Lewis大鼠風(fēng)濕性心瓣膜炎模型的比較研究
發(fā)布時間：2019-06-25 18:08
【摘要】：目的：風(fēng)濕性心臟�。≧heumatic heart disease，RHD）目前仍是我國較常見的心臟病之一，雖然已經(jīng)明確RHD發(fā)病是由感染A組鏈球菌(GroupA streptococcus, GAS)誘發(fā)自身免疫反應(yīng)所致，但對風(fēng)濕性心臟病的發(fā)生分子機制仍不完清楚。因此本研究采用三種方法建立lewis大鼠風(fēng)濕性心瓣膜炎模型，從多方面對各模型進(jìn)行評價和研究，為風(fēng)濕性心臟病機制研究提供較可靠的動物模型。 方法： lewis雌性大鼠24只,隨機分為: I、II、 III、 IV四組，每組6只。II組后足墊注射滅活GAS/完全弗氏佐劑（CFA）以1:1體積乳化的混合液，首次免疫后第7天腹部皮下注射上述抗原1次，每7天注射1次，注射4次后改為皮下注射滅活GAS。III組前4周操作同II組，第5周改為皮下注射滅活GAS/不完全弗氏佐劑（IFA）以1:1體積乳化的混合液。IV組首次免疫同II、III組，第7天尾靜脈注射未滅活GAS，每7天注射一次1次，共注射4次。I組為對照組，除不注射GAS外其余操作步驟同實驗組。第7周時處死每組3只大鼠，第12周時處死每組剩余3只，根據(jù)兩時間點再將各組分為A、B兩個組。行血清抗鏈球菌溶血素“O（”ASO）、類風(fēng)濕因子(RF)、C-反應(yīng)蛋白(CRP)檢查及心臟HE染色病理檢查。 結(jié)果:（1）體重改變：第7，12周各實驗組和對照組大鼠體重均數(shù)無差別(P0.05)。（2）實驗室檢查：IV組ASO在7周、12周時較其它組明顯升高(p0.05),12周時，實驗組ASO、CRP均較對照組升高（P0.05，P0.05）。（3）風(fēng)濕性心瓣膜炎發(fā)病率：第7周各實驗組發(fā)生心臟炎和瓣膜炎為：IIA組100%(3/3只)、IIIA組67%(2/3只)、IVA組100%(3/3只)；第12周各組發(fā)生心臟炎和瓣膜炎為：IIB組100%（3/3只）、IIIB組100%（3/3只）、IVB組100%（3/3只）。（4）心臟病理表現(xiàn)：第7周時，，IIA、IIIA組心臟HE染色病理均表現(xiàn)心肌間質(zhì)及瓣膜散在炎性細(xì)胞滲出，小血管周單核細(xì)胞浸潤，IVA組心肌間及瓣膜為較多灶狀炎性細(xì)胞滲出，以淋巴細(xì)胞為主；12周時，IIB組大鼠心臟病理表現(xiàn)心肌間水腫消失，心肌間及瓣膜少量炎性細(xì)胞浸潤，其中1只瓣膜出現(xiàn)輕微鈣化；IIIB組大鼠心臟HE染色病理表現(xiàn)心肌及瓣膜仍以散在炎性細(xì)胞浸潤為主，其中1只大鼠血心肌間較多風(fēng)濕細(xì)胞聚集。IVB組大鼠心臟病理提示心肌及瓣膜少量灶狀炎性細(xì)胞滲出。I組無一例發(fā)生心臟炎或瓣膜炎。 結(jié)論：在風(fēng)濕性心瓣膜炎模型的比較研究中，采用滅活GAS、未滅活GAS兩類菌的三種比較方法中，急性期兩類菌造模方法所致lewis大鼠風(fēng)濕性心瓣膜炎病理表現(xiàn)及實驗室檢查結(jié)果差異大。Lewis大鼠心瓣膜炎急性期，尾靜脈注射未滅活GAS組，心肌間質(zhì)、瓣膜顯微鏡下可見較多灶狀炎性滲出。滅活GAS和滅活GAS+IFA兩種方法病理表為散在淋巴細(xì)胞浸潤。同時GAS活菌組大鼠血ASO明顯升高。綜上用GAS活菌造模在成模效果上更具優(yōu)勢,因此更適合風(fēng)濕性心瓣膜炎急性期研究。
[Abstract]:Objective: rheumatoid heart disease (Rheumatic heart disease,RHD) is still one of the most common heart diseases in China. Although it has been confirmed that the pathogenesis of RHD is caused by autoimmune response induced by group A streptococcal (GroupA streptococcus, GAS) infection, the molecular mechanism of rheumatoid heart disease is still unclear. Therefore, three methods were used to establish the model of rheumatic valvular inflammation in lewis rats, and to evaluate and study the models from many aspects, so as to provide a reliable animal model for the study of the mechanism of rheumatic heart disease. Methods: 24 female lewis rats were randomly divided into four groups with 6 rats in each group. In group II, the inactivated GAS/ complete Freund's adjuvant (CFA) was injected with a mixture of inactivated Freund's adjuvant (CFA) at 1:1. The antigen was injected subcutaneously once every 7 days on the 7th day after the first immunization, and the inactivated GAS.III group was injected subcutaneally 4 weeks after the first immunization, and the inactivated GAS.III group was treated with the same group 4 weeks after the first immunization. At the 5th week, the inactivated GAS/ incomplete Freund's adjuvant (IFA) was emulsified at 1:1. Group IV was immunized with II,III group for the first time, uninactivated GAS, was injected intravenously every 7 days on the 7th day, and group I was injected 4 times as the control group. The other operation steps except GAS injection were the same as those in the experimental group. At the 7th week, 3 rats in each group were killed, and the remaining 3 rats in each group were killed at the 12th week. According to the two time points, each group was divided into two groups: group A and group B. Serum antistreptococcal hemolysin "O (" ASO), rheumatoid factor (RF), C-reactive protein (CRP) and cardiac HE staining were examined. Results: (1) body weight change: there was no difference in the average body weight between the experimental group and the control group at the 7th and 12th week (P 0.05). (2). The ASO in the IV group was significantly higher than that in the other groups at 7 weeks and 12 weeks (p0.05). At 12 weeks, the ASO,CRP in the experimental group was higher than that in the control group (P0.05). P05). (3) incidence of rheumatic valvular inflammation: at the 7th week, the incidence of carditis and valvulitis in each experimental group was 100% in IIA group (67% in), IIIA group (n = 3) and 100% (n = 3) in), IVA group (n = 3) at the 7th week. At the 12th week, carditis and valvular inflammation occurred in 100% of IIB group (3 鈮
本文編號：2505889
[Abstract]:Objective: rheumatoid heart disease (Rheumatic heart disease,RHD) is still one of the most common heart diseases in China. Although it has been confirmed that the pathogenesis of RHD is caused by autoimmune response induced by group A streptococcal (GroupA streptococcus, GAS) infection, the molecular mechanism of rheumatoid heart disease is still unclear. Therefore, three methods were used to establish the model of rheumatic valvular inflammation in lewis rats, and to evaluate and study the models from many aspects, so as to provide a reliable animal model for the study of the mechanism of rheumatic heart disease. Methods: 24 female lewis rats were randomly divided into four groups with 6 rats in each group. In group II, the inactivated GAS/ complete Freund's adjuvant (CFA) was injected with a mixture of inactivated Freund's adjuvant (CFA) at 1:1. The antigen was injected subcutaneously once every 7 days on the 7th day after the first immunization, and the inactivated GAS.III group was injected subcutaneally 4 weeks after the first immunization, and the inactivated GAS.III group was treated with the same group 4 weeks after the first immunization. At the 5th week, the inactivated GAS/ incomplete Freund's adjuvant (IFA) was emulsified at 1:1. Group IV was immunized with II,III group for the first time, uninactivated GAS, was injected intravenously every 7 days on the 7th day, and group I was injected 4 times as the control group. The other operation steps except GAS injection were the same as those in the experimental group. At the 7th week, 3 rats in each group were killed, and the remaining 3 rats in each group were killed at the 12th week. According to the two time points, each group was divided into two groups: group A and group B. Serum antistreptococcal hemolysin "O (" ASO), rheumatoid factor (RF), C-reactive protein (CRP) and cardiac HE staining were examined. Results: (1) body weight change: there was no difference in the average body weight between the experimental group and the control group at the 7th and 12th week (P 0.05). (2). The ASO in the IV group was significantly higher than that in the other groups at 7 weeks and 12 weeks (p0.05). At 12 weeks, the ASO,CRP in the experimental group was higher than that in the control group (P0.05). P05). (3) incidence of rheumatic valvular inflammation: at the 7th week, the incidence of carditis and valvulitis in each experimental group was 100% in IIA group (67% in), IIIA group (n = 3) and 100% (n = 3) in), IVA group (n = 3) at the 7th week. At the 12th week, carditis and valvular inflammation occurred in 100% of IIB group (3 鈮
本文編號：2505889
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