黄芪预防肿瘤坏死因子-α所致胰岛素抵抗

目的：探讨黄芪对大鼠注射肿瘤坏死因子α（ＴＮＦα）后发生胰岛素抵抗（ＩＲ）的预防作用。方法：取正常大鼠分别给予黄芪煎剂和等量蒸馏水预先灌胃１周，尾静脉注射小剂量ＴＮＦα４ｈ后，以葡萄糖－胰岛素耐量试验（ＧＩｎｓＴＴ）检测其胰岛素敏感性等一些指标的变化。结果：外源性ＴＮＦα可致正常大鼠出现高胰岛素血症，胰岛素敏感性Ｋ值下降，并有血浆胰高血糖素、促肾上腺皮质激素和血脂水平的升高，肝脏和红色股四头肌糖原含量减少，肝脏中甘油三酯（ＴＧ）含量升高。黄芪除对血脂和肝脏中ＴＧ无明显改善外，对其它指标均有不同程度的改善作用。结论：黄芪对外源性ＴＮＦα所致ＩＲ有明显的预防作用，可能与降低血中拮抗激素水平和增加组织糖原合成有关。     

肿瘤坏死因子α与胰岛素抵抗的研究

糖尿病是一种以血糖代谢紊乱为特点的常见的慢性疾病 ,其中 90 %以上为 2型 ,而胰岛素抵抗又为 2型糖尿病的根本病机之一。目前对 2型糖尿病的基本共识为 :2型糖尿病不是一种单基因病 ,其发生是多种基因相互作用的结果 ,即多种基因和环境因素共同参与了糖尿病的致病过程 ,其中环境因素(如肥胖 )在决定基因作用的外显方面起到重要的作用。肿瘤坏死因子α(TNFα)作为导致胰岛素抵抗的环境因素之一 ,正日益成为研究热点。1　TNFα的生物学效应八十年代 ,TNFα在细菌性感染动物中随其同源近亲淋巴毒素 (Iymphotoxin ,LT -α或TNF - β)一…     

Ⅱ型糖尿病肿瘤坏死因子-α与胰岛素抵抗关系的研究现状

胰岛素抵抗（IR）是多种疾病的病理生理基础之一，如Ⅱ型糖尿病、肥胖、高血压、高脂血症、冠心病和脑血管意外等。胰岛素抵抗病因复杂，为其防治带来困难。目前在Ⅱ型糖尿病的胰岛素抵抗机制研究中，主要集中在游离脂肪酸（FFA）、肿瘤坏死因子α（TNF-α）及过氧化物酶体激活型增殖体（PPARγ2）等方面，而TNF-α备受瞩目。TNF-α是激活的单核巨噬细胞及脂肪细胞分泌的一种细胞因子，具有广泛的生物活性。现已认识到TNF-α在免疫及免疫外系统中的重要作用以及其与许多疾病状态密切相关。国外大量报道提示，TNF-α可能是胰岛素抵…     

益脉降压胶囊对老年高血压病患者胰岛素抵抗及肿瘤坏死因子的影响

目的：观察益脉降压胶囊对老年气虚血瘀证型高血压病患者胰岛素抵抗（IR）及肿瘤坏死因子－α（TNF－α）的影响。方法：选择120例老年气虚血瘀证型Ⅱ型高血压病患者，随机分为治疗组（80例）和对照组（40例），分别口服益脉降压胶囊和卡托普利，两组疗程均为8周。结果：治疗前两组患者较健康对照组FBG无显著差异（P＞0．05），FPI、TNF－－α显著升高（P＜0．01），ISI显著降低（P＜0．01）；治疗后两组患者与其治疗前比较，FBG无明显变化（P＞0．05，FPI、TNF－α显著降低（P＜0．01或P＜0．05），ISI显著高于（P＜0．01或P＜0．05）；两组治疗后比较，治疗组FPI、TNF－α显著低于对照组（P＜0．01）（P＜0．05），ISI显著高于对照组（P＜0．01）；两组治疗前FPI与TNF－α含量变化均呈显著正相关（P＜0．01）；两组血压下降幅度比较无显著性差异（P＞0．05）。疗程结束后复查上述指标。     

肿瘤坏死因子-α诱导3T3-L1脂肪细胞胰岛素抵抗模型的建立

目的:应用肿瘤坏死因子d(TNF-α)诱导3T3-L1脂肪细胞,探讨建立可靠胰岛素抵抗(IR)细胞模型的方法.方法:3T3-L1前脂肪细胞经3-异丁基-1-甲基黄嘌呤、地塞米松、胰岛素诱导分化成3T3-L1脂肪细胞,将其与20,10,5μg·L-1TNF-α共孵育,100 nmol·L-1胰岛素作用30 min刺激脂肪细胞糖转运.以葡萄糖氧化酶法测定培养基上清液葡萄糖含量,观察TNF-α对脂肪细胞糖摄取的影响,鉴定IR模型.结果:TNF-α抑制胰岛素诱导前、后的脂肪细胞糖转运,抑制作用呈剂量依赖性,其中20 μg·L-1TNF-α的抑制率分别为79.2％和81.4％(P＜0.05).结论:肿瘤坏死因子α可诱导3T3-L1脂肪细胞产生IR,这种细胞模型简便、可靠.     

肿瘤坏死因子-α诱导脂肪细胞胰岛素抵抗模型的建立及评价指标

[目的]确定运用肿瘤坏死因子-α(TNF-α)建立胰岛素抵抗模型的最适时间与剂量,并通过检测TNF-α对葡萄糖转运体4(GLUT4)表达及膜转位的影响探讨模型成立的评价指标。[方法]用不同浓度(5、10、15、20、25 ng/mL)的TNF-α作用于3T3-L1脂肪细胞不同的时间(48、72、96 h),建立胰岛素抵抗模型。另外,分别采用蛋白免疫印迹法(Western blot)和高内涵筛选技术检测模型组细胞GLUT4蛋白表达及分布情况。[结果]与对照组相比,10 ng/mL TNF-α作用3T3-L1脂肪细胞96 h后的模型组的葡萄糖摄取及GLUT4的表达均有显著的降低;加入胰岛素后,对照组的葡萄糖摄取及GLUT4的表达有明显的升高,而模型组无明显变化;胰岛素抵抗模型中,GLUT4膜转位显著降低,差异有统计学意义。[结论] 10 ng/mL的TNF-α作用3T3-L1脂肪细胞96 h有利于建立胰岛素抵抗模型。此外,葡萄糖摄取结合GLUT4的蛋白表达及膜转位可作为胰岛素抵抗模型建立的评价标准。     

糖脂平对胰岛素抵抗大鼠血清肿瘤坏死因子-α水平及其脂肪组织mRNA表达的影响

目的观察糖脂平对喂养型胰岛素抵抗大鼠血清肿瘤坏死因子-α（TNF-α）水平及脂肪组织mRNA表达的影响,探讨其抗动脉粥样硬化（AS）的作用机制。方法将28只清洁级SD大鼠随机分为对照组、模型组、中药组和西药组,采用高脂高盐饲料喂养,造模成功后分别给予生理盐水、糖脂平和罗格列酮灌胃。给药8周后,用放免法测定各组大鼠血清TNF-α水平,反转录-聚合酶链反应（RT-PCR）方法测定附睾旁脂肪组织TNF-αmRNA表达水平。结果模型组大鼠血清TNF-α水平为（1.78±0.13）ng/mL,较对照组大鼠明显升高,糖脂平或罗格列酮灌胃可分别使模型大鼠血清TNF-α水平降至（1.46±0.13）ng/mL和（1.32±0.16）ng/mL,差异有统计学意义（P〈0.01）。模型组大鼠脂肪组织TNF-αmRNA表达量较对照组显著升高（P〈0.01）,与模型组相比,糖脂平或罗格列酮灌胃可分别使TNF-αmRNA下降30.2%和31.6%,差异有统计学意义（P〈0.01）。结论糖脂平改善胰岛素抵抗和抗AS作用可能与其降低血清TNF-α水平,抑制TNF-αmRNA过度表达有关。     

肿瘤坏死因子α和可溶性肿瘤坏死因子受体2与多囊卵巢综合征胰岛素抵抗机制的关系

目的 :探讨血浆肿瘤坏死因子α(TNFα)、可溶性肿瘤坏死因子受体 2 (STNFR2 )与多囊卵巢综合征 (PCOS)患者胰岛素抵抗 (IR)和血清雄激素 (T)水平的相互关系。方法 :将 5 0例PCOS患者分为PCOS肥胖组、PCOS非肥胖组 ,将正常肥胖妇女、正常非肥胖妇女各 2 5例作为肥胖对照组和非肥胖对照组。测定 4组的血清性激素六项、TNFα ,STNFR2水平及血清胰岛素浓度、胰岛素敏感指数(ISI)等 ,并做对比和相关性分析。结果 :PCOS肥胖组及肥胖对照组的TNFα水平明显高于非肥胖对照组 (P <0 .0 5 )。PCOS肥胖组和PCOS非肥胖组的STNFR2均高于非肥胖对照组 ,且以PCOS肥胖组升高更为明显 (P <0 .0 5 )。PCOS肥胖组和PCOS非肥胖组ISI较非肥胖对照组明显降低 (P <0 .0 5 )。PCOS肥胖组和PCOS非肥胖组血浆T水平均显著高于肥胖对照组和非肥胖对照组 (P <0 .0 5 )。在PCOS肥胖组和肥胖对照组中 ,血浆TNFα与其ISI均呈负相关 (P <0 .0 5 )。在PCOS肥胖组、PCOS非肥胖组和肥胖对照组中 ,血浆STNFR2与其ISI均呈负相关。各组TNFα和STNFR2水平与其对应血浆T浓度均无明显相关性 (P >0 .0 5 )。结论 :PCOS患者存在不同程度的IR ;TNFα与STNFR2水平的升高与PCOS患者发生IR有关而与T无关。     

电针对肥胖大鼠胰岛素抵抗及肿瘤坏死因子α的影响

目的:观察针刺对肥胖大鼠体重、血糖、胰岛素含量、脂肪组织中肿瘤坏死因子-α(TNF-α)水平的影响。方法:随机挑选10只普通饲料喂养为正常组。另一组80只高脂致肥饲料喂养,将造模成功的肥胖大鼠30只随机分为肥胖模型组和针刺组,每组各15只。采用实时定量PCR技术测定肿瘤坏死因子-α(TNF-α)基因表达水平,酶联免疫测定法测定血清中胰岛素(insu lin)的含量,生化比色法测定血清葡萄糖含量。结果:针刺治疗组体重、血糖、血清胰岛素、脂肪组织中TNF-α水平均较模型组有不同程度的降低,胰岛素敏感指数有所提高。结论:针刺可以改善肥胖大鼠胰岛素抵抗和糖代谢紊乱状态。     

A research on the quality of radix Astragali]

Milkvetch root (Radix Astragali) and its likes were determined in their contents of trace elements, total extracts and astragalin A. The result showed there was some relationship between the drug quality, trace-element contents, difference of species, growing areas and on-the-spot processing methods.     

Inhibition of lipopolysaccharide and interferon-gamma-induced expression of inducible nitric oxide synthase and tumor necrosis factor-alpha by Lithospermi radix in mouse peritoneal macrophages

Lithospermi radix (LR, root of Lithospermum erythrorhizon Siebold. et Zuccarinii) has been used to treat various conditions, such as septic shock, eczema and burns. In this study, the effect of LR on lipopolysaccharide (LPS) and recombinant interferon-gamma (rIFN-gamma)-induced production of nitric oxide (NO) and tumor necrosis factor (TNF)-alpha were examined using mouse peritoneal macrophages. At 0.01-1 mg/ml, LR inhibited the LPS/rIFN-gamma-induced expression of inducible nitric oxide synthase (iNOS) and TNF-alpha release. To clarify the mechanism involved, the effect of LR on the activation of nuclear factor (NF)-kappaB was examined. The LPS/rIFN-gamma-induced activation of NF-kappaB was almost completely blocked by LR at 1mg/ml without cytotoxicity. These findings demonstrate that the inhibition of the LPS/rIFN-gamma-induced production of NO and TNF-alpha by LR involves the inhibition of NF-kappaB activation.     

高效液相色谱-蒸发光散射检测测定黄芪中黄芪甲甙的含量

目的 :建立测定黄芪中黄芪甲甙含量的新方法。方法 :采用高效液相色谱 蒸发光散射检测法测定。结果 :黄芪甲甙在 2.02～10.12 μg与峰面积积分值呈良好的线性 (r=0.9997,n=5 ) ,平均回收率为100.5%。 结论 :为控制黄芪中黄芪甲甙的含量提供了新的方法。     

Effect of radix Astragali and radix ginseng in enhancing the metabolism of human myocardial cells in vitro]

Our experiment indicated that in Radix Astragali and Radix Ginseng treated human myocardial cell cultures the level of LDH and SDH elevated in varying degrees and in Radix Ginseng treated cells the cAMP showed higher levels but in Radix Ginseng treated ones the same was not observed. This suggests that the metabolism of myocardial cells is enhanced by Radix Astragali or Radix Ginseng.     

益元生血方对慢性再生障碍性贫血患者外周血γ—干扰素 …

目的：探讨益元生血方对慢性再生障碍性贫血患者外周血γ－干扰素,肿瘤坏互因子－α的影响,方法：３６例ＣＡＡ患者分为肾阴虚组和肾阳虚组,采用微量细胞病变抑制法及Ｌ５９５细胞毒法,检测使用益元生血方前后外周血γ－ＩＦＮ,ＴＮＦ－α水平,并与正常组比较。结果：外周血γ－ＩＦＮ,ＴＮＦ－α水平,治疗总组与正常组比较、治疗前有明显差异,治疗后无明显差异,肾阴虚组与肾阳虚组比较,治疗前后均有明显差异,且有效率肾     

针刺对胰岛素抵抗模型大鼠血清胰岛素抗体和肿瘤坏死因子α的影响

目的:探讨治疗胰岛素抵抗的有效方法及其作用机理。方法:40只SD大鼠随机平均分成①空白组、②模型1组、③模型2组、④针刺1组、⑤针刺2组。②③④⑤组采用高脂高糖高盐饲料喂养复制胰岛素抵抗模型成功后,①③⑤组给予普通饲料喂养,②④组给予高脂高糖高盐饲料饲养,④⑤组同时给予针刺治疗。2w后检测大鼠空腹血糖(FBG)、血浆胰岛素(INS)、胰岛素敏感指数(ISI)、血清胰岛素抗体(INS-Ab)和肿瘤坏死因子α(TNF-α)。结果:与①组比较,②组大鼠FBG、INS升高,ISI降低(均P<0.01);与②组比较,③④⑤组大鼠FBG、INS下降(均P<0.01),ISI上升(P<0.05,P<0.01);各组INS-Ab( )例数均为0;②组大鼠TNF-α较①组升高(P<0.01),③④⑤组大鼠TNF-α均较②组下降(P<0.01)。结论:针刺对胰岛素抵抗有逆转效应,饮食能促进此效应。其作用机理可能是通过降低TNF-α的分泌来实现的。     

Antiviral action of combined use of rhizoma Polygoni cuspidati and radix Astragali on HSV-1 strain]

OBJECTIVE: The clinical action of combined use of Rhizoma Polygoni Cuspidati and Radix Astragali on HSV-1 was investigated with a view to developing a new antiviral drug. METHOD: The action was analyzed by way of plaque reduction assay and median-effect principle. RESULTS: In the HEp-2 cell system, if the combination ratio of Rhizoma Polygoni Cuspidati and Radix Astragali was 1(ED50):1(ED50) then, (1) In directly annihilating HSV-1 F strain, when the plaque reduction rate was 20%-80%, and the combination index was < 1.0, there was synergism. (2) In inhibiting the multiplication of HSV-1 F strain, when the plaque reduction rate was 20%-60%, and the combination index was < 1.0, there was also synergism. (3) In blockading HSV-1 F strain infection, when the plaque reduction rate was 20%-90% and the combination index was < 1.0, there was synergism. So this ratio of 1(ED50):1(ED50) should be the first choice for combination. CONCLUSION: The treatment index of the above two Chinese medicinal herbs equals 10(3), and the cytotoxicity is not potentiated, indicating that the combination is helpful as a virucide for HSV-1 F strain.     

Protective effect of Astragali radix extract on interleukin 1beta-induced in fl ammation in human amnion

The aim of this study was to investigate the effect of Astragali radix extract on interleukin (IL)-6 and tumour necrosis factor (TNF)-alpha production and prostaglandin E(2) (PGE(2)) and leukotriene C(4) (LTC(4)) release from IL-1beta-stimulated human amnion. Primary monolayer cultures of amnion cells were established from women undergoing elective caesarean section before the onset of labour. Production of both IL-6 and TNF-alpha was stimulated in a concentration-dependent manner by proinflammatory cytokine IL-1beta (0.01-10 ng/mL). Astragalus extract inhibited IL-6 production by approximately 75% from cells under IL-1beta-stimulated conditions. Treatment of amnion cells with IL-1beta (0.01-10 ng/mL) resulted in a significant increase in PGE(2) release. Incubation of the cells with the extract for 24 h significantly inhibited IL-1beta-induced PGE(2) production. A concentration-dependent increase in LTC(4) production by amnion cells occurred in response to IL-1beta. Astragalus extract blocked the effect of IL-1beta in LTC(4) production in human amnion. These results indicate that Astragali radix has a broad antiinflammatory effect in human amnion and may be considered a promising agent to protect preterm labour.     

Nitric oxide and tumor necrosis factor-alpha production by Ixeris dentata in mouse peritoneal macrophages

Using mouse peritoneal macrophages, we have examined the mechanism by which Ixeris dentata (IXD) regulates nitric oxide (NO) production. When IXD was used in combination with recombinant interferon-gamma (rIFN-gamma), there was a marked cooperative induction of NO production. However, IXD had no effect on NO production by itself. The increased production of NO from rIFN-gamma plus IXD-stimulated cells was almost completely inhibited by pre-treatment with pyrrolidine dithiocarbamate (PDTC), an inhibitor of nuclear factor kappa B (NF-kappaB). Furthermore, treatment with IXD alone or rIFN-gamma plus IXD in peritoneal macrophages caused a significant increase in tumor necrosis factor-alpha (TNF-alpha) production. PDTC decreased TNF-alpha production induced by IXD significantly. These findings demonstrate that IXD increases the production of NO and TNF-alpha by rIFN-gamma-primed macrophages and suggest that NF-kappaB plays a critical role in mediating these effects of IXD.