腹主动脉瘤小鼠模型的病理形态学比较及抗血管紧张素治疗在其发病过程中的研究
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摘要
第一章三种腹主动脉瘤小鼠模型的建立以及比较
目的：建立三种小鼠腹主动脉瘤(AAA)模型,比较三种建模方法的不同特点,探讨其研究应用的可行性。
方法：取C57BL/6以及ApoE-/-雄性小鼠共30只,采用三种不同方法分别建立三种小鼠腹主动脉瘤模型：血管紧张素Ⅱ模型[Angiotensin Ⅱ (Ang Ⅱ) Model],猪胰蛋白酶模型[Porcine Pancreatic Elastase(PPE) Model],氯化钙模型[Calcium Chloride (CaCl2) Model];并用磷酸缓冲溶液(PBS)作为相应方法的对照。多普勒超声监测小鼠腹主动脉直径变化、成瘤部位,计算并比较不同小鼠腹主动脉瘤模型的建模方法、手术时间、成瘤时间、成瘤率以及死亡率等特点；
结果：三种方法均能建立成功的腹主动脉瘤模型。PPE模型建模方法难度较大,手术时间较长(52.6±5.1min),成瘤率高(100%),存活周期长(随访4周,存活率为95%),死亡率低(5%)；CaC12模型建模方法容易,手术时间较长(40.7±4.3min),成瘤率较低(50%),存活周期长(随访4周均存活,存活率为100%),死亡率低(0%)；AngⅡ模型建模方法容易,手术时间短(7.8±3.6min),成瘤率较高(70%),存活周期较短(随访4周,存活率为60%),死亡率较高(40%)。
结论：小鼠的PPE模型,CaC12模型以及Ang Ⅱ模型为三种较为稳定的腹主动脉瘤模型,能为深入理解人腹主动脉瘤的病理机制以及评价腹主动脉瘤的药物治疗提供较为稳定的研究平台。
第二章三种腹主动脉瘤小鼠模型的病理形态学比较以及病理机制的研究
目的：观察不同小鼠模型的病理形态学特点,探讨不同腹主动脉瘤模型的共同病理机制。
方法：采用HE染色、EVG染色、免疫组织化学等方法检测小鼠的腹主动脉瘤组织,与正常小鼠腹主动脉相比较,观察病组织中瘤壁弹性纤维、炎症细胞、新生血管、淋巴管生成等的表达差异。
结果：PPE模型腹主动脉瘤病理变化表现为外膜大量炎症细胞浸润(尤其以巨噬细胞为主,伴有T淋巴细胞以及少量B淋巴细胞)以及新生血管、淋巴管形成,弹力纤维变性,部分缺失断裂,厚度不均。Ang Ⅱ模型表现为瘤壁血肿形成,外膜有炎症细胞浸润(以巨噬细胞为主,少有T淋巴细胞及B淋巴细胞)以及少量新生血管、淋巴管形成。伴有部分弹力纤维变性,缺失。CaCl2模型病变部位主要在外膜和中膜,表现为外膜部分增厚,伴少量炎症细胞浸润,仅有少量新生血管及淋巴管形成,中膜弹性纤维变性,僵直,呈烧灼状,厚薄不均,部分缺失断裂。
结论：三种小鼠模型既存在不同的病理形态学特点,也存在共同病理形态学特征,表现为炎症细胞浸润,血管及淋巴管生成。PPE、AngⅡ模型较为真实的反映了人腹主动脉瘤的病理特点,是两种比较稳定的动物模型。
第三章抗血管紧张素治疗在腹主动脉瘤发生发展过程中的研究
目的：将血管紧张素受体阻滞剂应用于小鼠腹主动脉瘤模型,评价抗血管紧张素治疗在腹主动脉瘤中的应用价值。
方法：取C57BL/6小鼠、ApoE-/-小鼠各15只,分成实验组(10只/组)和对照组(5只/组),实验组在建模前一周按telmisartan (10mg/kg)剂量给小鼠喂药；另一组为对照组,正常饮食。分别用多普勒超声监测小鼠的腹主动脉直径变化,与对照组(未用药处理的腹主动脉瘤模型小鼠)相比较,比较不同小鼠的成瘤率,瘤体进展情况等。并应用HE染色、EVG染色、免疫组织化学、qRT-PCR等方法检测腹主动脉瘤组织,比较不同小鼠的病理形态学变化。
结果：telmisartan在10mg/kg的剂量下对小鼠无明显副作用,能够有效抑制弹力蛋白酶及血管紧张素灌注后的小鼠腹主动脉直径进行性增大,并且能够防止两种腹主动脉瘤小鼠模型的腹主动脉瘤形成。病理切片显示：telmisartan处理过的小鼠主动脉管壁血管生成明显减少,炎症细胞浸润显著减轻,弹性纤维以及管壁三层结构相对完整,无显著病理变化。
结论：抗血管紧张素治疗能够防止小鼠腹主动脉瘤的发生并控制疾病的进展。telmisartan能够发挥有效的抗动脉瘤生成作用；10mg/kg的剂量安全,有效。
Chapter1. The establishment and comparative study of three types of rodent abdominal aortic aneurysms models
Objective:To investigate the feasibility of the animal research application by establishment and comparison of three different types of models.
Method:C57BL/6(20) and ApoE-/-(10) mice were used to eastablish three different abdominal aortic aneurysm (AAA) models by PPE intraluminal infusion for about5min, CaC12solution gauze adventitial infusion for15min and Ang Ⅱ minipump continuous subcutaneous infusion for28days. PBS infusion was accordingly applied for the control groups. Doppler ultrasound was applied to detect the diameter of the abdominal aortic and the location of the aneurysm. The time of operaion and aneurysm formation was recorded; the percentage of the aneurysm formation and mortality of animal models were also calculated.
Result:Three types of AAA models were successfully established. The process of PPE model establishment was more challenged, consequently the operation time was longer (52.6±5.1min), compared to40.7±4.3min in CaC12model and7.8±3.6min in Ang Ⅱ model, but the percentage of the aneurysm formation of PPE model was100%and the survival time of PPE and CaCl2model are longer than Ang Ⅱ model, almost all alive in4weeks follow-up compared to60%alive in Ang Ⅱ model. The process of CaCl2and Ang Ⅱ model establishment was relatively easy, however, the mortality of Ang Ⅱ model was much higher than PPE and CaCl2model.
Conclusion:PPE, CaCl2and Ang Ⅱ AAA models are stable models for further animal research. Moreover, the findings of our study support that the three types of animal models of AAAs may provide intriguing mechanistic insights into the human disease and are suitable for evaluation of medicine therapy in AAA.
Chapter2. The comparison study of morphology and pathogenesis in three different types of abdominal aortic aneurysm models
Objective:To observe the pathomorphological characteristics of three different models of abdominal aortic aneurysm (AAA) and investigate the common pathogenesis in the three different models of AAA.
Methods:As compared to the aortae of normal mice, HE, EVG, Immunohistochemistry staining technique were applied to detect the Morphological and phathological changes in the tissue specimens, such as the pattern of elastin degeneration was recorded, the quantity of different inflammatory cells infiltration, angiogenesis and lymphangiogenesis were counted.
Results:In PPE model, there was extensive destruction of the elastic lamellae and the adventitial region was occupied by a pronounced inflammatory infiltrate, predominantly containing macrophages. Neutrophils were present on the peripheral aspects of the adventitia surrounding the aorta; One fascinating aspect of angiotensin Ⅱ model is the aneurysm localization to the suprarenal segment of the aorta. The precipitating event that occurs within days of AngⅡ infusion appears to be medial macrophage accumulation in the region that is prone to AAA formation, associated with elastin degradation. Subsequently there were gross dissections of the aortas leading to prominent vascular hematomas and enhanced extracellular matrix deposition and infiltration of other leukocyte populations, primarily macrophages. The dilated region of the aorta gradually regained circumferential elastin fibers and completely re-endothelialized. Prominent neovascularization was present throughout the lumen of the remodeled tissue; In CaC12models, the abluminal incubation of calcium chloride also led to structural disruption of the medial layer and inflammatory responses. This inflammation occurred on the luminal and medial aspect of the artery. But, there is no obvious angiogenesis and lymphangiogenesis in this model.
Conclusion:Although there were different pathomorphological changes in the three types of AAA models, the common pathological charateristics were still existed, such as transmural inflammatory cells infiltration, adventitial angiogenesis and lymphangiogenesis and so on. Since the similar pathogenesis as human, PPE and Ang Ⅱ model were considered to be kind of ideal models for animal research.
Chapter3. The application of anti-angiotension in the development of abdominal aortic aneurysm
Object:To elucidate the effect of angiotension on the progression of AAA and validate the therapeutic effect of anti-angiotension based treatment on AAA
Method:The C57BL/6(15) and ApoE-/-male mice were devided into two groups:treated group and control. AAA was induced either in male ApoE-/-mice by subcutaneous infusion of1OOOng/kg/min Ang Ⅱ for28days or in mail C57BL/6mice by transient intra-aortic infusion of PPE. In the treated group, all the mice were daily treated with10mg/kg telmisartan7days before aneurym establishment; Doppler ultrasound was applied to detect the diameter of the abdominal aortic and the location of the aneurysm. The percentage of the aneurysm formation and mortality of animal models were also calculated. Morover, histopathology and gene profiling were used to evaluate therapeutic efficacy.
Results:The telmisartan almost completely prevented PPE-induced AAA formation in C57BL/6mice and suppressed Ang Ⅱ-induced increase in systolic blood pressure, preserved medial elastin and smooth musclesm and attenuated macrophage infiltration and angiogenesis within aortic adventitia. Moreover, ARB therapy dramatically downregulated the gene expression levels of certain proteinases, chemokines and their receptors, Cytokines, and adhesion molecules at the aneurismal lesions. There was no obvious side effect in the dose of1Omg/kg.
Conclusion:The application of telmisartan can play a significant anti-angiotension effect, which can successfully prevent the progression and formation of AAA; and the anti-angiotension therapy is highly efficacious and safe in suppressing experimental AAA.
目的：建立三种小鼠腹主动脉瘤(AAA)模型,比较三种建模方法的不同特点,探讨其研究应用的可行性。
方法：取C57BL/6以及ApoE-/-雄性小鼠共30只,采用三种不同方法分别建立三种小鼠腹主动脉瘤模型：血管紧张素Ⅱ模型[Angiotensin Ⅱ (Ang Ⅱ) Model],猪胰蛋白酶模型[Porcine Pancreatic Elastase(PPE) Model],氯化钙模型[Calcium Chloride (CaCl2) Model];并用磷酸缓冲溶液(PBS)作为相应方法的对照。多普勒超声监测小鼠腹主动脉直径变化、成瘤部位,计算并比较不同小鼠腹主动脉瘤模型的建模方法、手术时间、成瘤时间、成瘤率以及死亡率等特点；
结果：三种方法均能建立成功的腹主动脉瘤模型。PPE模型建模方法难度较大,手术时间较长(52.6±5.1min),成瘤率高(100%),存活周期长(随访4周,存活率为95%),死亡率低(5%)；CaC12模型建模方法容易,手术时间较长(40.7±4.3min),成瘤率较低(50%),存活周期长(随访4周均存活,存活率为100%),死亡率低(0%)；AngⅡ模型建模方法容易,手术时间短(7.8±3.6min),成瘤率较高(70%),存活周期较短(随访4周,存活率为60%),死亡率较高(40%)。
结论：小鼠的PPE模型,CaC12模型以及Ang Ⅱ模型为三种较为稳定的腹主动脉瘤模型,能为深入理解人腹主动脉瘤的病理机制以及评价腹主动脉瘤的药物治疗提供较为稳定的研究平台。
第二章三种腹主动脉瘤小鼠模型的病理形态学比较以及病理机制的研究
目的：观察不同小鼠模型的病理形态学特点,探讨不同腹主动脉瘤模型的共同病理机制。
方法：采用HE染色、EVG染色、免疫组织化学等方法检测小鼠的腹主动脉瘤组织,与正常小鼠腹主动脉相比较,观察病组织中瘤壁弹性纤维、炎症细胞、新生血管、淋巴管生成等的表达差异。
结果：PPE模型腹主动脉瘤病理变化表现为外膜大量炎症细胞浸润(尤其以巨噬细胞为主,伴有T淋巴细胞以及少量B淋巴细胞)以及新生血管、淋巴管形成,弹力纤维变性,部分缺失断裂,厚度不均。Ang Ⅱ模型表现为瘤壁血肿形成,外膜有炎症细胞浸润(以巨噬细胞为主,少有T淋巴细胞及B淋巴细胞)以及少量新生血管、淋巴管形成。伴有部分弹力纤维变性,缺失。CaCl2模型病变部位主要在外膜和中膜,表现为外膜部分增厚,伴少量炎症细胞浸润,仅有少量新生血管及淋巴管形成,中膜弹性纤维变性,僵直,呈烧灼状,厚薄不均,部分缺失断裂。
结论：三种小鼠模型既存在不同的病理形态学特点,也存在共同病理形态学特征,表现为炎症细胞浸润,血管及淋巴管生成。PPE、AngⅡ模型较为真实的反映了人腹主动脉瘤的病理特点,是两种比较稳定的动物模型。
第三章抗血管紧张素治疗在腹主动脉瘤发生发展过程中的研究
目的：将血管紧张素受体阻滞剂应用于小鼠腹主动脉瘤模型,评价抗血管紧张素治疗在腹主动脉瘤中的应用价值。
方法：取C57BL/6小鼠、ApoE-/-小鼠各15只,分成实验组(10只/组)和对照组(5只/组),实验组在建模前一周按telmisartan (10mg/kg)剂量给小鼠喂药；另一组为对照组,正常饮食。分别用多普勒超声监测小鼠的腹主动脉直径变化,与对照组(未用药处理的腹主动脉瘤模型小鼠)相比较,比较不同小鼠的成瘤率,瘤体进展情况等。并应用HE染色、EVG染色、免疫组织化学、qRT-PCR等方法检测腹主动脉瘤组织,比较不同小鼠的病理形态学变化。
结果：telmisartan在10mg/kg的剂量下对小鼠无明显副作用,能够有效抑制弹力蛋白酶及血管紧张素灌注后的小鼠腹主动脉直径进行性增大,并且能够防止两种腹主动脉瘤小鼠模型的腹主动脉瘤形成。病理切片显示：telmisartan处理过的小鼠主动脉管壁血管生成明显减少,炎症细胞浸润显著减轻,弹性纤维以及管壁三层结构相对完整,无显著病理变化。
结论：抗血管紧张素治疗能够防止小鼠腹主动脉瘤的发生并控制疾病的进展。telmisartan能够发挥有效的抗动脉瘤生成作用；10mg/kg的剂量安全,有效。
Chapter1. The establishment and comparative study of three types of rodent abdominal aortic aneurysms models
Objective:To investigate the feasibility of the animal research application by establishment and comparison of three different types of models.
Method:C57BL/6(20) and ApoE-/-(10) mice were used to eastablish three different abdominal aortic aneurysm (AAA) models by PPE intraluminal infusion for about5min, CaC12solution gauze adventitial infusion for15min and Ang Ⅱ minipump continuous subcutaneous infusion for28days. PBS infusion was accordingly applied for the control groups. Doppler ultrasound was applied to detect the diameter of the abdominal aortic and the location of the aneurysm. The time of operaion and aneurysm formation was recorded; the percentage of the aneurysm formation and mortality of animal models were also calculated.
Result:Three types of AAA models were successfully established. The process of PPE model establishment was more challenged, consequently the operation time was longer (52.6±5.1min), compared to40.7±4.3min in CaC12model and7.8±3.6min in Ang Ⅱ model, but the percentage of the aneurysm formation of PPE model was100%and the survival time of PPE and CaCl2model are longer than Ang Ⅱ model, almost all alive in4weeks follow-up compared to60%alive in Ang Ⅱ model. The process of CaCl2and Ang Ⅱ model establishment was relatively easy, however, the mortality of Ang Ⅱ model was much higher than PPE and CaCl2model.
Conclusion:PPE, CaCl2and Ang Ⅱ AAA models are stable models for further animal research. Moreover, the findings of our study support that the three types of animal models of AAAs may provide intriguing mechanistic insights into the human disease and are suitable for evaluation of medicine therapy in AAA.
Chapter2. The comparison study of morphology and pathogenesis in three different types of abdominal aortic aneurysm models
Objective:To observe the pathomorphological characteristics of three different models of abdominal aortic aneurysm (AAA) and investigate the common pathogenesis in the three different models of AAA.
Methods:As compared to the aortae of normal mice, HE, EVG, Immunohistochemistry staining technique were applied to detect the Morphological and phathological changes in the tissue specimens, such as the pattern of elastin degeneration was recorded, the quantity of different inflammatory cells infiltration, angiogenesis and lymphangiogenesis were counted.
Results:In PPE model, there was extensive destruction of the elastic lamellae and the adventitial region was occupied by a pronounced inflammatory infiltrate, predominantly containing macrophages. Neutrophils were present on the peripheral aspects of the adventitia surrounding the aorta; One fascinating aspect of angiotensin Ⅱ model is the aneurysm localization to the suprarenal segment of the aorta. The precipitating event that occurs within days of AngⅡ infusion appears to be medial macrophage accumulation in the region that is prone to AAA formation, associated with elastin degradation. Subsequently there were gross dissections of the aortas leading to prominent vascular hematomas and enhanced extracellular matrix deposition and infiltration of other leukocyte populations, primarily macrophages. The dilated region of the aorta gradually regained circumferential elastin fibers and completely re-endothelialized. Prominent neovascularization was present throughout the lumen of the remodeled tissue; In CaC12models, the abluminal incubation of calcium chloride also led to structural disruption of the medial layer and inflammatory responses. This inflammation occurred on the luminal and medial aspect of the artery. But, there is no obvious angiogenesis and lymphangiogenesis in this model.
Conclusion:Although there were different pathomorphological changes in the three types of AAA models, the common pathological charateristics were still existed, such as transmural inflammatory cells infiltration, adventitial angiogenesis and lymphangiogenesis and so on. Since the similar pathogenesis as human, PPE and Ang Ⅱ model were considered to be kind of ideal models for animal research.
Chapter3. The application of anti-angiotension in the development of abdominal aortic aneurysm
Object:To elucidate the effect of angiotension on the progression of AAA and validate the therapeutic effect of anti-angiotension based treatment on AAA
Method:The C57BL/6(15) and ApoE-/-male mice were devided into two groups:treated group and control. AAA was induced either in male ApoE-/-mice by subcutaneous infusion of1OOOng/kg/min Ang Ⅱ for28days or in mail C57BL/6mice by transient intra-aortic infusion of PPE. In the treated group, all the mice were daily treated with10mg/kg telmisartan7days before aneurym establishment; Doppler ultrasound was applied to detect the diameter of the abdominal aortic and the location of the aneurysm. The percentage of the aneurysm formation and mortality of animal models were also calculated. Morover, histopathology and gene profiling were used to evaluate therapeutic efficacy.
Results:The telmisartan almost completely prevented PPE-induced AAA formation in C57BL/6mice and suppressed Ang Ⅱ-induced increase in systolic blood pressure, preserved medial elastin and smooth musclesm and attenuated macrophage infiltration and angiogenesis within aortic adventitia. Moreover, ARB therapy dramatically downregulated the gene expression levels of certain proteinases, chemokines and their receptors, Cytokines, and adhesion molecules at the aneurismal lesions. There was no obvious side effect in the dose of1Omg/kg.
Conclusion:The application of telmisartan can play a significant anti-angiotension effect, which can successfully prevent the progression and formation of AAA; and the anti-angiotension therapy is highly efficacious and safe in suppressing experimental AAA.
引文
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