Lewis大鼠风湿性心瓣膜炎模型的比较研究
发布时间：2019-06-25 18:08
【摘要】：目的：风湿性心脏病（Rheumatic heart disease，RHD）目前仍是我国较常见的心脏病之一，虽然已经明确RHD发病是由感染A组链球菌(GroupA streptococcus, GAS)诱发自身免疫反应所致，但对风湿性心脏病的发生分子机制仍不完清楚。因此本研究采用三种方法建立lewis大鼠风湿性心瓣膜炎模型，从多方面对各模型进行评价和研究，为风湿性心脏病机制研究提供较可靠的动物模型。 方法： lewis雌性大鼠24只,随机分为: I、II、 III、 IV四组，每组6只。II组后足垫注射灭活GAS/完全弗氏佐剂（CFA）以1:1体积乳化的混合液，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次后改为皮下注射灭活GAS。III组前4周操作同II组，第5周改为皮下注射灭活GAS/不完全弗氏佐剂（IFA）以1:1体积乳化的混合液。IV组首次免疫同II、III组，第7天尾静脉注射未灭活GAS，每7天注射一次1次，共注射4次。I组为对照组，除不注射GAS外其余操作步骤同实验组。第7周时处死每组3只大鼠，第12周时处死每组剩余3只，根据两时间点再将各组分为A、B两个组。行血清抗链球菌溶血素“O（”ASO）、类风湿因子(RF)、C-反应蛋白(CRP)检查及心脏HE染色病理检查。 结果:（1）体重改变：第7，12周各实验组和对照组大鼠体重均数无差别(P0.05)。（2）实验室检查：IV组ASO在7周、12周时较其它组明显升高(p0.05),12周时，实验组ASO、CRP均较对照组升高（P0.05，P0.05）。（3）风湿性心瓣膜炎发病率：第7周各实验组发生心脏炎和瓣膜炎为：IIA组100%(3/3只)、IIIA组67%(2/3只)、IVA组100%(3/3只)；第12周各组发生心脏炎和瓣膜炎为：IIB组100%（3/3只）、IIIB组100%（3/3只）、IVB组100%（3/3只）。（4）心脏病理表现：第7周时，，IIA、IIIA组心脏HE染色病理均表现心肌间质及瓣膜散在炎性细胞渗出，小血管周单核细胞浸润，IVA组心肌间及瓣膜为较多灶状炎性细胞渗出，以淋巴细胞为主；12周时，IIB组大鼠心脏病理表现心肌间水肿消失，心肌间及瓣膜少量炎性细胞浸润，其中1只瓣膜出现轻微钙化；IIIB组大鼠心脏HE染色病理表现心肌及瓣膜仍以散在炎性细胞浸润为主，其中1只大鼠血心肌间较多风湿细胞聚集。IVB组大鼠心脏病理提示心肌及瓣膜少量灶状炎性细胞渗出。I组无一例发生心脏炎或瓣膜炎。 结论：在风湿性心瓣膜炎模型的比较研究中，采用灭活GAS、未灭活GAS两类菌的三种比较方法中，急性期两类菌造模方法所致lewis大鼠风湿性心瓣膜炎病理表现及实验室检查结果差异大。Lewis大鼠心瓣膜炎急性期，尾静脉注射未灭活GAS组，心肌间质、瓣膜显微镜下可见较多灶状炎性渗出。灭活GAS和灭活GAS+IFA两种方法病理表为散在淋巴细胞浸润。同时GAS活菌组大鼠血ASO明显升高。综上用GAS活菌造模在成模效果上更具优势,因此更适合风湿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
本文编号：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
本文编号：2505889
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