速效救心丸抗动脉粥样硬化作用及机制的研究
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摘要
目的:本实验通过建立大鼠动脉粥样硬化(Atherosclerosis,AS)模型,观察速效救心丸对AS的预防性干预作用,并探讨速效救心丸的抗AS的作用及其可能的作用机制。
方法:采用高脂饮食加大剂量钙负荷(一次性腹腔注射维生素D_360万U/kg)方法建立大鼠AS模型。选用健康雄性成年Sprague-Dawlay(SD)大鼠60只,随机分为6组:①正常对照组(N):普通饲料;②模型组(M):高脂饲料:③速效救心丸低剂量治疗组(SXL):高脂饲料+SX60mg·kg~(-1)·d~(-1);④速效救心丸中剂量治疗组(SXM):高脂饲料+SX600mg·kg~(-1)·d~(-1);⑤速效救心丸高剂量治疗组(SXH):高脂饲料+SX1800mg·kg~(-1)·d~(-1);⑥西药阿托伐他汀组(Astorvastatin,ATO):高脂饲料+可托伐他汀4mg·kg~(-1)·d~(-1);各治疗组药物自造模第一天开始灌胃给予,正常对照组及模型组给予等量生理盐水灌胃,共饲养12周。光镜下行HE、Masson染色观察主动脉的病理变化,透射电镜下观察主动脉超微结构改变;生化方法测定血清中总胆固醇(total cholesterol,TC)、甘油三酯(triglyceride,TG)、低密度脂蛋白(low density lipoprotein,LDL)、高密度脂蛋白(high density lipoprotein,HDL)、丙二醛(malondialdehyde,MDA)的含量及超氧化物歧化酶(superoxide dismutase,SOD)活性;酶联免疫吸附双抗体夹心方法测定血清中氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL);免疫组织化学法检测三磷酸腺苷结合盒转运体A1(ATP bindingcassette transporter A1,ABCA1)和血红素氧合酶-1(heme oxygenase-1,HO-1)在主动脉的表达情况。
结果:
1.主动脉形态学改变:
(1)光镜下观察:HE染色可见正常组大鼠主动脉内皮细胞连续完整,内膜光滑;模型组大鼠血管内膜明显增厚,不光滑,内皮细胞呈连续性缺失,内皮下间隙增宽,内有脂质沉积;中膜明显增厚,平滑肌细胞增殖增生明显,排列不规则,向内膜迁移,弹力纤维排列紊乱,部分断裂,局部向管腔突出,细胞间隙可见脂质沉积。速效救心丸低剂量组病理改变与横型组相比,并无明显改善;但中、高剂量组及西药组主动脉内膜比较光滑,局部轻微增厚,内皮细胞部分缺失,弹力纤维排列基本整齐,病理改变较模型组明显减轻,并且高剂量和西药组效果更明显。MASSON染色可见:正常组大鼠主动脉内膜胶原含量极少,弹力纤维完整,排列规则;模型组主动内膜明显增厚,增厚的内膜下大量着色较重的蓝染胶原纤维,弹力纤维明显减少,排列极其紊乱,扭曲断裂;速效救心丸低剂量抑制血管胶原纤维的作用不明显;中、高剂量组和西药组主动脉血管内膜及中膜蓝染的胶原纤维减少,着色轻,弹力纤维排列基本整齐,以高剂量组和西药组效果最明显。
(2)透射电镜下观察:正常组大鼠主动脉内膜薄,内皮完整,内皮细胞呈长梭形,连接紧密,内弹力板完整连续,中膜平滑肌细胞大小均匀,细胞器结构正常;模型组主动脉内膜增厚,不光滑,不连续,内皮细胞间连接破坏,微绒毛缺失,胞膜缺失,为裸核,粗面内质网扩张呈圆形,有严重脱颗粒现象,吞饮小泡明显减少,内皮下间隙宽窄不一。速效救心丸低剂量组血管超微结构改变基本和模型组相同;中、高剂量组和西药组的超微结构则明显减轻,内皮细胞较完整,细胞之间连接较好,内皮下间隙明显变规则、清晰,平滑肌细胞迁移明显减少。
2.血清中指标的改变:模型组大鼠血清中TC、TG、LDL和HDL均高于正常对照组,两者差异有统计学意义(P＜0.05),预防性给药后,速效救心丸低剂量组大鼠血脂各项水平变化不明显(P＞0.05),而中、高剂量组和西药组能明显降低各组大鼠血清中TC、TG和LDL水平,升高HDL水平,尤以高剂量组和西药组用药最明显(P＜0.01)。
模型组大鼠血清中SOD活性明显低于正常组,差异有统计学意义(P＜0.05),MDA及ox-LDL含量显著高于正常组(P＜0.05)。速效救心丸预防组中低剂量组对SOD及ox-LDL影响不明显,差异没有统计学意义(P＞0.05);中、高剂量组和西药组能升高SOD含量、降低MDA及ox-LDL含量,与模型组相比,差异有统计学意义(P＜0.05)。
3.主动脉壁ABCA1表达量的改变:模型组主动脉壁ABCA1表达高于正常组(P＜0.05),速效救心丸低、中剂量对其表达无明显影响(P＞0.05),高剂量组主动脉壁ABCA1表达高于模型组(P＜0.05),而西药组则抑制ABCA1的表达(P＜0.05)。
4.主动脉管壁HO-1表达量的改变:模型组主动脉壁HO-1表达高于正常组(P＜0.05),速效救心丸低剂量对其表达无明显影响(P＞0.05),中、高剂量及阿托伐他汀组主动脉壁HO-1表达高于模型组(P＜0.05)。
结论:高脂饮食加一次性大剂量VitD3负荷共同作用可成功建立大鼠早期AS模型。速效救心丸具有降血脂、抗脂质过氧化等抑制AS的形成的作用,其可能的机制是:(1)速效救心丸可降低AS大鼠血清TC、TG、LDL、MDA、ox-LDL水平,升高HDL、SOD水平;(2)速效救心丸可以上调主动脉管壁ABCA1和HO-1的表达;(3)速效救心丸可以减轻血管内皮细胞的损伤,抑制平滑肌细胞、胶原纤维的增生,改善AS病理变化。
Objective:To investigate the anti-atherosclerosis effects of SuXiao JiuXin Wan and its possible mechanism through animal model of experimental atherosclerosis.
Method:Experimental atherosclerosis in rats was produced by feeding with atherogenic-diet and vitaminD_3 administration(600,000 IU/kg by intraperitoneal injected at one time)for 12 weeks.60 male mature Sprague-Dawlay rats were divided into 6 groups randomly and equally:1.normal group(normal diet);2.AS model group (atherogenic-diet);3.SXL group(atherogenic-diet and SX 60mg·kg~(-1)·d~(-1));4.SXM group(atherogenic-diet and SX 600mg·kg~(-1)·d~(-1));5.SXH group(atherogenic-diet and SX 1800mg·kg~(-1)·d~(-1));6.Astorvastatin group(atherogenic-diet and Astorvastatin 4mg·kg~(-1)·d~(-1)).SX or Astorvastatin was given by gavage from the beginning of the first week to the end of the experiment.At the same time,normal saline was given to the rats of normal group and model group with the same volume and the same way. After 12 weeks treatment,all rats were killed,Aortas were taken and sectioned. Hematoxylin and eosin(H&E),masson were used for morphological investigation by light microscope.The changes of aortas' ultrastructure were observed by electron microscope.Blood was collected to detect the levels of serum total cholesterol(TC), triglyceride(TG),low density lipoprotein(LDL),high density lipoprotein(HDL), malonaldehyd(MDA),superoxide dismutase(SOD)by biochemistry method.The serum levels of oxidized low lipoprotein were mearsured by enzyme-linked immunosorbent assay(ELISA)method.The expression of ATP binding cassette transporter A1(ABCA1)and heme oxygenase-1(HO-1)on aorta were examined by immunohistochemistry.
Results:
1.Pathomorphological changes in the aorta
(1)Pathologic staining:HE stain:In the normal group,the structure of the aortic wall was well-constructed.The intima was thin and endothelia were intact.The smooth muscle cells didn't proliferate.In the model group,Some endothelial ceils were lost and the intima thicked.The smooth muscle ceils proliferated and lined up in disorder.The structures and arrangements of elastic fibers were in disorder and the fibrous tissues proliferated.Compared with the model group,the pathological changes lessened in the SXM、SXH and ATO groups.(2)Masson stain:In the normal group,the structures and arrangements of elastic fibers were intact and in order.In the model group,the vascular smooth cells and collagen fibers proliferated significantly. Compared with the model group,the extents of these changes lessened obviously in the SXM、SXH and ATO groups.
(2)Electron microscope examination:In the model group,aortic tunica intima was destroyed and thicked,the structure arrangement was disorder as well.There were mass foam cells between tunica intima and runica media,furthermore,there were some fatty vesicles in intima.The smooth muscle cell proliferated greatly.Compared with the model group,the pathological changes of aortic ultrastructure alleviated obviously in the SXM、SXH and ATO groups
2.In the model group,TC、TG、LDL and HDL were increased compared with the normal group(P＜0.05).Compared with the model group,the serum lipid profile did not change appreciably in the SXL group(P＞0.05),while the levels of TC、TG and LDL were declined and the level of HDL was increased evidently in the SXM、SXH and ATO groups(P＜0.05).SXH group has the best results among the three SX treatment groups.
In the model group,the serum SOD activity was declined and the MDA、ox-LDL level were increased compared with the normal group(P＜0.05).Compared with the model group,the serum SOD、MDA、and ox-LDL level did not change appreciably in the SXL group(P＞0.05),while the serum SOD activity was increased and the MDA、ox-LDL level were decreased definitely in the SXM、SXH and ATO groups(P＜0.05).
3.The expression of ABCA1of aortic in the model group was enhanced compared with the normal group(P＜0.05).Compared with the model group,the expression of ABCA1 of aortic was not influenced in the SXL、SXM groups(P＞0.05),while,it was increased in the SXH group and decreased in the ATO group.(P＜0.05).
4.The expression of HO-1 of aortic in the model group was enhanced compared with the normal group(P＜0.05).Compared with the model group,the expression of HO-1 of aortic was not influenced in the SXL group(P＞0.05),while,it was increased in the SXM、SXL and ATO group(P＜0.05).
Conclusions:The rat model of early atherosclerosis can be established successfully by atherogenic-diet and vitamin D_3 administration(600,000 IU/kg by intraperitoneal injected at one time).The results suggest that the SuXiao JiuXin Wan can ameliorate the atherosclerotic changes and its protection effect may be involve in regulating plasma lipid metabolic disorder,enhancing anti-oxidant capacity and so on. (1)SX has obvious effect on decreasing the serum levels of TC、TG、LDL、MDA and ox-LDL,and increasing the serum level of HDL、SOD in AS rats;(2)SX can increase the expression of ABCA1、HO-1 of aortic;(3)Morphological changes of aorta show a significant effect of protecting aorta endothelial cell,decreasing the proliferation of vascular smooth muscle cell and collagen fibers in AS rats.
方法:采用高脂饮食加大剂量钙负荷(一次性腹腔注射维生素D_360万U/kg)方法建立大鼠AS模型。选用健康雄性成年Sprague-Dawlay(SD)大鼠60只,随机分为6组:①正常对照组(N):普通饲料;②模型组(M):高脂饲料:③速效救心丸低剂量治疗组(SXL):高脂饲料+SX60mg·kg~(-1)·d~(-1);④速效救心丸中剂量治疗组(SXM):高脂饲料+SX600mg·kg~(-1)·d~(-1);⑤速效救心丸高剂量治疗组(SXH):高脂饲料+SX1800mg·kg~(-1)·d~(-1);⑥西药阿托伐他汀组(Astorvastatin,ATO):高脂饲料+可托伐他汀4mg·kg~(-1)·d~(-1);各治疗组药物自造模第一天开始灌胃给予,正常对照组及模型组给予等量生理盐水灌胃,共饲养12周。光镜下行HE、Masson染色观察主动脉的病理变化,透射电镜下观察主动脉超微结构改变;生化方法测定血清中总胆固醇(total cholesterol,TC)、甘油三酯(triglyceride,TG)、低密度脂蛋白(low density lipoprotein,LDL)、高密度脂蛋白(high density lipoprotein,HDL)、丙二醛(malondialdehyde,MDA)的含量及超氧化物歧化酶(superoxide dismutase,SOD)活性;酶联免疫吸附双抗体夹心方法测定血清中氧化低密度脂蛋白(oxidized low density lipoprotein,ox-LDL);免疫组织化学法检测三磷酸腺苷结合盒转运体A1(ATP bindingcassette transporter A1,ABCA1)和血红素氧合酶-1(heme oxygenase-1,HO-1)在主动脉的表达情况。
结果:
1.主动脉形态学改变:
(1)光镜下观察:HE染色可见正常组大鼠主动脉内皮细胞连续完整,内膜光滑;模型组大鼠血管内膜明显增厚,不光滑,内皮细胞呈连续性缺失,内皮下间隙增宽,内有脂质沉积;中膜明显增厚,平滑肌细胞增殖增生明显,排列不规则,向内膜迁移,弹力纤维排列紊乱,部分断裂,局部向管腔突出,细胞间隙可见脂质沉积。速效救心丸低剂量组病理改变与横型组相比,并无明显改善;但中、高剂量组及西药组主动脉内膜比较光滑,局部轻微增厚,内皮细胞部分缺失,弹力纤维排列基本整齐,病理改变较模型组明显减轻,并且高剂量和西药组效果更明显。MASSON染色可见:正常组大鼠主动脉内膜胶原含量极少,弹力纤维完整,排列规则;模型组主动内膜明显增厚,增厚的内膜下大量着色较重的蓝染胶原纤维,弹力纤维明显减少,排列极其紊乱,扭曲断裂;速效救心丸低剂量抑制血管胶原纤维的作用不明显;中、高剂量组和西药组主动脉血管内膜及中膜蓝染的胶原纤维减少,着色轻,弹力纤维排列基本整齐,以高剂量组和西药组效果最明显。
(2)透射电镜下观察:正常组大鼠主动脉内膜薄,内皮完整,内皮细胞呈长梭形,连接紧密,内弹力板完整连续,中膜平滑肌细胞大小均匀,细胞器结构正常;模型组主动脉内膜增厚,不光滑,不连续,内皮细胞间连接破坏,微绒毛缺失,胞膜缺失,为裸核,粗面内质网扩张呈圆形,有严重脱颗粒现象,吞饮小泡明显减少,内皮下间隙宽窄不一。速效救心丸低剂量组血管超微结构改变基本和模型组相同;中、高剂量组和西药组的超微结构则明显减轻,内皮细胞较完整,细胞之间连接较好,内皮下间隙明显变规则、清晰,平滑肌细胞迁移明显减少。
2.血清中指标的改变:模型组大鼠血清中TC、TG、LDL和HDL均高于正常对照组,两者差异有统计学意义(P＜0.05),预防性给药后,速效救心丸低剂量组大鼠血脂各项水平变化不明显(P＞0.05),而中、高剂量组和西药组能明显降低各组大鼠血清中TC、TG和LDL水平,升高HDL水平,尤以高剂量组和西药组用药最明显(P＜0.01)。
模型组大鼠血清中SOD活性明显低于正常组,差异有统计学意义(P＜0.05),MDA及ox-LDL含量显著高于正常组(P＜0.05)。速效救心丸预防组中低剂量组对SOD及ox-LDL影响不明显,差异没有统计学意义(P＞0.05);中、高剂量组和西药组能升高SOD含量、降低MDA及ox-LDL含量,与模型组相比,差异有统计学意义(P＜0.05)。
3.主动脉壁ABCA1表达量的改变:模型组主动脉壁ABCA1表达高于正常组(P＜0.05),速效救心丸低、中剂量对其表达无明显影响(P＞0.05),高剂量组主动脉壁ABCA1表达高于模型组(P＜0.05),而西药组则抑制ABCA1的表达(P＜0.05)。
4.主动脉管壁HO-1表达量的改变:模型组主动脉壁HO-1表达高于正常组(P＜0.05),速效救心丸低剂量对其表达无明显影响(P＞0.05),中、高剂量及阿托伐他汀组主动脉壁HO-1表达高于模型组(P＜0.05)。
结论:高脂饮食加一次性大剂量VitD3负荷共同作用可成功建立大鼠早期AS模型。速效救心丸具有降血脂、抗脂质过氧化等抑制AS的形成的作用,其可能的机制是:(1)速效救心丸可降低AS大鼠血清TC、TG、LDL、MDA、ox-LDL水平,升高HDL、SOD水平;(2)速效救心丸可以上调主动脉管壁ABCA1和HO-1的表达;(3)速效救心丸可以减轻血管内皮细胞的损伤,抑制平滑肌细胞、胶原纤维的增生,改善AS病理变化。
Objective:To investigate the anti-atherosclerosis effects of SuXiao JiuXin Wan and its possible mechanism through animal model of experimental atherosclerosis.
Method:Experimental atherosclerosis in rats was produced by feeding with atherogenic-diet and vitaminD_3 administration(600,000 IU/kg by intraperitoneal injected at one time)for 12 weeks.60 male mature Sprague-Dawlay rats were divided into 6 groups randomly and equally:1.normal group(normal diet);2.AS model group (atherogenic-diet);3.SXL group(atherogenic-diet and SX 60mg·kg~(-1)·d~(-1));4.SXM group(atherogenic-diet and SX 600mg·kg~(-1)·d~(-1));5.SXH group(atherogenic-diet and SX 1800mg·kg~(-1)·d~(-1));6.Astorvastatin group(atherogenic-diet and Astorvastatin 4mg·kg~(-1)·d~(-1)).SX or Astorvastatin was given by gavage from the beginning of the first week to the end of the experiment.At the same time,normal saline was given to the rats of normal group and model group with the same volume and the same way. After 12 weeks treatment,all rats were killed,Aortas were taken and sectioned. Hematoxylin and eosin(H&E),masson were used for morphological investigation by light microscope.The changes of aortas' ultrastructure were observed by electron microscope.Blood was collected to detect the levels of serum total cholesterol(TC), triglyceride(TG),low density lipoprotein(LDL),high density lipoprotein(HDL), malonaldehyd(MDA),superoxide dismutase(SOD)by biochemistry method.The serum levels of oxidized low lipoprotein were mearsured by enzyme-linked immunosorbent assay(ELISA)method.The expression of ATP binding cassette transporter A1(ABCA1)and heme oxygenase-1(HO-1)on aorta were examined by immunohistochemistry.
Results:
1.Pathomorphological changes in the aorta
(1)Pathologic staining:HE stain:In the normal group,the structure of the aortic wall was well-constructed.The intima was thin and endothelia were intact.The smooth muscle cells didn't proliferate.In the model group,Some endothelial ceils were lost and the intima thicked.The smooth muscle ceils proliferated and lined up in disorder.The structures and arrangements of elastic fibers were in disorder and the fibrous tissues proliferated.Compared with the model group,the pathological changes lessened in the SXM、SXH and ATO groups.(2)Masson stain:In the normal group,the structures and arrangements of elastic fibers were intact and in order.In the model group,the vascular smooth cells and collagen fibers proliferated significantly. Compared with the model group,the extents of these changes lessened obviously in the SXM、SXH and ATO groups.
(2)Electron microscope examination:In the model group,aortic tunica intima was destroyed and thicked,the structure arrangement was disorder as well.There were mass foam cells between tunica intima and runica media,furthermore,there were some fatty vesicles in intima.The smooth muscle cell proliferated greatly.Compared with the model group,the pathological changes of aortic ultrastructure alleviated obviously in the SXM、SXH and ATO groups
2.In the model group,TC、TG、LDL and HDL were increased compared with the normal group(P＜0.05).Compared with the model group,the serum lipid profile did not change appreciably in the SXL group(P＞0.05),while the levels of TC、TG and LDL were declined and the level of HDL was increased evidently in the SXM、SXH and ATO groups(P＜0.05).SXH group has the best results among the three SX treatment groups.
In the model group,the serum SOD activity was declined and the MDA、ox-LDL level were increased compared with the normal group(P＜0.05).Compared with the model group,the serum SOD、MDA、and ox-LDL level did not change appreciably in the SXL group(P＞0.05),while the serum SOD activity was increased and the MDA、ox-LDL level were decreased definitely in the SXM、SXH and ATO groups(P＜0.05).
3.The expression of ABCA1of aortic in the model group was enhanced compared with the normal group(P＜0.05).Compared with the model group,the expression of ABCA1 of aortic was not influenced in the SXL、SXM groups(P＞0.05),while,it was increased in the SXH group and decreased in the ATO group.(P＜0.05).
4.The expression of HO-1 of aortic in the model group was enhanced compared with the normal group(P＜0.05).Compared with the model group,the expression of HO-1 of aortic was not influenced in the SXL group(P＞0.05),while,it was increased in the SXM、SXL and ATO group(P＜0.05).
Conclusions:The rat model of early atherosclerosis can be established successfully by atherogenic-diet and vitamin D_3 administration(600,000 IU/kg by intraperitoneal injected at one time).The results suggest that the SuXiao JiuXin Wan can ameliorate the atherosclerotic changes and its protection effect may be involve in regulating plasma lipid metabolic disorder,enhancing anti-oxidant capacity and so on. (1)SX has obvious effect on decreasing the serum levels of TC、TG、LDL、MDA and ox-LDL,and increasing the serum level of HDL、SOD in AS rats;(2)SX can increase the expression of ABCA1、HO-1 of aortic;(3)Morphological changes of aorta show a significant effect of protecting aorta endothelial cell,decreasing the proliferation of vascular smooth muscle cell and collagen fibers in AS rats.
引文
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