黄芩有效成分SBM对炎症模型及免疫功能的影响

目的研究通过常温超高压方法得到的黄芩有效成分SBM的抗炎作用,并初步探讨其作用机制。方法观察SBM体外对淋巴细胞增殖、IL-1β合成的影响;观察给药后对佐剂性关节炎大鼠原发性及继发性病变、免疫功能及对甲醛诱导足肿胀、醋酸诱导腹腔渗出的影响。结果SBM(31.25～500mg.L-1)体外可明显抑制ConA诱导的小鼠脾淋巴细胞增殖及LPS诱导的腹腔巨噬细胞合成IL-1β;SBM(20mg.kg-1)灌胃给药可明显抑制佐剂性关节炎大鼠原发性及继发性足肿胀,并可抑制脾淋巴细胞增殖、IL-1β合成;SBM(20mg.kg-1)灌胃给药还可明显抑制甲醛诱导的大鼠足肿胀及醋酸诱导的腹腔渗出。结论SBM可通过抑制免疫细胞的功能及促炎因子的产生发挥抗炎作用。     

三叶青藤醇提物的镇痛抗炎作用

目的:研究三叶青藤醇提物的镇痛及抗炎作用。方法:采用小鼠热水缩尾法和醋酸扭体法观察镇痛作用;采用二甲苯致小鼠耳肿胀、角叉菜胶诱导大鼠足肿胀的试验模型观察抗炎作用;并测定角叉菜胶诱导大鼠足肿胀炎性渗出液中前列腺素E2(PGE2)的含量。结果:三叶青藤醇提物能明显提高小鼠的痛阈值,但未能减少小鼠的扭体次数。同时,三叶青藤醇提物能显著减轻小鼠耳肿胀和大鼠足爪肿胀反应,能明显减少大鼠角叉菜胶性炎症渗出液中PGE2含量。结论:三叶青藤醇提物没有明确的镇痛作用,但有显著的抗炎作用,其机制可能与抑制PGE2的合成有关。     

溃结康胶囊的抗炎作用机制

目的:研究渍结康胶囊的抗炎作用及其可能的机制.方法:通过小鼠耳肿胀、大鼠角叉菜胶足跖肿胀、大鼠棉球肉芽肿等实验观察其抗炎作用,并测定小鼠足爪中前列腺素E2(PGE2)、丙二醛(MDA)的含量.结果:溃结康胶囊能明显抑制二甲苯所致的小鼠耳肿胀,角叉菜胶所致大鼠足跖肿胀以及棉球肉芽肿的增生,并减少PGE2、MDA在炎症组织中的产生;对摘除肾上腺的小鼠亦可抑制二甲苯所致的耳肿胀.结论:溃结康胶囊具有一定的抗炎作用,其作用与抑制PGE2合成及脂质过氧化有关.     

虎杖提取物抗炎作用的实验研究

[目的]考察虎杖的乙酸乙酯提取物的抗炎作用及初步机制。[方法]分别以地塞米松、阿司匹林和环磷酰胺为阳性对照药,采用虎杖的乙酸乙酯提取物对小鼠和大鼠的多种炎症模型进行抑制实验。[结果]虎杖的乙酸乙酯提取物对角叉菜胶所致大鼠足跖肿胀有显著抑制作用(P<0.00 J);对小鼠、大鼠纸片法所致肉芽肿有显著抑制作用(P<0.01);对腹腔注射醋酸所致小鼠毛细血管通透性增高有显著抑制作用(P<0.01);对角叉菜胶所致小鼠肿胀足中炎症介质PGE2合成有显著抑制作用(P<0.001);对三硝基氯苯诱导的小鼠迟发性超敏反应有显著抑制作用(P<0.01);对肾上腺切除大鼠纸片法致肉芽肿(P<0.01)及角叉菜胶所致足跖肿胀(P<0.05)有显著抑制作用,但其抑制率均较正常大鼠相应实验抑制率有所降低。[结论]虎杖的乙酸乙酯提取物有一定的抗炎作用,其作用机制可能是抑制炎症介质PGE2的合成、抑制细胞免疫及与垂体-肾上腺皮质系统有关。     

仙鹤草提取物镇痛抗炎试验的实验研究

目的:初步探讨中药仙鹤草提取物的镇痛抗炎作用.方法:取仙鹤草的水提取物和乙醇提取物,应用醋酸致小鼠扭体法、小鼠热板法、二甲苯致小鼠耳廓肿胀法和大鼠角叉菜胶足跖肿胀法研究其镇痛抗炎作用.结果:仙鹤草乙醇提取物和水提起物可减少醋酸致小鼠扭体次数,延长小鼠舔足时间,减轻二甲苯致小鼠耳廓肿胀程度,减小角叉菜胶致足跖肿胀程度;乙醇提取物作用强于水提取物.结论:中药仙鹤草乙醇提取物具有明显的镇痛抗炎作用.     

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。     

白英提取物镇痛抗炎作用的实验研究

目的：初步探讨中药白英提取物的镇痛抗炎作用？方法：取白英的水提取物和乙醇提取物,应用醋酸致小鼠扭体法、小鼠热板法研究是镇痛作用;应用二甲苯致小鼠耳廓肿胀法和大鼠角叉莱胶足跖肿胀法研究其镇痛抗炎作用、结果：白英水提取物和乙醇提取物可减少醋酸致小鼠扭体次数,延长小鼠舔足时间;减轻二甲苯致小鼠耳廓肿胀程度,减小角叉莱胶致足跖肿胀程度。但水提取物作用强于乙醇提取物。结论：中药白英有一定的镇痛抗炎作用,其水提取物的镇痛抗炎作用比乙醇提取物效果明显。     

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.     

半边莲不同提取物镇痛抗炎作用

目的研究半边莲不同溶剂提取物的镇痛抗炎作用。方法制备半边莲水提取物和75%乙醇提取物,采用醋酸扭体实验和热板实验测定半边莲提取物镇痛作用,二甲苯致小鼠耳廓肿胀实验和10%蛋清致小鼠足跖肿胀实验测定半边莲提取物抗炎作用。结果半边莲水提取物可明显抑制醋酸所致小鼠扭体反应（P＜0.01）;给予半边莲水提取物和醇提取物1,2 h,小鼠热板痛阈值明显提高（P＜0.05或P＜0.01）;半边莲提取物能抑制二甲苯所致小鼠耳廓肿胀（P＜0.05或P＜0.01）;半边莲提取物在致炎后0.5,1,2,4 h能显著抑制10%蛋清所致小鼠足跖肿胀（P＜0.05或P＜0.01）。结论半边莲提取物有明显的镇痛和抗炎作用。     

梅花鹿鹿角托盘提取物的抗炎镇痛作用

目的:探讨梅花鹿鹿角托盘提取物的抗炎镇痛作用。方法:通过小鼠足肿胀、耳郭肿胀的实验研究梅花鹿鹿角托盘提取物的抗炎作用;采用热板法和醋酸扭体法研究梅花鹿鹿角托盘提取物的镇痛作用。结果:梅花鹿鹿角托盘提取物腹腔注射给药能有效地抑制角叉菜胶引起的足肿胀和二甲苯引起的小鼠耳郭肿胀;显著提高热板实验小鼠的痛阈,并能抑制醋酸引起的小鼠扭体反应次数,延长疼痛潜伏期。结论:梅花鹿鹿角托盘提取物腹腔注射给药具有抗炎镇痛作用。     

当归A_3活性部位对小鼠巨噬细胞环氧化酶-2活性及基因表达的影响

目的研究当归A3活性部位对小鼠巨噬细胞RAW264.7环氧化酶-2(cyclooxygenase-2,COX-2)活性及基因表达的影响。方法采用酶联免疫法(enzyme-line immu-nosorbnent assay,ELISA)检测前列腺素E2(prostaglandin E2,PGE2)产量及COX-2活性,采用RT-PCR和Western blot法检测COX-2 mRNA及蛋白表达水平。结果 A3(20、40、80mg.L-1)剂量依赖性地抑制LPS诱导的RAW264.7细胞PGE2产量、COX-2活性、COX-2 mRNA及蛋白表达水平增高。结论 A3能够直接抑制PGE2产量,此作用可能与抑制COX-2基因表达有关。     

广西山银花绿原酸体外抗炎作用及分子机制研究

目的研究广西山银花绿原酸体外抗炎效应并探讨其分子机制。方法分离大鼠腹腔巨噬细胞(peritoneal macro-phages,PMΦ),MTT比色法分析绿原酸对PMΦ生长活性的影响,LPS长时间刺激PMΦ,酶联免疫吸附法(ELISA)法检测细胞上清液中肿瘤坏死因子(TNF-α)、白细胞介素-6(IL-6)和前列腺素E2(PGE2)含量,用PGE2的含量表示COX-2的活性;A23187短时间刺激PMΦ,放射免疫分析法测定培养上清液6-酮-前列腺素F1α(6-keto-PGF1α)的含量,以此表示COX-1的活性。结果绿原酸在31.25～1 000 mg.L-1范围内对细胞无抑制作用;除绿原酸50 mg.L-1组TNF-α含量与LPS刺激组无统计学意义外,其余各浓度组TNF-α、IL-6及PGE2含量与LPS刺激组比较差异有显著性,呈剂量依赖性;绿原酸体外低浓度抑制6-keto-PGF1α生成,高浓度则诱导6-keto-PGF1α生成。结论绿原酸具有体外抗炎作用。其作用机制可能与抑制TNF-α、IL-6等炎症因子的活化以及影响花生四烯酸(AA)代谢有关。     

Anti-Inflammation activity of<Emphasis Type="Italic">Actinidia polygama</Emphasis>

The fruit of Actinidia polygama (AP) has long been used as a folk medicine in Korea for treating pain, rheumatic arthritis and inflammation. The present investigation was carried out to determine the in vivo and in vitro anti-inflammatory activity of AP using several animal models of inflammation. The 70% ethanol extract of the fruit of AP significantly inhibited acetic acid-induced, vascular permeability in a dose dependent manner (23%, 38%, and 41% inhibition at doses of 200 mg/kg, 500 mg/kg and 1000 mg/kg, respectively). This effect was maintained in AP water-soluble fraction (APW). The APW fraction also showed significant inhibitory activity against the rat paw edema induced by a single treatment of carrageenan. In vitro experiments were performed to demonstrate the inhibitory activities of APW (100 microg/ml) on lipopolysaccharide (LPS)-induced nitric oxide (NO) and prostaglandin E2 (PGE2) production. The results showed that APW dose-dependently suppressed LPS-induced NO production in RAW 264.7 macrophages without a notable cytotoxic effect and also decreased inducible NO synthase (iNOS) protein expression. APW also showed a significant inhibitory effect in LPS-induced PGE2 production and cyclooxygenase-2 (COX-2) expression.     

Inhibitory effects of 2,3,5,4'-tetrahydroxystilbene-2-O-beta-D-glucoside on experimental inflammation and cyclooxygenase 2 activity

The inhibitory effects of 2,3,5,4'-tetrahydroxystilbene-2-O-beta-d-glucoside (THSG), extracted from the roots of Polygonum multiflorum Thunb, on inflammatory activity in animal models and cyclooxygenase-2 (COX-2) activity in lipopolysaccharide (LPS)-induced mouse RAW264.7 macrophage cells were investigated. The carrageenin (CGN)-induced rat paw oedema model and dimethylbenzene-induced mouse ear oedema model were prepared; MTT assay, semi-quantitative RT-PCR, Western blot and ELISA were adopted. THSG 2.3, 4.6 and 9.2 mg kg(- 1) by oral administration inhibited mouse ear oedema and the percentage of inhibition of THSG 9.2 mg kg(- 1) is 87%. THSG 3.2, 6.4 and 12.8 mg kg(- 1) by oral administration dose-dependently inhibited rat paw oedema and the percentage of inhibition of THSG 12.8 mg kg(- 1) is 56% at 6 h. Indomethacin 13 and 9 mg kg(- 1) showed 90% and 57% inhibition in the same animal models, respectively. LPS 1 microg ml(- 1) significantly up-regulated prostaglandin E(2) (PGE(2)) production (inducing COX-2 activity) by 35% (exogenous arachidonic acid, AA), which was dose-dependently decreased by THSG 1, 10, and 100 micromol L(- 1) and the percentage of inhibition of THSG 10 micromol L(- 1) was 40%. NS-398 10 micromol L(- 1) decreased PGE(2) production by 42%. THSG 1, 10, 100 micromol L(- 1) was shown to markedly inhibit the LPS-induced COX-2 protein and mRNA expression in RAW264.7 cells (P < 0.05) but had no effect on COX-1 protein and mRNA (P>0.05). In summary, the data showed that THSG possessed an anti-inflammatory effect, which was perhaps related to the inhibition of COX-2 enzyme activity and expression in RAW264.7 macrophage cells.     

Distribution and regulation of cyclooxygenase-2 in carrageenan-induced inflammation

1 We characterized the regulation of cyclooxygenase-2 (COX-2) at the mRNA, protein and mediator level in two rat models of acute inflammation, carrageenan-induced paw oedema and mechanical hyperalgesia. 2 Carrageenan was injected in the hind paw of rat at low (paw oedema) and high doses (hyperalgesia). COX-2 and prostaglandin E2 (PGE2) levels were measured by RT-PCR and immunological assays. We also determined the distribution of COX-2 by immunohistochemistry. 3 The injection of carrageenan produced a significant and parallel induction of both COX-2 and PGE2. This induction was significantly higher in hyperalgesia than in paw oedema. This was probably due to the 9 fold higher concentration of carrageenan used to provoke hyperalgesia. 4 Immunohistochemical examination showed COX-2 immunoreactivity in the epidermis, skeletal muscle and inflammatory cells of rats experiencing hyperalgesia. In paw oedema however, only the epidermis showed positive COX-2 immunoreactivity. 5 Pretreatment with indomethacin completely abolished the induction of COX-2 in paw oedema but not in hyperalgesia. 6 These results suggest that multiple mechanisms regulate COX-2 induction especially in the more severe model. In carrageenan-induced paw oedema, prostanoid production have been linked through the expression of the COX-2 gene which suggest the presence of a positive feedback loop mechanism.     

穿心莲内酯对巨噬细胞环氧化酶2及其产物表达的影响

目的研究穿心莲内酯对巨噬细胞环氧化酶2(COX-2)表达及其主要产物前列腺素E2(PGE2)生成的影响。方法取生长良好的小鼠巨噬细胞RAW264.7,加入不同浓度的穿心莲内酯(终浓度1、10、50μmol/L)进行预干预,1h后再加入脂多糖(LPS,终浓度1μg/mL)刺激,并设空白组和穿心莲内酯单独作用组作为对照组。取培养18h细胞上清,用Elisa法检测PGE2生成量;取培养24h细胞,提取总蛋白,用WesternBlot法检测穿心莲内酯对COX-2蛋白表达的影响。结果 LPS可以显著诱导RAW264.7细胞COX-2表达和PGE2的生成,与对照组比较P<0.01;穿心莲内酯预干预可以抑制LPS诱导的COX-2蛋白表达,下调PGE2的生成。结论穿心莲内酯可通过降低LPS诱导的巨噬细胞COX-2表达和PGE2生成,发挥抗炎作用,这可能是其抗炎的作用机制之一。     

Role of cyclooxygenases in oedema-forming activity of bothropic venoms.

The venoms of Bothrops asper (BaV) and Bothrops jararaca (BjV), two of the most medically important poisonous snakes of Latin America, cause pronounced oedema in the victims through poorly understood mechanisms. In the present study, we examined the possible role of cyclooxygenases (COX) in the genesis of mouse paw oedema caused by BaV and BjV injections. BaV at 2.5 microg/paw and BjV at 0.75 microg/paw induced significant oedema that persisted for up to 6h following subplantar injection. Treatment with indomethacin (2 mg/kg), rofecoxib, (10 mg/kg), or dexamethasone (2 mg/kg) significantly reduced the BaV- and BjV-induced oedema formation. Treatment with SC-560 (30 mg/kg) significantly reduced the oedema formation induced by BjV but had no effect on that induced by BaV. Both venoms induced significant increases in the levels of prostaglandin E(2) (PGE(2)) and the expression of COX-1 and COX-2 in paw tissue. The peak of oedema formation and PGE(2) release correlated with marked expression of COX-2 in the paw tissue. These results demonstrate that injection of BaV and BjV results in a rapid increase in oedema formation that is, at least partially, mediated by arachidonic acid metabolites formed by COX-2. In the case of BjV, COX-1-derived prostanoids also appear to contribute significantly to the inflammatory changes.     

白芍总甙对大鼠腹腔巨噬细胞产生前列腺素E_2的作用及部分机制研究

白芍总甙（ＴＧＰ，０．０１～１００ｍｇ·Ｌ－１）对亚适浓度Ａ２３１８７（０．１μｍｏｌ·Ｌ－１）激活的大鼠腹腔巨噬细胞（ＰＭΦ）产生的前列腺素Ｅ２（ＰＧＥ２）呈现低浓度促进和高浓度抑制的双向调节作用。而ＴＧＰ对最适浓度Ａ２３１８７（１μｍｏｌ·Ｌ－１）激活的ＰＭΦ产生的ＰＧＥ２呈浓度依赖性的抑制作用，其ＩＣ５０为１６．７ｍｇ·Ｌ－１。在整体模型上，ＴＧＰ（５０ｍｇ·ｋｇ－１×１０ｄ）能使佐剂性关节炎（ＡＡ）大鼠ＰＭΦ产生过高的ＰＧＥ２恢复正常水平。采用Ｆｕｒａ－２／ＡＭ荧光法测定ＴＧＰ对Ａ２３１８７（１μｍｏｌ·Ｌ－１）诱导正常大鼠ＰＭΦ胞内游离钙离子浓度［Ｃａ２＋］ｉ，发现ＴＧＰ（≤１０ｍｇ·Ｌ－１）对ＰＭΦ［Ｃａ２＋］ｉ无明显影响，而ＴＧＰ在（１０～１００ｍｇ·Ｌ－１）时，对ＰＭΦ［Ｃａ２＋］ｉ有一定抑制作用。提示高浓度ＴＧＰ对ＰＧＥ２的负向调节作用可能与抑制细胞内钙有关。     

COX expression and PGE(2) and PGD(2) production in experimental acute and chronic gastric lesions

Prostaglandin E(2) and D(2) (PGE(2) and PGD(2)) production and cyclooxygenase-2 (COX-2) expression during the resolution of acute and chronic gastric inflammatory lesions in Wistar rats have been investigated. Differences between ibuprofen, nonselective COX inhibitor, and rofecoxib, specific COX-2 inhibitor, on the development of the induced responses were also analysed. In an acute model, by instillation of HCL, the greatest injury was observed early with a rapid and progressive restoration. Maximal up-regulation of COX-2 protein was detected at 6 h and was accompanied by increase of PGE(2) synthesis but not PGD(2). Both drugs stimulated COX-2 expression in accordance to their capacity of inhibiting this enzymatic activity, driving to delay in the healing. In a chronic model, by acetic acid-induced gastric ulcers, COX-2 was expressed at 7 days and was also associated with PGE(2) increase. Ibuprofen and rofecoxib also augmented COX-2 protein and inhibited PGE(2) levels. However, PGD(2) production was augmented when none signal of COX-2 protein could be detected. Together, this study confirms the role played by COX-2 enzyme in the resolution of acute and chronic gastric inflammatory process, PGE(2) being the principal product. The antiinflammatory effect of nonsteroidal antiinflammatory drugs (NSAIDs) could be mediated not only through the inhibition of COX activity but also through the induction of antiinflammatory PGs production-such as PGD(2)-although further studies would be needed to clarify the mechanisms of this activity and the possible implicated processes.