关节鼠

The results show that: This tablet can decrease the rat"s footpad swell induced by Freud"s, inhibit the permeability of the blood capillary in inflammatory joint and decrease the 11-2 level in serum while increasing the rat"s body weight,(2) It can lower the rat"s temperature and the permeability of the blood capillary in inflammatory joint induced by collagen and inhibit the delayed type hypersensitivity,It can lower the stickiness of full blood and the accumulation of erythrocyte obviously inblood stasis model rats,lt can inhibit the formation of hemolysin and decrease the index of carbon granule clearance in mice, It can lower the permeability of celiac blood capillary and inhibit the granulomatous hyperplasia by sc cotton ,It can inhibit the pain induced by acetic acid and raise the pain threshold value of heat stimulation.

结果表明：关络通片能明显降低佐剂性关节炎大鼠左右足趾肿胀度，降低大鼠炎症关节的通透性，抑制其IL-2含量，对大鼠体重增长缓慢有一定的改善作用；能改善Ⅱ型胶原诱导性关节炎大鼠的表征指标及炎症关节的通透性，对其迟发型超敏反应有一定的抑制作用；对血瘀模型大鼠，能显著性降低其全血粘度、血浆粘度、红细胞压积；能抑制小鼠的溶血素抗体生成，抑制小鼠网状内皮系统的吞噬能力，具有一定的抑制机体免疫功能的作用，能抑制小鼠腹腔毛细血管通透性增高，抑制大鼠棉球肉芽组织增生，具有一定的抗炎作用；能抑制小鼠醋酸扭体反应、提高小鼠热板痛阈值，具有一定的镇痛作用。

And observed the changes of pawl swelling, multi-arthritis and hestopathology in joint inflammation.

以AA大鼠作为实验模型，分别予以FSN与雷公藤多甙进行灌胃治疗，对照观察大鼠关节肿胀和多关节炎情况，以及关节内病理组织学变化。

Anti-CCII antibody level was higher in experiment group than that in the normal group by ELISA(P.001). Besides, typical arthritis pathology was showed by roentgenography and histopathology.

与正常对照组相比，实验组大鼠脚踝与脚趾均有明显的肿胀；ELISA结果显示：实验组大鼠血清中抗CCII抗体水平较正常对照组明显高(P.001)； X线摄片结果和病理学分析结果显示，实验组大鼠的关节呈现典型的RA关节样病变和病理组织学特征。

The pathological findings showed that ZBT could alliviate the synovial tissues inflammatory congestion, edema, remit the inflammatory cell infiltration and inhibit the proliferation of synovial cells, therefore reduce the degree of destruction of the articular cartilage and subcartilaginous bone tissue. Inhibited the disablement of the woulded limbs.

结果：止痹痛药酒能轻模型鼠关节肿胀度，对免疫注射后继发病变具有良好的治疗作用，说明该药具有抗炎免疫作用，病理学观察证实该药能减轻关节滑膜的充血水肿和炎细胞浸润、抑制滑膜细胞增生，减轻关节软骨和软骨下骨组织的破坏程度，抑制模型鼠患肢的致残。

Barometz. The following factors were determined: blood rheology indexes in mouse, weight of mouse and their organs' weight, turgenscence of the feet of mouse, content of trace elements in blood in mouse, content of Interleukin-1β(IL-1β) and tumor necrosis factor in the joint fluid in mouse.

对以下指标进行测试：大鼠的血液流变学指标，大鼠的体重；大鼠的脏器重量；大鼠的足跖肿胀程度；大鼠的血中微量元素含量；大鼠关节腔炎症介质白细胞介素-1β(Interleukin.1β，IL-1β)和肿瘤坏死因子(tumor necrosis factor，TNF-α)的含量。

Results:(1) FSN can inhibit secondary joints swelling and multi-arthritis evidently, improve the whole condition of rats; at the same time, it can also lighten the synovial inflammation and hyperplasia of lesion joints distinctly, and prevent the joint cartilage and bone from destruction; the collective efficiency of FSN is better than TWP.(2) FSN can raise AA rats low LTT of spleen to normal nearly, remedy the disorder of Th / Ts and Thl / Th2 cells balance in peripheral blood, restrain exorbitant TNF- a ? IL-1 produced by PM O , thereof exert anti-inflammatory and immunoregulation effect.(3) Inside the lesion joints, FSN can depress abnormal hyper-expression of TNF- a mRNA and NF-kB in synovial tissues, as well as advance the expression of Caspase-3 (a proteolytic enzyme of apoptosis), reduce synovial immflamination and proliferation.(4) FSN can lower the expression of VEGF in synovial tissue,reduce neogenetic veins, so inhibit the growth of pannus tissue and the damage of cartilage and bone by that.(5) The above effect of FSN are in proportion to its dosage.Conclusions: FSN has inhibitory effects on symptom and condition of experimental RA, which is better than TWP as a whole.

结果：(1)FSN有明显的抗炎作用，可显著抑制AA大鼠足跖肿胀与多关节炎，改善大鼠的全身情况，同时明显减轻病变关节滑膜炎症与增生，防止关节软骨及骨质的破坏，其综合作用优于TWP；(2)FSN还能使AA大鼠低下的脾LTT恢复至接近正常，纠正外周血中T细胞亚群Th／Ts及Th1／Th2平衡紊乱，抑制大鼠PHφ过高的TNF-α、IL-1分泌，而发挥抗炎和免疫调节作用；(3)在病变关节局部，FSN能显著抑制AA大鼠滑膜细胞异常增高的TNF-αmRNA的表达，降低滑膜组织中NF-kB表达，并增加凋亡蛋白酶Caspase-3表达，从而抑制滑膜的炎症与增殖；(4)FSN还可下调滑膜组织中VEGF表达，减少血管新生，由此抑制血管翳的形成及其对软骨和软骨下骨的侵蚀；(5)FSN的上述作用皆呈现一定的量效依赖关系，高剂量组作用优于低剂量组。

FSN can raise AA rats low LTT of spleen to normal nearly, remedy the disorder of Th/Ts and Th1/Th2 cells balance in peripheral blood, restrain exorbitant TNF-α、IL-1 produced by PMφ, thereof exert anti-inflammatory and immunoregulation effect.(3) Inside the lesion joints, FSN can depress abnormal hyper-expression of TNF-αmRNA and NF-kB in synovial tissues, as well as advance the expression of Caspase-3 (a proteolytic enzyme of apoptosis), reduce synovial immflammation and proliferation.(4) FSN can lower the expression of VEGF in synovial tissue, reduce neogenetic veins, so inhibit the growth of pannus tissue and the damage of cartilage and bone by that.(5) The above effect of FSN are in proportion to its dosage. Conclusions: FSN has inhibitory effects on symptom and condition of experimental RA, which is better than TWP as a whole.

结果：(1)FSN有明显的抗炎作用，可显著抑制AA大鼠足跖肿胀与多关节炎，改善大鼠的全身情况，同时明显减轻病变关节滑膜炎症与增生，防止关节软骨及骨质的破坏，其综合作用优于TWP；(2)FSN还能使AA大鼠低下的脾LTT恢复至接近正常，纠正外周血中T细胞亚群Th/Ts及Th1/Th2平衡紊乱，抑制大鼠PMφ过高的TNF-α、IL-1分泌，而发挥抗炎和免疫调节作用；(3)在病变关节局部，FSN能显著抑制AA大鼠滑膜细胞异常增高的TNF-αmRNA的表达，降低滑膜组织中NF-kB表达，并增加凋亡蛋白酶Caspase-3表达，从而抑制滑膜的炎症与增殖；(4)FSN还可下调滑膜组织中VEGF表达，减少血管新生，由此抑制血管翳的形成及其对软骨和软骨下骨的侵蚀；(5)FSN的上述作用皆呈现一定的量效依赖关系，高剂量组作用优于低剂量组。

TyPe II collagen induced arthritisln the rat ank1e joint andoVathumin as antigen induced arthritis WA in the rabbit knee joint wereestab1ish2 Qualitative evaluation of me in skin, muscle, synovium, cedilagearound joint and blood was performed by OMA3 The CIA rats were treated on day 7 after hind paw swelling and erythemaAnimals were injected intravenously with ase at a dose of 10mg/kg,tWenty minuots 1ater, one ankle of the rats random1y assigned was exPosedlaser irradiation at l00J/cm fOr l000 seconds, and another ankle wasM grouP wihout laser The other two groups is unmanipulatedcontrol group and untreated CIA group Bimaleolar ankle widthmeasuremellts were taken in all animals every tWo days using amicrometer The histopathology of the ank1e Joint was assessed at day 21after disease onset4 The pro1iferating cell nuclear antigen WCNA of CIA treated by PDT andthe HMME group without laser was doterdrined by immunohistochemiStry5 The AfA rabbits were treated on day 7 after knee swelling and erythemaThe theraPy invo1ved lntravenous injection of l0mg/kg HMME, fOl1owedby 20 minues period in dim light, and transdermal light treatment with\l00 J/cm2 fOr l000 seconds The inner sides of the treated Anees wereirradiated at first, and then the outer side did 24 hours later, the synovialtissue of the Anees joint were removed and in situ cel1 aPoptosis wasdetCCted With tednal deoxync1eotidyl transferase-mediated dUTP nickend labelingR6suIt8:l The pathologic changes of CIA and AIA include subsynovial inflammation,opovial hyPerplasia, pannus formation, cartilage and bone destructionresemble RA.2 The studies demonstrated that there are different uptake of HMME withinskin, muscle, synovium, cartilage and b1ood, and the synovium cou1draPidly uPtake more ase than skin and cartilage at the firSt 30 minuesaller intravenous injection of HMME3 The bimaleolar anke width had no different among PDT treated group,H group withollt 1aser and untreated CIA group But hlstologicalevaluation showed statiStical1y significallt reductions in synovialhyperplasia, pannus formation and cart1lage reosion, bone destruction andtotal score in PDT treated group4 Image analysis showed that the ratlo bforeen the areas of the coufltedobect to that of the entire area in PDTtreated grOup is lower than that in conirol group, but the integrated oPticaldensity had no different between the two groups5 Imape analysis showed that the ratio between the area of the countedobject to that of the e

治疗组在大鼠出现踝关节红肿后1周，炎症达到高峰时进行PDT治疗。随机治疗大鼠一侧的踝关节，另。2。一一侧作单纯HMME 对照。治疗方法是大鼠麻醉后尾静脉注入 HMME10ngkg，20分钟后踝关节照光，激光波长627.sum，功率密度 100mwcm'，照射时间1000秒，能量密度100）／。治疗后避光喂养72 小时。隔日一次测量大鼠的踝关节左右横径，治疗后两周取关节进行病理d 观察。 4。大鼠CIA模型用上述方法进行PDT治疗后，治疗组和单纯HMME 组用兔疫组化SP法检测石蜡切片的核增殖抗原。 5。兔AIA模型在关节炎出现第七天进行PDT治疗，随机治疗一侧膝关节，另一侧作自身对照。兔耳静脉注入I'arrainrelomg／Kg，20分钟后，膝关节用金蒸气激光照射，激光能量密度100）儿旷。24 ／J'时后取膝关节滑膜作病理检查，并用脱氧核昔酸末端转移酶介导的缺口末端标记法原位检测凋亡细胞。结果： 1。模型观察：CIA大鼠炎症高峰期滑膜下炎细胞浸润明显，滑膜细胞明显增殖，炎症达到高峰后二周，血管缀形成，并侵蚀和破坏软骨和骨， CIA模型病理改变与人类RA相似。兔AIA模型膝关节滑膜病理可见滑膜细胞增生，滑膜下炎细胞浸润，也与人类RA滑膜改变相似。 2。关节周围组织中光敏剂含量的测定结果表明，各组织对HMME 的吸收速度和吸收量不同，荧光值一时间曲线不同，滑膜组织比皮肤和软骨对 HMME的吸收多，在 2 0分钟时即有明显差异。 3.PDT对CIA模型的治疗结果表明：PDT治疗后关节炎组、单纯 HMME组和治疗组踝关节左右横径统计学检验差异没有显著性，但病理评分PDT治疗组滑膜增生、血管资形成及软骨破坏、骨破坏和总分比关节炎对照组和HMME对照组好，统计学检验差异有显著性。。3＿军医进修学院硕士学位论文中文摘要 4.PDT治疗组PCNA阳性细胞较对照组少，图像分析结果表明面密度（阳性染色的面积总和与统计视野面积的比值）治疗组小于对照组，统计学检验差异有显著性。。 5.PDT治疗组凋亡阳性细胞较对照组明显增多，图像分析结果单位视野内阳性细胞数和面密度PDT治疗组高于对照组，统计学检验差异有显著性。凋亡细胞核直径PDT治疗组较小，与对照组相比，统计学检验差异有显著性。结论：二。CIA、AIA的病理改变类似人类RA，可作为研究RA病因、发病机制、检查及治疗方法的模型。 2。各组织对HMME的吸收速度和吸收量不同，滑膜组织比皮。

Results(1) Group of electroacupuncture in Shu and dense wave can significantlyreduce the degree of ankle swelling(P＜0.05, P＜0.01), which shows thatelectroacupuncture has obvious anti-inflammatory and repercussive roles;(2) Theresults of HE staining showed that group of electroacupuncture in Shuand dense wave can significantly reduce inflammatory cell infiltration,inhibit synovial cell proliferation, and decrease proliferation of granulationtissue in rats joints;(3) group of electroacupuncture in dense-wave can increase the pain thresholdof experimental rats (P＜0.05, P＜0.01), reduce the content of peripheral painmediums, such as K~+, DA and 5-HT(P＜0.05, P＜0.01), which shows thatelectroacupuncture has significant analgesic effect;(4) In the local lesion of joints, electroacupuncture can significantly reducethe content of IL-1β, IL-8, TNF-a, increase IL-4 content, decrease theexpression of COX-2mRNA, and significantly promote the expression ofHSP-70 protein in synovial tissues of acute gouty arthritis rats (P＜0.05,P＜0.01),thus restrain the occurrence of synovial tissue inflammation.

结果：(1)电针疏密波组能显著减轻踝关节肿胀度(P＜0.05，P＜0.01)，表明电针有明显的抗炎消肿作用；(2)HE染色显示：电针疏密波组可使大鼠关节炎症细胞浸润明显减轻，滑膜细胞增生明显被抑制，肉芽组织增生明显减少；(3)电针密波组能提高实验性大鼠痛阈(P＜0.05，P＜0.01)，降低外周疼痛介质K~+、DA、5-HT的含量(P＜0.05，P＜0.01)，表明电针有明显的镇痛作用；(4)在病变关节局部，电针能显著降低急性痛风性关节炎大鼠滑膜组织IL-1β、IL-8、TNF-α含量(P＜0.05，P＜0.01)，升高IL-4的含量(P＜0.05，P＜0.01)，并降低关节滑膜内COX-2mRNA的表达(P＜0.05，P＜0.01)，可促使急性痛风性关节炎大鼠滑膜内HSP-70蛋白表达显著增加(P＜0.05，P＜0.01)，从而抑止滑膜组织炎症发生。

Results T-2 toxin could cause rat articular chondroncytes degeneration, necrosis, and appeared many blank areas free cells. Weigert/Van Gieson staining showed obvious collagen fasciculi emergence could be seen. Scanning electronic microscope showed the surface of articular cartilage was wave and rough. Collagen fasciculi ruptured and stack up, and presented a typical 揳rticular dryness?phenomenon. ELISA results indicated, at the stage of 3 month, the level of rat serum CTX-II in T-2 toxin group was higher than that in control group, and the difference had a markedly significance.

结果 T－2毒素可致大鼠关节软骨细胞变性、坏死，出现大面积无细胞区，胶原染色可见明显的&胶原显现&；扫描电镜显示，关节面起伏不平，表面粗糙，胶原纤维断裂、剥脱，关节表面布满裂片状凸起，呈典型的关节&干燥&现象；ELISA检测结果表明， T-2毒素组大鼠血清CTX-II水平在3个月时较对照组明显增加，差异具有统计学意义。

But we don't care about Battlegrounds.

但我们并不在乎沙场中的显露。

Ah! don't mention it, the butcher's shop is a horror.

啊！不用提了。提到肉，真是糟透了。