活血化瘀法对慢性盆腔炎雌性大鼠血清前炎症细胞因子TNF-α、IL-1β、IL-8水平的影响

目的：探讨活血化瘀法对慢性盆腔炎雌性大鼠血清前炎症细胞因子肿瘤坏死因子-α（TNF-α）、白介素-1β（IL-1β）、白介素-8（IL-8）水平的影响。方法：采用混合细菌加机械损伤方法,建立慢性盆腔炎大鼠模型,将60只造模后大鼠随机分为慢性盆腔炎造模组（模型组）、桂枝茯苓胶囊治疗高、中、低剂量组（高、中、低剂量实验组）、少腹逐瘀胶囊治疗组（对照组）,各组均为12只,另选假手术慢性盆腔炎造模大鼠（假手术组）、正常饲养未干预大鼠（正常组）各12只。运用酶联免疫吸附测定法,分别检测各组大鼠血清TNF-α、IL-1β、IL-8的水平。结果：（1）血清TNF-α、IL-8水平,模型组较正常组、假手术组明显升高（P〈0.01）;中剂量实验组较模型组明显降低（P〈0.01）,且接近正常组水平（P〉0.05）;中剂量实验组较对照组降低,差异有统计学意义（P〈0.05）,高、低剂量实验组均较对照组升高（P〉0.05或P〈0.01）;中剂量实验组较高、低剂量实验组明显降低（P〈0.01）。（2）血清IL-1β水平,模型组较正常组、假手术组明显升高（P〈0.01）;高、中剂量实验组、对照组较模型组明显降低（P〈0.01）,且接近正常组水平（P〉0.05）;高、中剂量实验组较对照组降低,但差异无统计学意义（P〉0.05）;高、中剂量实验组较低剂量实验组明显降低（P〈0.01）。结论：活血化瘀法通过影响慢性盆腔炎大鼠血清前炎症细胞因子TNF-α、IL-1β、IL-8水平,以抑制炎症反应,这可能是活血化瘀法治疗慢性盆腔炎和预防、缓解盆腔粘连的作用机制之一。     

牛王刺对CIA大鼠Treg/Th17细胞平衡影响的实验研究

目的:观察牛王刺(CD)水提液对CIA诱导大鼠Treg/Th17细胞平衡的影响,探讨牛王刺抗类风湿性关节炎的作用机制。方法:CIA诱导建立关节炎模型,将50只SD大鼠随机分为正常组,模型组,阳性组,牛王刺水提液低、高剂量组,采用ELISA法检测各组血清IL-1β、IL-6及TNF-α含量,Western Bolt法检测大鼠滑膜IL-1β,IL-6,TNF-α,IL-17,RORγt,Foxp3的蛋白表达水平。结果:与正常组比较,CIA诱导模型组大鼠血清中IL-1β、IL-6及TNF-α水平显著增高(P0.01),滑膜中IL-1β,IL-6,TNF-α,IL-17,RORγt的蛋白表达水平显著升高(P0.01),而Foxp3的蛋白表达水平显著下降(P0.01);与模型组比较,牛王刺治疗组的血清中IL-1β、IL-6及TNF-α水平明显下降(P0.05),滑膜中IL-1β,IL-6,TNF-α,IL-17,RORγt的蛋白表达水平明显下降(P0.05),Foxp3的蛋白表达水平明显上升(P0.05),高剂量组尤为明显。结论:牛王刺可调节CIA诱导关节炎大鼠Treg/Th17细胞平衡,抑制炎性细胞因子生成,这可能是牛王刺抗RA的治疗作用机制之一。     

胰岛素不同时机给药对脓毒症大鼠炎性反应的影响

目的:通过注射内毒素(LPS)建立的大鼠脓毒症模型,观察胰岛素不同时机给药对血清和肝细胞因子表达的影响。方法:将81只大鼠分为九组,即A组腹腔注射等渗盐水;B组腹腔注射LPS;C、D、E、F、G、H、I组分别在腹腔注射LPS前30 min和注射后0、1、3、6、12、24 h给予胰岛素治疗。观察各组大鼠LPS注射后24和48h血清白细胞介素-1β(IL-1β)、IL-6、肿瘤坏死因子α(TNF-α)和IL-10的变化,以及LPS注射48 h后肝组织IL-1β、IL-6、TNF-α和IL-10的变化。结果:注射LPS后24和48 h,大鼠血IL-1β、IL-6、TNF-α和IL-10均显著增加。LPS注射48 h后,肝组织中IL-1β、TNF-α、IL-6和IL-10蛋白水平也明显增加。在注射LPS前30 min或注射后6 h内给予胰岛素,能明显降低注射后24和48 h血清中的IL-1β、TNF-α和IL-6水平(P0.05);而IL-10水平则仅在注射LPS前或注射同时给予胰岛素,才较LPS组明显增加(P0.05)。在LPS注射前30 min或注射后6 h内给予胰岛素,注射后48 h肝内的IL-1β和TNF-α水平较LPS组明显降低(P0.05);而肝的IL-6水平仅在LPS注射前30min或与同时给予胰岛素时,才较LPS组明显降低(P0.05)。结论:胰岛素对脓毒症大鼠有抑制炎性细胞因子,增加抗炎介质释放等保护作用。在注射LPS 6 h内给予胰岛素可发挥良好的抗炎保护作用,而在注射LPS 6 h后给予胰岛素治疗其抗炎保护作用明显减弱。     

复方木尼孜其颗粒对盆腔炎性疾病后遗症的作用

目的:研究复方木尼孜其颗粒对盆腔炎性疾病后遗症的作用及其机理,为临床上选择复方木尼孜其颗粒治疗盆腔炎性疾病后遗症提供依据。方法:进行慢性盆腔炎大鼠模型子宫组织修复实验和血清IL-2细胞因子的检测实验,以此探讨复方木尼孜其颗粒对盆腔炎性疾病后遗症的影响。结果:①各给药组慢性盆腔炎大鼠模型宫腔粘连或扩张、子宫壁结构病变、子宫内膜上皮细胞变性、子宫壁炎细胞浸润、子宫内膜充血水肿情况均好于模型组。②各给药组的IL-2水平均高于模型组。结论:①各给药组对慢性盆腔炎大鼠模型均有减轻子宫病变的作用,其中大剂量给药组对子宫的修复作用明显优于模型组。②给药组的IL-2水平较高,表现出一定程度的增强细胞免疫功能的作用。     

钙对染铅大鼠免疫损伤的干预作用

目的研究不同剂量钙对染铅大鼠免疫损伤的干预作用。方法 60只(50±5)g清洁级SD雄性大鼠随机分为对照、染铅、试验Ⅰ、试验Ⅱ、试验Ⅲ共5组。饲养60 d后,采全血测定白细胞数及血清IgG含量;取脾脏计算脾脏指数,观察其细胞形态变化;提取脾脏中总的RNA,测定TNF-α、IL-1β和IL-6基因的相对表达量。结果铅暴露会导致大鼠机体脾脏指数、白细胞数、血清IgG含量和细胞因子TNF-α、IL-1β、IL-6 m RNA表达量显著下降,脾脏淋巴细胞减少,而补充一定剂量钙可使脾脏指数、白细胞数和血清IgG含量显著升高,明显改善脾脏病理性变化,同时细胞因子TNF-α、IL-1β、IL-6的相对表达量显著增加。结论补充适量的钙可缓解铅致大鼠机体免疫功能下降。     

慢性盆腔炎患者促炎因子与抗炎因子的关系

目的:探讨慢性盆腔炎患者血清促炎因子与抗炎因子的表达与相关性。方法:选择87例慢性盆腔炎患者作为病例组,选择同期健康体检妇女69例作为对照组,ELISA法检测血清TNF-α、IL-1β、IL-6和抗炎细胞因子IL-4、IL-10的表达。结果:病例组患者血清TNF-α、IL-1β和IL-6表达高于对照组(P<0.05),而血清IL-4和IL-10表达低于对照组(P<0.05);病例组患者血清促炎因子的表达与抗炎因子的表达呈负相关(P<0.05)。结论:慢性盆腔炎患者促炎因子过度激活,而抗炎因子被抑制,并且二者表达具有一定的相关性,共同促进慢性盆腔炎的发生发展。     

蠲痛饮对大鼠子宫内膜异位症TNF-α、IL-1β和ICAM-1影响

目的:探讨蠲痛饮对大鼠子宫内膜异位症血清和腹腔液中细胞因子IL-1β、TNF-0[以及异位内膜ICAM-1表达影响.方法:采用SD大鼠自体移植建立EMS大鼠模型,将60只大鼠随机分为正常组、模型组、蠲痛饮低剂量组、中剂量组、高剂量组、丹那唑组6组,持续用药28天,Elisa法检测TNF-α、IL-1β含量以及S-P法检测ICAM-1的表达.结果:模型组腹腔液和血清IL-1β、TNF-α含量以及异位内膜ICAM-1表达明显高于正常组,蠲痛饮能显著减低内异症大鼠血清及腹腔液中IL-1β、TNF-α含量和减少异位内膜组织ICAM-1表达(P＜0.05).结论:子宫内膜异位症的发病与细胞因子IL-1β,TNF-α以及异位内膜ICAM-1异常表达有关.蠲痛饮通过抑制炎症因子IL-1β、TNF-α的分泌改善全身和局部免疫水平,抑制异位子宫内膜的黏附而达到治疗目的.     

急性坏死性胰腺炎大鼠血细胞因子含量的变化和意义

目的探讨急性坏死性胰腺炎大鼠血清TNF-α、IL-1β、IL-6和IL-10含量的变化及其意义。方法选择标准W istar大鼠64只,随机分为2组:假手术组(SO,n=32)和急性坏死性胰腺炎组(ANP,n=32)。以牛磺胆酸钠复制急性坏死性胰腺炎大鼠模型。动态观察同组不同时间,不同组同时间的血清中内毒素(ET)、TNF-α、IL-1β、IL-6和IL-10含量变化。结果在4 h、8 h、12h和16 h的血清中ET、TNF-α、IL-1β、IL-6和IL-10(ANP组IL-10除16h外),ANP组显著高于SO组(P<0.05),且在ANP组ET、TNF-α、IL-1β和IL-6随病程进展而升高(P<0.01),在ANP组IL-10水平随病程进展降低(P<0.01)。结论ET、TNF-α、IL-1β、IL-6和IL-10参与了大鼠ANP的病理过程,促炎细胞因子TNFα-、IL-1β和IL-6介导了ANP时的炎性细胞因子瀑布样级联反应,抗炎细胞因子IL-10的负调控作用减弱。     

肺灌注PM2.5对高血压大鼠心血管系统的炎性作用

目的 观察大气细颗粒物对机体心血管系统的炎性作用,探寻其可能作用机制.方法 在上海市某非工业区采集大气PM2.5,选取雄性自发性高血压(spontantously hypertensive,SH)和Wsitar Kyoto(WKY)大鼠各24只作为实验对象,设低、中、高3个剂量组和1个对照组,染毒剂量分别是1.6、8.0、40.0mg/kg,采用气管滴注法进行PM2.5染毒,观察不同染毒剂量组、不同机体内血清高敏C-反应蛋白(high sensitive C-reaction protein,hsCRP)的水平,同时检测心肌白细胞介素1-β(IL-1β)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)和MIP-2细胞因子的mRNA表达水平,了解机体肺灌注PM2.5后心血管系统的炎性反应,从而探索PM2.5对心血管系统的毒性效应及其可能机制.结果 大鼠PM2.5染毒后,WKY和SH大鼠各染毒组血清hsCRP水平与对照组比较,差异均有统计学意义,且随染毒剂量增加而增加,即存在剂量-反应关系.同时在相同染毒剂量下,WKY和SH大鼠hsCRP水平差异有统计学意义.此外,心肌组织中IL-1β、IL-6、TNF-α和MIP-2的mRNA表达水平总体上随染毒剂量增加有增加趋势,同时相同染毒剂量时,在SH大鼠体内上述各细胞因子的mRNA表达较WKY大鼠高.PM2.5对SH大鼠的心血管系统的炎性反应可能大于对WKY大鼠的作用.结论 PM2.5引起WKY和SH大鼠心血管系统出现明显的炎性反应,且对SH大鼠的作用更为明显,提示PM2.5对机体心血管系统有一定的损伤作用.     

橙皮素对矽尘暴露大鼠肺组织中细胞因子的影响

目的探讨橙皮素干预对二氧化硅染尘大鼠肺组织损伤的拮抗作用及其对细胞因子的影响。方法将54只健康SPF级Wistar雄性大鼠随机分为6组,分别为阴性对照(生理盐水)组、二氧化硅(50 mg/ml)模型组、吡非尼酮(100 mg/kg)对照组和低(100 mg/kg)、中(200 mg/kg)、高剂量(400 mg/kg)橙皮素治疗组,每组9只。二氧化硅模型组、吡非尼酮对照组和不同剂量橙皮素治疗组均给予1 ml二氧化硅溶液(50 mg/ml)一次性经气管灌注造模;24 h后,吡非尼酮对照组和各剂量橙皮素治疗组采用灌胃方式进行干预,染毒容量为10 ml/kg,每天1次,连续28 d;阴性对照组和二氧化硅模型组均给予等容积生理盐水。检测大鼠肺组织中转化生长因子-β1(TGF-β1)、肿瘤坏死因子-α(TNF-α)、白细胞介素-1β(IL-1β)、IL-4、IL-10、干扰素-γ(IFN-γ)的水平,并进行肺组织肺泡炎及纤维化评分。结果与阴性对照组比较,二氧化硅模型组、吡非尼酮对照组和各剂量橙皮素治疗组大鼠的肺泡炎和肺纤维化评分均较高,差异有统计学意义(P0.05);且随着橙皮素染毒剂量的升高,大鼠的肺泡炎和肺纤维化评分均呈下降趋势。与二氧化硅模型组比较,吡非尼酮对照组和各剂量橙皮素治疗组大鼠的肺泡炎和肺纤维化评分均较低,差异有统计学意义(P0.05)。与阴性对照组比较,二氧化硅模型组、吡非尼酮对照组和各剂量橙皮素治疗组大鼠肺组织中TGF-β1、IL-1β、TNF-α、IL-4、IL-10和IFN-γ的水平均较高,差异有统计学意义(P0.05);且随着橙皮素染毒剂量的升高,大鼠肺组织中TGF-β1、IL-1β的水平均呈下降趋势,TNF-α、IL-4、IL-10的水平均呈先上升后下降的趋势,而IFN-γ的水平呈上升趋势。与二氧化硅模型组比较,吡非尼酮对照组和各剂量橙皮素治疗组大鼠肺组织中TGF-β1、IL-1β、TNF-α、IL-4的水平均降低,除低剂量橙皮素治疗组IL-1β和吡非尼酮对照组IL-4外,差异均有统计学意义(P0.05);而中、高剂量橙皮素治疗组大鼠肺组织中IL-10的水平和高剂量橙皮素治疗组大鼠肺组织中的IFN-γ水平均较高,差异有统计学意义(P0.05)。结论橙皮素可能通过抑制促炎因子的释放、促进抗炎因子的分泌从而减轻二氧化硅对肺组织的损伤作用,进而抑制矽肺纤维化的形成和发展。     

Pelvic inflammatory disease

The real prevalence of pelvic inflammatory disease (PID) is unknown since many women are either asymptomatic or have atypical symptoms. It is often difficult to detect, manage, and prevent PID. Since PID has obstetric, gynecologic, and contraceptive-related causes, its prevalence is quite high. About 70% of PID hospital admissions in sub-Saharan Africa are a result of reproductive tract infections (RTIs) while this figure is 34% in Asia and 31% in developed countries. Only 10-20% of lower RTIs ascend into the upper genital tract and an even smaller percentage of women with PID develop chronic sequelae. Still, just 1 episode carries an increased risk of a tubal infertility, ectopic pregnancy, chronic pelvic pain, considerable pain during coitus, a new episode, and menstrual irregularities. Neisseria gonorrhoea and Chlamydia trachomatis are the most common causative organisms of PID. In Africa, the risk factors for PID are the same as they are for sexually transmitted diseases (STDs): multiple sex partners, young age at first intercourse, high frequency of coitus, and a high rate of acquiring new partners. The largest percentage of women with RTIs are monogamous women who are infected and constantly reinfected by their promiscuous husbands. The primary means to prevent PID are promotion of safer sexual behavior and condom usage. Secondary measures include accessible, acceptable, and effective STD services and education and counseling during case management. WHO suggests that STD treatment become part of the primary health care system. It has developed flow charts on syndromic diagnosis for urethral discharge in men and genital ulcer disease in women. Health workers should assume increased PID risk if the partner has had a history of urethral discharge and/or treatment for gonorrhea or nongonococcal urethritis. Partner notification is also needed for case management, but stigmatization in some countries poses a problem. WHO also recommends use of drugs which have a 95% STD cure rate.     

Pelvic inflammatory disease

This article discusses the etiology, epidemiology, diagnosis, and treatment of pelvic inflammatory disease (PID). PID, which affects at least 1 million women in the US each year, has serious consequences: about 15% of cases become sterile after 1 infection, 15% develop chronic pain requiring surgery, and the ectopic pregnancy rate among women who do become pregnant is 10 times that among women without infection. The goal is to prevent PID by identifying cervicitis and endometritis before salpingitis develops and by advocating contraceptive methods that will reduce attack rates. Also important are prompt, accurate diagnosis and effective therapy. Sexually transmitted organisms are responsible for 50-75% of acute primary spontaneous salpingitis. Epidemiologic factors influence the rate of cervicitis and the development of salpingitis from cervicitis. These factors include age, number of sexual partners, frequency of sexual intercourse, and OC use. OC users have 1/2-1/4 the expected rate of both gonococcal and chlamydial salpingitis. The tremendous range of clinical signs and symptoms makes the diagnosis of salpingitis difficult, implying a need for physical and laboratory determinations. It is suggested that laparoscopy be more widely used to diagnose acute pain. Adequate treatment includes both antibiotic administration and close follow up to assess the clinical response and antibiotic compliance.     

Etiopathogenesis of inflammatory bowel diseases

The pathogenesis of IBD is only partly understood; various environmental and host (e.g. genetic-, epithelial-, immune and non-immune) factors are involved. It is a multifactorial polygenic disease with probable genetic heterogeneity, some genes are associated with IBD itself, while others increase the risk of ulcerative colitis (UC) or Crohn's disease (CD) or are associated with disease location and/or behaviour. The role of environmental factors, in particular, enteric antigens, smoking and non-steroid anti-inflammatory drug use has been well established. However uptil now no proof of a role of any unique pathogenic bacteria or special dietary and/or psychosocial factor has been identified. In this hypothesis, the disease may develop in a genetically predisposed host as a consequence of disregulated immune response to environmental, in particular, enteric antigens, resulting in a continuous immune-mediated inflammation (in CD predominantly Th-1, in UC a modified Th-2 mechanisms are involved) and not in tolerance. As a consequence, the permeability of mucosa and the antigen challenge increases, in contrast, the disregulated immune response is unable to downregulate the inflammatory process. This will result in a continuous inflammation and tissue damage. The pathogenesis of CD is thought to be mainly an antigen driven, T-lymphocyte dependent process, while in UC the role of epithelial factors and activated granulocytes are essential.     

Radiology of inflammatory bowel disease

Plain radiographs and barium studies remain the primary imaging procedures in patients with known or suspected Crohn's disease or ulcerative colitis. The newer imaging modalities such as radionuclide studies, ultrasound and angiography have an important role in selected cases.