红曲抗炎作用的实验研究

目的：研究红曲的抗炎作用。方法：急性抗炎模型采用巴豆油致小鼠耳肿胀模型和角叉菜胶致大鼠足肿胀模型，慢性抗炎模型采用棉球植入小鼠腹腔致肉芽肿模型。以布洛芬作阳性对照，并设洛伐他汀高、低剂量组。比较红曲与洛伐他汀的抗炎作用。结果：红曲对巴豆油致小鼠耳肿胀、角叉菜胶致大鼠足肿胀和棉球致小鼠腹腔肉芽肿均有显著的抑制作用，与洛伐他汀的抗炎作用相近。结论：红曲具有显著的抗炎作用。     

祛痘新肤乳抗炎作用的实验研究

［摘要］目的考察祛痘新肤乳的抗炎作用。方法采用二甲苯致小鼠耳肿胀、角叉菜胶致大鼠足肿胀及棉球肉芽肿模型观察祛痘新肤乳的抗炎作用。结果局部外用祛痘新肤乳显著抑制二甲苯引起的小鼠耳肿胀、角叉菜胶导致的大鼠足肿胀及大鼠棉球肉芽肿。结论祛痘新肤乳具有显著的抗炎作用，并呈现一定的量效关系。     

益母草抗炎镇痛作用的实验研究

目的 探讨益母草的抗炎、镇痛的药理作用.方法 采用二甲苯致小鼠耳廓肿胀,角叉菜胶致大鼠足跖肿胀,小鼠棉球肉芽肿实验观察益母草的抗炎作用,采用热刺激和化学刺激致小鼠疼痛,观察其镇痛作用.结果 益母草对小鼠耳肿胀,大鼠足跖肿胀及小鼠棉球性肉芽肿均有显著抑制作用,能显著提高小鼠热板实验中的痛阈,减少扭体次数.结论 益母草具有显著的抗炎、镇痛的药理作用.     

咽炎合剂的抗炎、抑菌作用

目的:研究咽炎合剂的抗炎、抑菌作用。方法:采用醋酸致小鼠腹腔毛细管通透性亢进、二甲苯致小鼠耳肿胀、角叉菜胶致大鼠足肿胀、大鼠琼脂肉芽肿等模型研究抗炎作用;采用培养基药物浓度稀释法进行体外抗菌试验。结果:咽炎合剂能降低小鼠耳廓肿胀度,减轻角叉菜胶所致大鼠足肿胀程度,降低大鼠肉芽肿琼脂块质量;对金黄色葡萄球菌、流感杆菌、肺炎链球菌均有不同程度的抑制作用。结论:咽炎合剂具有显著的抗炎、抑菌作用。     

炎康颗粒的抗炎作用及机制研究

目的 研究炎康颗粒的抗炎作用,并探讨其作用机制.方法 采用巴豆油致小鼠耳肿胀实验模型、角叉菜胶致雄性大鼠足跖肿胀实验模型,观察炎康颗粒对急性炎症的作用;采用大鼠棉球肉芽肿实验模型,观察炎康颗粒对慢性炎症的作用;采用摘除双侧肾上腺的大鼠进行角叉菜胶致足跖肿胀实验及棉球肉芽肿实验,以观察炎康颗粒抗炎作用与下丘脑-垂体肾上腺轴(HPAA)的关系.结果 炎康颗粒8、16 g(生药)/kg连续给药1周,明显抑制小鼠耳肿胀;4、8g(生药)/kg明显抑制由角叉菜胶诱导的大鼠足趾肿胀;明显抑制大鼠棉球肉芽的增生.摘除肾上腺后,炎康颗粒连续给药1周,无明显抗炎作用.结论 炎康颗粒对急性炎症和慢性炎症均有明显的防治作用,其抗炎作用依赖于HPAA系统,并与减少白细胞介素有关.     

头顶一棵珠抗炎和免疫作用的实验研究

目的探讨头顶一棵珠的抗炎和免疫作用.方法抗炎实验采用巴豆油致小鼠耳廓肿胀等常规抗炎模型;免疫实验采用对小鼠体内碳粒廓清功能影响等的方法.结果头顶一颗珠提取物可明显抑制巴豆油致小鼠耳廊肿胀及角叉菜胶引起的大鼠足跖肿胀,能显著抑制大鼠棉球肉芽肿的增重及2.4-二硝基氯苯致小鼠迟发型超敏反应,明显增加免疫器官重量及指数,增强吞噬功能.结论头顶一颗珠有明显的抗炎和免疫调节作用.     

健胃康颗粒剂抗炎镇痛作用的研究

目的观察健胃康颗粒剂的抗炎、镇痛作用。方法采用小鼠耳肿胀、大鼠角叉菜胶足跖肿胀、大鼠棉球肉芽肿等实验模型观察其抗炎作用;以小鼠热板法和扭体法研究其镇痛作用。结果健胃康颗粒剂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;并可提高小鼠的热痛阈值,减少小鼠的扭体次数。结论健胃康颗粒剂具有抗炎、镇痛作用。     

刺茎楤木根皮抗炎和免疫作用的研究

目的探讨刺茎楤木根皮的抗炎和免疫作用。方法抗炎实验采用巴豆油致小鼠耳廓肿胀等常规抗炎模型;免疫实验采用对小鼠体内碳粒廓清功能影响等的方法。结果刺茎楤木根皮提取物可明显抑制巴豆油致小鼠耳廊肿胀及角叉菜胶引起的大鼠足跖肿胀,能明显抑制大鼠棉球肉芽肿的增重及2,4二硝基氯苯(DNCB)致小鼠迟发型超敏反应(DTH),增强吞噬功能。结论刺茎楤木根皮有明显的抗炎和免疫调节作用。     

刺茎楤木根皮抗炎和免疫作用的研究

目的探讨刺茎楤木根皮的抗炎和免疫作用。方法抗炎实验采用巴豆油致小鼠耳廓肿胀等常规抗炎模型;免疫实验采用对小鼠体内碳粒廓清功能影响等的方法。结果刺茎楤木根皮提取物可明显抑制巴豆油致小鼠耳廊肿胀及角叉菜胶引起的大鼠足跖肿胀,能明显抑制大鼠棉球肉芽肿的增重及2,4二硝基氯苯(DNCB)致小鼠迟发型超敏反应(DTH),增强吞噬功能。结论刺茎楤木根皮有明显的抗炎和免疫调节作用。     

苦瓜霜抗炎作用的研究

目的：研究苦瓜霜的抗炎作用。方法：观察二甲苯致小鼠耳肿胀度;测定角叉菜胶致大鼠足踝关节周长;测定大鼠棉球肉芽肿重量;观察组胺致大鼠毛细血管通透性。结果：苦瓜霜明显抑制二甲苯致小鼠耳肿胀;明显抑制角叉菜胶致大鼠足肿胀;明显抑制大鼠棉球肉芽肿增生;明显抑制组胺致大鼠毛细血管通透性。结论：苦瓜霜具有明显的抗炎作用。     

小儿清热感冒口服液抗炎解热镇咳的药效学研究

目的：研究小儿清热感冒口服液的抗炎、解热和镇咳作用。方法：在冰醋酸致小鼠腹腔毛细血管通透模型，角叉菜胶致小鼠足肿胀模型，干酵母致大鼠发热模型，百、白、破三联疫苗致家兔发热模型，以及枸橼酸诱导豚鼠咳嗽模型上观察小儿清热感冒口服液口服给药对实验动物的抗炎、解热和镇咳作用。结果：小儿清热感冒口服液可明显抑制冰醋酸所致小鼠腹腔毛细血管通透性增高，减轻角叉菜胶所致小鼠脚肿胀，降低干酵母致大鼠和百、白、破三联疫苗致家兔的体温升高，显著抑制枸橼酸诱导的豚鼠咳嗽。结论：小儿清热感冒口服液治疗小儿风热感冒疗效较好可能与其具有良好的解热、抗炎、镇咳等作用有关。     

Late inflammatory swelling by carrageenan in rat's subcutaneous neck tissue

When injected subcutaneously in the dorsum of neck in albino rats, carrageenan produced inflammatory swelling which reached peak after about 16 hr. The occurrence of the peak inflammatory swelling was delayed but not significantly reduced in severity by aspirin or indomethacin which were administered repeatedly. Phenylbutazone significantly reduced and dexamethasone almost completely inhibited it. In rat hind paw model, subplantar carrageenan injection produced peak inflammatory swelling after about 4 hr which was significantly reduced by all anti-inflammatory drugs mentioned above. It is interesting that an inflammagen when injected at different sites in the same species elicits responses which differ in the time course and drug responses.     

他汀类药物对多发性硬化的辅助治疗作用

他汀类药物可通过减少T细胞激活、抑制 T细胞迁移、使Th1类细胞反应向Th2类细胞反应 转化以及下调中枢神经系统炎症介质来抑制多发性 硬化的自身免疫反应。这些反应并非通过调节胆固 醇代谢,而是通过其抗炎症作用而达到的。临床上 采用他汀类药物治疗多发性硬化已经取得初步成 功。他汀类药物是多发性硬化治疗中有希望的辅助 药物。     

A sensitive and relevant model for evaluating anti-inflammatory activity-papaya latex-induced rat paw inflammation.

A new model employing latex of papaya as an inflammagen has been developed for testing anti-inflammatory activity. The latex (exudate) was harvested from the unripe papaya fruit, which had been dried under vacuum. The latex was then suspended in 0.05 M sodium acetate buffer. This suspension when injected in rat hind paw produced concentration-dependent inflammation. Of the 0.25% of this suspension, 0.1 ml was found ideal for evaluating anti-inflammatory activity of test drugs. This concentration produced 70%-100% inflammation lasting for about 5 hr with a maximum effect at h 3. The test drugs employed were prednisolone, aspirin, indomethacin, phenylbutazone, ibuprofen, piroxicam, chloroquine, levamisole, and a mixture of boswellic acids. For comparison, these drugs were also tested against carrageenan-induced inflammation. All the test drugs--steroidal, aspirin, and non-aspirin-like--showed anti-inflammatory activity against latex-induced inflammation. The activity of chloroquine, levamisole, and boswellic acids was significantly more against latex as compared with that of the carrageenan model. The inflammation caused by latex may be attributed to both its hydrolytic enzymes--papain and chymopapain--and glutathione, the activator of these enzymes. These enzymes seem to act like lysosomal enzymes that are released in inflammatory disease processes which mediate inflammation by stimulating the synthesis of prostaglandins. The papaya latex-induced inflammation model appears to be a sensitive, broad-based, and relevant one likely to prove useful for discovering new and effective drugs against inflammation and rheumatoid arthritis.     

Atherosclerosis is an inflammatory disorder after all

Inflammation has been increasingly recognized as an important player in the pathophysiology of numerous human disorders. Accumulating evidence has led to the conclusion that atherosclerosis is an inflammatory disease, although it was believed to be a disorder of high cholesterol levels in the bloodstream for over a century. Cholesterol does contribute to the pathogenesis of atherosclerosis, but through inflammatory mechanisms. Statins lower cholesterol levels and hence reduce inflammation in the vasculature and prevent heart disease. Statins may also exert anti-inflammatory effects through mechanisms independent of cholesterol lowering. Adhesion molecules, cytokines, oxidative stress, etc. appear to contribute to the inflammatory state of atherosclerosis and therapeutic approaches directed toward these markers or targets have the potential to be effective in reducing inflammation and treating atherosclerosis.     

Protective effect of simvastatin and rosuvastatin on trinitrobenzene sulfonic acid-induced colitis in rats

Objective:Statins have anti-inflammatory effects that are not directly related to their cholesterol lowering activity. This study was carried out to evaluate the effect of simvastatin or rosuvastatin on the extent of colonic mucosal damage and on the inflammatory response in trinitrobenzene sulfonic acid (TNBS)-induced ulcerative colitis.Result:Disease activity index score in TNBS-treated rats, as determined by weight loss, stool consistency, fecal occult blood, were significantly lowers in simvastatin or rosuvastatin-treated rats than TNBS-treated animals. Simvastatin or rosuvastatin counteracted the reduction in colon length, decreased colon weight, neutrophil accumulation, and tumor necrosis factor-alpha level in TNBS-induced colitis. Simvastatin and rosuvastatin also inhibited the increase in oxidative stress levels after TNBS administration.Conclusions:These results suggest that simvastatin and rosuvastatin significantly ameliorate experimental colitis in rats, and these effects could be explained by their anti-inflammatory and antioxidant activity.KEY WORDS: Rosuvastatin, simvastatin, trinitrobenzene sulfonic acid, tumor necrosis factor-α, ulcerative colitis     

蜂毒肽在治疗炎性疾病中的研究进展

炎性疾病是指因过度炎症反应所引发的或伴有炎症并发症的一类可影响人类健康的病症。目前临床上可通过抑制炎症反应达到治疗炎性疾病的目的,而常用的抗炎药虽然疗效明确,但都存在明显的不良反应,易给机体造成二次伤害,故抗炎新药亟待开发。蜂毒肽是从蜂毒中分离出的主要有效成分,具有较强的抗炎活性,其可通过介导炎症通路信号传递、抑制炎症细胞活性及炎症介质分泌等途径治疗多种炎性疾病,且疗效较好,具有较为广阔的临床应用前景。本文主要对蜂毒肽在治疗不同炎性疾病中的作用特点、蜂毒肽主要不良反应及应对策略进行了总结,以为后期蜂毒肽抗炎应用的临床开发提供参考。     

Statins and cardiovascular risk in rheumatic diseases

Chronic inflammatory rheumatic diseases are associated with an increased risk of cardiovascular (CV) atherosclerotic events. The inflammatory state, which is the hallmark of chronic rheumatic diseases, is the important driving force for accelerated atherogenesis. Since the control of traditional risk factors alone is insufficient in reducing the risk, much attention has been directed towards the potential use of statins. Statins, a family of drugs that suppress cholesterol biosynthesis by inhibiting the hydroxymethyl glutaryl coenzyme A reductase, have been shown to significantly reduce CV-related morbidity and mortality. In addition to lower lipid levels, several non-lipid lowering pleiotropic effects, including anti-inflammatory and immunomodulatory activities, make statins potential therapeutic agents in chronic rheumatic diseases. However, lipid metabolism in chronic rheumatic diseases is complex, since inflammatory states can induce alterations in lipid levels and function, so that cholesterol target levels from general guidelines may not be adequate in chronic inflammatory rheumatic diseases. Larger trials are needed to refine the precise benefits and health-utility associated with this therapy.