除了与抗氧化应激损伤有关外,尚与增强胆碱能神经元功能与多巴胺神经功能有关。     

Protection against radiation induced damage to spermatogenesis by Podophyllum hexandrum

Aqueous extract of rhizome of Podophyllum hexandrum (RP-1) has been found to render protection against lethal whole body irradiation (10 Gy), damage to haemopoietic and gastrointestinal tissue etc. in mice. In order to assess its suitability from clinical point of view its effects were investigated on male germinal tissue in mice. Swiss albino strain 'A' male mice (10-12 weeks) were exposed to varied radiation doses (0.5, 2.0, 5.0 and 10 Gy) with and without 200 mg/kg b.w. of RP-1 and sacrificed at different time periods (10, 35 and 70 days) to collect the tissue. Administration of RP-1, 2 h before irradiation rendered a significant increase in the testis weight, repopulating tubules, resting primary spermatocytes, stem cell survival index, sperm counts and reduction in abnormalities of sperm morphology, at all the time periods studied here. RP-1 treatment alone did not generate any adverse effects. These results reveal that RP-1, if put to clinical application, will not be harmful to the testicular system.     

Protection of brain cells against AMPA-induced damage by Asiasari Radix extracts

We determined whether Asiasari Radix (AR) extracts have protective actions in brain cells. Methanol extracts of Asiasari Radix (fraction 1) have significant inhibitory effects on the AMPA-induced rat cortical depolarization in the grease gap assay. In differentiated PC12 cells, it almost completely protected against AMPA-induced cell death. In addition, it had some protective actions in C6 glial cells death induced by AMPA. The methanol extracts (fraction 1) of AR were subsequently fractionated into chloroform-(fraction 2), chloroform/methanol-(3:1) (fraction 3), methanol-soluble (fraction 4) and methanol-insoluble, water-soluble fractions (fraction 5). Among these, fraction 4 had the strongest inhibitory effects against AMPA-induced cell death in the PC 12 cells and also dramatically inhibited AMPA-induced depolarization of rat brain cortex in the grease gap assay. Interestingly, fraction 4 blocked the Zn-induced oxidative damages in C6 glial cells.     

葛根素注射液对慢性乙醇中毒小鼠记忆障碍的改善作用

 目的,探讨葛根素注射液对慢性乙醇中毒小鼠记忆障碍的改善作用及其脑内机制。方法每日给予30%乙醇连续4周造成小鼠慢性乙醇中毒，同时每日ip 20,100 mg·kg^-1葛根素注射液治疗4周，用Y-迷宫检测小鼠分辨学习和记忆行为的变化，用紫外分光光度计和荧光分光光度计分别检测脑组织SOD，脂褐素生化指标；用电镜和计算机图像分析仪观测小鼠海马CA₃区Gray Ⅰ型突触界面结构参数的变化。结果葛根素注射液100 mg·kg^-1可显著改善长期给予乙醇造成的小鼠学习记忆功能障碍；显著提高脑组织SOD的活性，使小鼠脑内脂褐素含量明显下降；同时使海马突触后致密物质(PSD)厚度显著增加，突触间隙宽度显著减小。结论葛根素注射液能改善慢性乙醇中毒引起的小鼠学习记忆功能障碍，该作用可能与其提高脑组织抗氧化能力，改变海马突触界面结构有关。     

丹参配方颗粒对乙醇所致PC12细胞损伤的保护作用

目的研究丹参配方颗粒对乙醇损伤大鼠肾上腺嗜铬细胞瘤(PC12)细胞的保护作用及其机制。方法用乙醇和不同质量浓度丹参配方颗粒溶液处理PC12细胞;MTT法检测细胞存活率,乳酸脱氢酶(LDH)法检测丹参配方颗粒对乙醇致PC12细胞损伤的保护作用;应用原位末端转移酶标记法(TUNEL)和Annexin V/PI标记染色检测PC12细胞凋亡情况:相关试剂盒测定总超氧化物歧化酶(T-SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化氢酶(GSH-Px)的活性和丙二醛(MDA)的量;DCFH-DA染色法检测胞内活性氧(ROS)水平。结果丹参配方颗粒能够抑制乙醇导致的PC12细胞的损伤和死亡,显著降低乙醇诱导的PC12细胞的凋亡率(P0.05),提高细胞的T-SOD、CAT和GSH-Px酶活性(P0.05),降低MDA和ROS水平(P0.05)。结论丹参配方颗粒能有效保护乙醇损伤的PC12细胞,其作用机制与提高细胞抗氧化能力有关。     

Protection against galactosamine and tert-butyl hydroperoxide induced hepatocyte damage by Melothria maderaspatana extract

The aqueous extract of Melothria maderaspatana is used by traditional medical practitioners to treat jaundice in man. The effect of Melothria maderaspatana extract on damage induced in freshly isolated rat hepatocytes by D-galactosamine and tert-butyl hydroperoxide (TBH) has been investigated. On incubation of hepatocytes with galactosamine or TBH in the presence of the plant extract, a significant dose-dependent protection against hepatocyte damage was observed, with maximum protection at a concentration of 500 μg/mL. At this concentration the galactosamine-induced release of lactate dehydrogenase (LDH) and aspartate amino-transferase (AST) were reduced by 40.7% ± 4.2% and 37.7% ± 6.1% respectively, compared with control incubations. The TBH-induced lipid peroxidation (estimated from malondialdehyde production) was decreased by 26.0 ± 3.7% together with a 38.4% ± 4.4% and 40.8 ± 7.6% reduction in the release of cellular LDH and AST respectively into the incubation medium. On post-treatment with the plant extract the protective activity was found to decrease with increase in time of exposure of the cells to either of the toxins. The direct protective effects of Melothria extract on hepatocytes support the use of this plant as a herbal remedy.     

秃疮花提取物对CCl4诱导的小鼠急性肝细胞微粒体损伤的影响

目的:探讨研究秃疮花提取物(DLE)对CCl4诱导的小鼠急性损伤肝细胞微粒体的影响。方法:小鼠灌胃给予不同剂量的DLE,连续2周。最后一次给药24h后CCl4造成急性肝损伤。制备肝细胞微粒体悬液,检测抗氧化酶SOD、CAT、GSH-Px的活性;测量肝细胞微粒体悬液中的MDA水平;观察NADPH-细胞色素C(P450)还原酶活性及ATPase活性的变化。结果:与模型组相比,不同剂量的DLE给药组肝细胞微粒体悬液中MDA含量显著减少;抗氧化酶SOD、GSH-Px活性显著增加;肝细胞微粒体NAD-PH-细胞色素C(P450)还原酶活性降低,Na+K+-ATPase和Ca2+-ATPase活性显著上升。结论:DLE对CCl4诱导的小鼠肝微粒体损伤具有很好的保护作用。其作用机理与DLE具抗氧化和自由基活性清除有关。     

Protection afforded by aqueous extracts of Phyllanthus species against cytotoxicity induced by lead and aluminium salts

Oral administration of aqueous extracts of Phyllanthus emblica L. fruit and P. niruri L. leaves to laboratory bred albino mice for a week, significantly reduced the cytotoxic action of lead nitrate and aluminium sulphate. The frequency of chromosomal breakages, gaps and rearrangements induced by three concentrations of these salts was decreased when compared to the control animals which had received the salts alone. The plant extracts were equally effective in modifying the clastogenic effects of both lead nitrate and aluminium sulphate.     

川芎嗪对花生四烯酸诱导血管内皮细胞凋亡的保护作用

目的　研究川芎嗪 (TMP)对花生四烯酸 (AA,16 0μm ol/ L )诱导的血管内皮细胞株 ECV 30 4损伤和凋亡的保护作用及其机制。方法　 MTT法检测细胞存活率 ,比色法测乳酸脱氢酶 (L DH)释放率和细胞丙二醛(MDA)含量 ,Hoechst 332 5 8荧光染色法观察细胞核形态变化并测定细胞凋亡率 ,琼脂糖凝胶电泳检测 DNA降解。结果　 TMP(0 .2 5～ 1.0 m mol/ L)能浓度依赖性地抑制 AA引起的细胞存活率下降 (P<0 .0 5 ) ,并降低细胞L DH释放率和 MDA含量 (P<0 .0 5 )。 AA处理 2 4 h后的细胞呈典型的凋亡核固缩表现 ,凝胶电泳显示 DNA凋亡梯带 ,TMP(0 .2 5～ 1.0 m mol/ L)能降低其凋亡率 (P<0 .0 5 )。结论　 TMP对 AA引起的 ECV30 4细胞损伤和凋亡具有保护作用 ,其机制可能与其抗脂质过氧化作用有关     

Protection by garlic against adriamycin induced alterations in the oxido-reductive status of mouse red blood cells

The effects of oral garlic supplementation on the activities of (a) the antioxidant enzymes superoxide dismutase (SOD) and glutathione peroxidase (GPX) and (b) lipid peroxidation, as assessed by malondialdehyde (MDA) production in red blood cells of normal mice and those subject to oxidative stress by chronic administration of the anti-tumour drug adriamycin has been investigated. As expected, adria-mycin administration resulted in a significant increase in MDA generation (by 105.4%) and a decrease in GPX activity (by 23.8%) in the red blood cells. Although garlic had no significant effects on the basal levels of the antioxidant enzymes or MDA generation in red blood cells of normal mice (untreated with adriamycin), at doses of 20 mg/kg or 100 mg/kg, garlic was able to decrease significantly the adriamycin induced changes in the oxido-reductive status of the red blood cells. Thus, on administration of adriamycin to mice fed diets containing 20 mg/kg or 100 mg/kg garlic, the drug-induced increase in MDA generation was 38.2% and 22.5% respectively, less than that produced by adriamycin in mice fed normal diets, containing no garlic (105.4%). Similarly, in mice fed diets providing 20 mg/kg and 100 mg/kg garlic, adriamycin was able to decrease GPX activity by only 15.1% and 7.6% respectively, less than that produced by adriamycin in rats fed normal diets, containing no garlic (23.9%).