桂产藿香蓟乙醇提取物抗炎作用及其机制研究

目的：探讨桂产藿香蓟乙醇提取物的抗炎作用及其作用机制。方法：采用二甲苯诱导小鼠耳廓肿胀,观察桂产藿香蓟乙醇提取物对二甲苯诱导小鼠耳廓肿胀的影响;采用角叉菜胶致小鼠足肿胀法,观察桂产藿香蓟乙醇提取物对角叉菜胶致小鼠足肿胀的影响,并分别测定小鼠炎性组织中丙二醛（MDA）、前列腺素E2（PGE2）和超氧化物歧化酶（SOD）的活性;采用角叉菜胶致大鼠足肿胀法,观察桂产藿香蓟乙醇提取物对角叉菜胶诱导大鼠足肿胀的影响,同时测定大鼠血清肿瘤坏死因子（TNF-α）、白介素-1β（IL-1β）和白介素-6（IL-6）的含量。结果：与空白对照组比较,桂产藿香蓟乙醇提取物能显著抑制小鼠耳廓肿胀及足肿胀（P〈0.05或0.01）,其中高、中、低剂量组（6.0,3.0,1.5g·kg-1）耳廓肿胀和足肿胀抑制率分别为29.24%,16.42%,11.21%和28.66%,18.79%,13.13%,并能降低小鼠炎足中炎性组织PGE2、MDA含量,提高其SOD活力（P〈0.05或0.01）;显著抑制大鼠的足肿胀（P〈0.05或0.01）,其中在3h时高、中、低剂量组（6.0,3.0,1.5g·kg-1）的足肿胀抑制率分别为43.69%,36.01%,23.29%,并能显著降低肿胀足大鼠血清TNF-α、IL-1β和IL-6的含量（P〈0.05或0.01）。结论：桂产藿香蓟乙醇提取物抗炎作用显著,其机制可能与清除氧自由基、减少炎症因子和致炎细胞因子的释放有关。     

川黄柏醇提物的抗炎作用及机制的研究

目的 观察川黄柏醇提物(AEPC)的抗炎作用并探讨其机制.方法 采用乙酸致小鼠腹腔毛细血管通透性增加和角叉菜胶诱导大鼠胸膜炎模型来观察AEPC的抗炎作用;测定胸膜炎大鼠胸腔渗出液中前列腺素E2(PGE2)、肿瘤坏死因子-α(TNF-α)和白细胞介素-1β(IL-1β)的含量及肺组织中TNF-α、IL-1β、丙二醛(MDA)的含量,探讨其抗炎机制.结果 与模型组比较,AEPC中、高剂量可显著抑制小鼠腹腔毛细血管通透性增加;还可抑制胸膜炎大鼠胸腔液中PGE2、TNF-α、IL-1β含量的升高;AEPC高剂量能抑制胸膜炎大鼠肺组织中TNF-α、IL-1β、MDA含量的升高,中剂量能抑制肺组织中IL-1β含量的升高.结论 AEPC具抗炎作用,其抗炎机制可能与影响炎症介质的产生和抗氧化作用有关.     

水苏碱抗炎活性的研究

目的:研究水苏碱的抗炎活性及其相关作用机制。方法:通过二甲苯致小鼠耳廓肿胀法和棉球致大鼠肉芽肿实验考察水苏碱的抗炎作用;通过检测角叉菜胶致大鼠胸膜炎性渗出液中蛋白质含量和白细胞(WBC)数及前列腺素E(2PGE2)、白细胞介素1(IL-1)、肿瘤坏死因子α(TNF-α)、一氧化氮(NO)含量,结合血清中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性测定,初步研究水苏碱抗炎有关的作用机制。结果:24、12mg.kg-1剂量下水苏碱可显著降低模型大鼠胸膜炎性渗出液中蛋白质含量和WBC数,降低炎症部位PGE2、IL-1、TNF-α含量,同时降低模型大鼠血清中MDA含量,提高血清SOD活性(P<0.01或P<0.05)。12mg.kg-1剂量下水苏碱可显著降低模型大鼠炎症部位NO含量(P<0.05)。结论:水苏碱在一定剂量内具有较强抗炎作用,其抗炎作用可能与改善细胞膜通透性、降低炎性因子水平、减少脂质过氧化反应等作用相关。     

侧柏总黄酮的抗炎作用

目的研究侧柏总黄酮的抗炎作用。方法以二甲苯致小鼠耳肿胀及角叉菜胶诱发大鼠足爪肿胀模型分别探讨侧柏总黄酮对小鼠耳片肿胀及大鼠足爪肿胀的抑制作用。测定大鼠足爪组织中一氧化氮 (NO)及前列腺素E2 (PGE2 )的含量。结果侧柏总黄酮在 12 5～ 5 0 0mg·kg-1内呈剂量依赖地抑制二甲苯诱导的小鼠耳肿胀 ,2 5 0mg·kg-1剂量能显著抑制大鼠足爪肿胀 ,其作用强于2 0mg·kg-1的地塞米松。侧柏总黄酮能抑制大鼠炎症足爪组织NO及PGE2 的生物合成。结论侧柏总黄酮具有较强的抗炎作用 ,其抗炎作用可能与抑制NO及PGE2 的生物合成或释放有关。     

瑶药破骨风的水提工艺优化及其水提物的抗炎镇痛作用研究

目的:优化瑶药破骨风的水提取工艺,并考察其水提物的抗炎镇痛作用。方法:采用单因素试验和正交试验,以阿魏酸含量、干膏率为指标,考察提取时间、液料比、提取次数3个因素对水提取工艺的影响,优选最佳工艺,并进行验证试验。以阿司匹林为阳性对照,采用二甲苯致小鼠耳廓肿胀法和角叉菜胶致小鼠足肿胀法观察低、中、高剂量(3、6、12 g/kg,以生药计)的破骨风水提物的抗炎作用,采用热板致小鼠疼痛反应和醋酸致小鼠扭体反应考察其镇痛作用;采用酶联免疫吸附法(ELISA)测定小鼠以角叉菜胶致炎后血清中肿瘤坏死因子α(TNF-α)和白细胞介素1β(IL-1β)的含量,采用紫外分光光度法检测小鼠血清和炎性组织中前列腺素E2(PGE2)的含量。结果:最优提取工艺为提取时间120 min,液料比16∶1(m L/g),提取3次。与模型组比较,破骨风水提物低、中、高剂量组小鼠耳廓肿胀度、足肿胀率均显著降低,扭体次数显著减少,疼痛反应痛阈值显著升高(P<0.05或P<0.01);与模型组比较,该水提物低、中、高剂量组小鼠血清中的TNF-α、IL-1β、PGE2含量与炎性组织中的PGE2含量均显著减少(P<0.05或P<0.01)。结论:优选的瑶药破骨风水提工艺效率高、稳定可行;其水提物对模型小鼠具有明显的抗炎镇痛作用,可能是通过降低体内TNF-α、IL-1β、PGE2水平发挥作用。     

羧胺三唑对角叉菜胶诱导急性炎症的抗炎作用

目的:探讨羧胺三唑(CAI)对角叉菜胶诱导的大鼠足爪急性炎症的预防作用及部分机制.方法:采用角叉菜胶诱导大鼠足爪急性炎症模型,测量足爪肿胀度以及足爪组织中髓过氧化物酶(MPO)、NO、前列腺素2(PGE2)、TNF-α、IL-1β、中性粒细胞趋化因子-1(CNCI-1)和诱导一氧化氮合酶(iNOS).结果:CAI能明显减轻大鼠足爪炎性肿胀,显著降低炎症足爪中MPO、NO、PGE2、TNF-α、IL-1β和CNCI-1含量及iNOS蛋白表达.结论:CAI可能通过减少炎症介质和中性粒细胞浸润来发挥对角叉菜胶诱导急性炎症的抗炎作用.     

猪胆干膏的抗炎作用及作用机制的研究

目的 研究猪胆干膏的抗炎作用.方法 采用二甲苯致小鼠耳肿胀,醋酸致小鼠腹腔毛细血管通透性增加,角叉菜胶致大鼠足跖肿胀等模型观察猪胆干膏的抗炎作用,并测定前列腺素E2（PGE2）、一氧化氮（NO）含量及超氧化物歧化酶（SOD）活性.结果 猪胆干膏能显著抑制二甲苯所致小鼠耳肿胀,降低小鼠毛细血管通透性,减轻大鼠足跖肿胀,并降低炎症组织PGE2和NO含量,增强血清SOD活性.结论 猪胆干膏具有明显的抗炎作用,其抗炎机制可能与降低血管通透性、抑制炎症介质生成及增强清除氧自由基、抗脂质过氧化的能力有关.     

杭白菊总黄酮抗炎作用及其机制初探

目的：观察杭白菊总黄酮抗炎作用并对其机制进行初步研究。方法：采用二甲苯致小鼠耳肿胀、醋酸致小鼠腹腔毛细血管通透性增加、角叉菜胶致小鼠足跖肿胀及大鼠气囊炎炎症模型,观察杭白菊总黄酮对不同炎症模型的抗炎作用,并测定蛋白质、白细胞数（WBC）、前列腺素E2（PGE2）、丙二醛（MDA）含量及超氧化物歧化酶（SOD）活性。结果：杭白菊总黄酮能显著降低小鼠毛细血管通透性,抑制小鼠二甲苯致耳肿胀,减轻小鼠足跖肿胀,降低炎症组织PGE2含量,抑制角叉菜胶致大鼠气囊炎模型中渗出液中总蛋白质含量和白细胞数,降低血浆MDA含量,增强血浆SOD活性。结论：杭白菊总黄酮具有明显的抗炎作用,其抗炎作用可能与其降低血管通透性、抑制PGE2等炎症介质生成及增强清除氧自由基、抗脂质过氧化能力有关。     

双黄连口服液解热抗炎作用的实验研究

目的 探讨双黄连口服液的解热抗炎作用.方法 采用2,4-二硝基苯酚致大鼠发热法研究双黄连口服液的解热作用,采用二甲苯致小鼠耳肿胀法和角叉菜胶致大鼠足肿胀法研究双黄连口服液的抗炎作用.结果 与空白对照组比较,双黄连口服液能显著降低2,4-二硝基苯酚致大鼠发热模型的体温(P＜0.05),并能显著抑制二甲苯致小鼠耳肿胀及角叉菜胶致大鼠足肿胀的炎症反应(P＜0.05).结论 双黄连口服液具有显著的解热、抗炎作用.     

玉郎伞提取物抗炎作用及机制研究

目的:研究玉郎伞(YLS)的抗炎作用及其可能的机制.方法:采用二甲苯致小鼠耳肿胀和角叉菜胶致小鼠足肿胀模型,考察YLS水提取物(TYLS,以生药计剂量分别为80,40 g·kg-1)及其总黄酮(FYLS,0.14,0.07 g·kg-1)的抗炎作用,连续灌胃给药7 d后测定小鼠耳肿胀度和炎症足前列腺素E2(PGE2)及一氧化氮(NO)的含量.采用去除双侧肾上腺小鼠足肿胀模型,观察TYLS(以生药计剂量分别为80,40 g·kg-1)及FYLS(0.14,0.07 g·kg-1)灌胃给药对二甲苯致小鼠耳肿胀的影响.正常大鼠灌胃TYLS(以生药计剂量分别为60,30 g·kg-1)及FYLS(0.1,0.05 g·kg-1)7 d后,测定大鼠肾上腺中维生素C和胆固醇含量及肾上腺重量.结果:TYLS及FYLS对二甲苯致小鼠耳肿胀、角叉菜胶致正常小鼠足肿胀均有显著的抑制作用,但对去肾上腺小鼠二甲苯所致耳肿胀无抑制作用(P0.05);可降低炎症渗出物中PGE2含量,但对NO含量无显著影响(P0.05);可降低正常大鼠肾上腺中维生素C和胆固醇的含量,对肾上腺指数无明显影响.结论:YLS具有明显抗炎作用,其作用可能与抑制PGE:产生,激动下丘脑-垂体一肾上腺轴有关,但对NO无显著抑制作用.     

Effect of itraconazoles on the production of pro-inflammatory substances in mouse macrophage-like cells

BACKGROUND, MATERIALS AND METHODS: Synthetic triazoles are widely used for the treatment of fungal infection. In order to understand their possible anti-inflammatory action, we investigated the effect of itraconazole and its hydroxylated derivative (hydroxyitraconazole) on the production of various pro-inflammatory substances by mouse macrophage-like RAW264.7 cells. RESULTS: These compounds did not apparently show any growth inhibitory or stimulatory effects over a wide range of concentrations (0.2-50 μg/ml). Itraconazoles dose-dependently increased the production of prostaglandin E? (PGE?) and tumor necrosis factor-α (TNF-α) without affecting the production of interleukin-1β (IL-1β) and nitric oxide (NO). LPS treatment significantly enhanced the production of NO, PGE?, TNF-α and IL-1β. The addition of itraconazoles to LPS-stimulated RAW264.7 cells significantly reduced the production of NO, but rather enhanced the production of PGE?, TNF-α and IL-1β. ESR spectroscopy demonstrated that itraconazoles did not significantly scavenge NO and superoxide anion radicals, indicating that the inhibition of NO production by itraconazoles is not due to their radical-scavenging activity. Hydroxyitraconazole was slightly more cytostatic, and more efficiently inhibited NO production, but enhanced the production of other pro-inflammatory substances. CONCLUSION: These data suggest that itraconazoles regulate NO and other pro-inflammatory substances differently in activated macrophages.     

吡格列酮对脂多糖诱导的星形胶质细胞炎性细胞因子释放的影响

目的研究吡格列酮对脂多糖(LPS)诱导的星形胶质细胞炎症介质释放的抑制作用及其信号传导通路。方法神经胶质酸性蛋白(glial fibrillary acid protein,GFAP)免疫荧光染色法鉴定星形胶质细胞纯度。ELISA方法检测IL-1β、IL-6和TNF-α蛋白表达量的变化。Griess法测定培养细胞上清液中一氧化氮(NO)含量。结果星形胶质细胞经GFAP免疫荧光鉴定,其阳性率可达95%以上。LPS组能明显增加星形胶质细胞分泌IL-1β、IL-6、TNF-α及NO。吡格列酮能明显抑制LPS引起的这些作用,并呈一定浓度依赖性。过氧化物酶体增殖物激活受体γ(PPARγ)的特异性阻断剂GW9662能明显对抗吡格列酮对LPS引起的IL-1β、IL-6、TNF-α及NO增加的抑制作用。与LPS组相比,JNK特异性阻断剂SP600125(5μmol·L-1)亦能有效对抗LPS诱导星形胶质细胞IL-1β、IL-6、TNF-α及NO分泌的增加;特异性iNOS抑制剂SMT可明显抑制LPS引起的NO分泌增加。结论吡格列酮能明显改善LPS诱导的大鼠皮层星形胶质细胞的损伤,这种作用可能与激活PPARγ、抑制JNK信号传导通路有关。     

Acetyl-α-boswellic acid and Acetyl-β-boswellic acid protects against caerulein-induced pancreatitis via down-regulating MAPKs in mice

This study is to investigate the protective effect of Acetyl-α-boswellic acid and Acetyl-β-boswellic mixture(α/β-ABA), which is the active ingredients isolated from Frankincense, on actue pancreatitis and its mechanism. Our experimental results showed that 2 μM α/β-ABA reduced production of NO, TNF-α, IL-6, IL-10 and IL-1β in RAW264.7 cells that were stimulated with lipopolysaccharide (LPS) which indicates its anti-inflammatory role. In pancreatitis model induced by caerulein, intra-gastrical administration of 100 mg/kg α/β-ABA relieved inflammatory cells infiltration significantly and attenuated the serum elevation of amylase TNF-α and IL-6 remarkably in mice. Furthermore, α/β-ABA down-regulated mitogen-activated protein kinase (MAPK) family phosphorylated proteins in pancreas, including phosphorylated p38, ERK1/2 and JNK, to reduce the serum inflammatory factors. Finally, α/β-ABA alleviated the pancreatic edema and inflammatory cell infiltration in pancreatitis mice model. This study suggests that α/β-ABA may be targeted for drug development against pancreatitis via modulating MAPKs pathway.     

Effects of platycodin D on IL-1β-induced inflammatory response in human osteoarthritis chondrocytes

Platycodin D (PYD), a major saponin derived and isolated from the roots of Platycodon grandiflorum, has been reported to have anti-inflammatory and anti-tumor effects. The present study aimed to investigate the effects of PYD on IL-1β-stimulated human osteoarthritis chondrocytes. Chondrocytes were treated with PYD 1 h before IL-1β treatment. The levels of MMP1, MMP13, IL-8, RANTES, PGE2, and NO were measured in this study. The expression of LXRα, NF-κB, and IκBα were detected by western blot analysis. The results showed that PYD significantly inhibited IL-1β-induced MMP1, MMP13, IL-8, RANTES, PGE2, and NO production. PYD also suppressed IL-1β-induced NF-κB activation. Furthermore, the expression of LXRα was up-regulated by PYD in a dose-dependent manner. In addition, LXRα siRNA inhibited the effects of PYD on MMP1, MMP13, PGE2, and NO production in human osteoarthritis chondrocytes. In conclusion, these results suggested that PYD attenuated IL-1β-induced inflammatory response in osteoarthritis chondrocyte by activating LXRα.     

葡萄籽中原花青素的抗炎作用和机制

目的：研究葡萄籽中原花青素（PA）的抗炎作用及机制。方法：用巴豆油诱导的小鼠耳肿和角叉菜胶诱导的大鼠足肿模型,研究PA对炎症的影响。NOS活性用NADPH黄递酶染色法,NO含量用Griess重氮化反应法,β-NAG用对硝基酚比色法,MDA用TBA荧光法测定,IL－1β,TNFα和PGE2含量用放免法测定。结果：PA 10－40mg/kg ip剂量依赖性地抑制角叉菜胶诱导的大鼠足肿和巴豆油诱导的小鼠耳肿。PA 10mg/kg减少大鼠致炎足MDA生成,抑制炎症渗出液中NOS的β－NAG活性,降低IL－1β、TNF和PGE2含量。其作用强于地塞米松2mg/kg。结论：PA对大鼠和小鼠实验性炎症有明显的抗炎作用。其抗炎机理和清除氧自由基、抗脂质过氧化和减少细胞因子的生成有关。     

蟛蜞菊内酯对脂多糖诱导RAW264.7细胞环氧化酶2、NO及TNF-α的影响

目的:研究蟛蜞菊内酯对脂多糖(lipopo-lysaccharide,LPS)诱导RAW264.7巨噬细胞环氧化酶2(COX-2)、NO及TNF-α的作用。方法:ELISA方法检测0.2、2、20μmol/L不同浓度蟛蜞菊内酯对终浓度为10μg/mL LPS诱导RAW264.7细胞产生TNF-α、NO及前列腺素E2(PGE2)的影响,Western blot方法检测蟛蜞菊内酯对LPS诱导COX-2酶蛋白表达的影响。结果:LPS能够明显诱导小鼠RAW264.7细胞产生的COX-2酶蛋白,蟛蜞菊内酯低中高3个浓度均能抑制LPS诱导产生的COX-2酶蛋白表达。PGE2可以被LPS诱导增加,与空白组比有显著差异。蟛蜞菊内酯低中高3个浓度均能抑制LPS诱导产生的PGE2、NO和TNF-α,呈现剂量依赖性。结论:蟛蜞菊内酯抗炎的作用机制可能为抑制COX-2的蛋白表达,进而抑制PGE2的生成,也可能与抑制NO和TNF-α生成有关。     

Soyasaponin Ab inhibits lipopolysaccharide-induced acute lung injury in mice

Soyasaponin Ab (SA) has been reported to have anti-inflammatory effect. However, the effects of SA on lipopolysaccharide (LPS)-induced acute lung injury (ALI) have not been reported. The aim of this study was to investigate the anti-inflammatory effects of SA on LPS-induced ALI and clarify the possible mechanism. The mice were stimulated with LPS to induce ALI. SA was given 1 h after LPS treatment. 12 h later, lung tissues were collected to assess pathological changes and edema. Bronchoalveolar lavage fluid (BALF) was collected to assess inflammatory cytokines and nitric oxide (NO) production. In vitro, mice alveolar macrophages were used to investigate the anti-inflammatory mechanism of SA. Our results showed that SA attenuated LPS-induced lung pathological changes, edema, the expression of cycloxygenase-2 (COX-2) and inducible nitric oxide synthase (iNOS) in lung tissues, as well as TNF-α, IL-6, IL-1β, and NO production in mice. Meanwhile, SA up-regulated the activities of superoxide dismutase (SOD) and catalase decreased by LPS in mice. SA also inhibited LPS-induced TNF-α, IL-6 and IL-1β production as well as NF-κB activation in alveolar macrophages. Furthermore, SA could activate Liver X Receptor Alpha (LXRα) and knockdown of LXRα by RNAi abrogated the anti-inflammatory effects of SA. In conclusion, the current study demonstrated that SA exhibited protective effects against LPS-induced acute lung injury and the possible mechanism was involved in activating LXRα, thereby inhibiting LPS-induced inflammatory response.     

红毛五加有效成分的抗炎机制初步研究

目的对红毛五加茎皮中有效成分的抗炎机制进行初步研究。方法以LPS刺激小鼠巨噬细胞样细胞RAW264.7,测定红毛五加萃取物氯仿洗脱部分对细胞上清液PGE2、TNF-α、NO、IL-10水平的影响。结果纯氯仿洗脱部分40mg/L剂量组产生的PGE2为(79.57±12.50)pg/mL,TNF-α为(291.6±40.7)pg/mL,NO为(26.2±2.9)μmol,与LPS刺激组相比,差异均有统计学意义。10mg/L剂量组产生的PGE2为(95.20±11.20)pg/mL,TNF-α为(358.6±37.9)pg/mL,NO为(28.3±3.2)μmol,与LPS刺激组相比,差异均有统计学意义。纯氯仿洗脱部分40mg/L剂量组、10mg/L剂量组产生的IL-10分别为(229.4±39.0)pg/mL、(243.7±47.7)pg/mL,与LPS刺激组相比,无统计学意义。结论红毛五加正丁醇萃取部分经氯仿洗脱部分能够抑制炎症因子PGE2、TNF-α、NO的产生而发挥抗炎作用。