CAJ | 학술논문

背景:原儿茶醛对引起动脉钙化的氧化应激、炎症、钙离子失衡等机制有作用,维生素E对引起动脉钙化氧化应激、免疫紊乱、炎症、血脂异常等机制也有作用,“软脉1号”制剂由原儿茶醛与维生素E两药组成.目的:用超生理剂量维生素D 3联合高脂乳剂建立小鼠动脉钙化模型,探讨“软脉1号”制剂对小鼠动脉钙化的预防作用.方法:清洁级KM小鼠40只,随机摸球法均分为正常对照组、模型组、普伐他汀钠组和“软脉1号”制剂组,后3组建立小鼠动脉钙化模型,然后分别给药干预.实验6周后眼球取血处死小鼠,制作胸主动脉苏木精-伊红染色病理切片,观察胸主动脉、血脂、红细胞和血红蛋白的变化.结果与结论:模型组可见胸主动脉有大量黑色钙质沉积于中层弹性纤维中,波浪状的弹性纤维已无法辨清,间距扩大甚至断裂,部分平滑肌细胞坏死消失,内外弹性膜结构不完整,血清总胆固醇、高密度脂蛋白升高(P <0.05),血红蛋白、平均红细胞血红蛋白含量降低(P <0.05).普伐他汀钠组胸主动脉血管病变无明显改善,总胆固醇、低密度脂蛋白、高密度脂蛋白、血红蛋白、平均红细胞血红蛋白、红细胞数较模型组均无显著性意义.“软脉1号”制剂组小鼠胸主动脉血管病变明显减轻,黑色钙质在弹性纤维中沉积较少,内弹性膜与中层弹性纤维均呈粉染、清晰,弹性纤维间距减少,可见呈波浪状的弹性纤维,内外弹性膜的结构比较完整.与模型组比较,“软脉1号”制剂组总胆固醇下降(P <0.05),血红蛋白、平均红细胞血红蛋白含量升高(P <0.05),其他指标均无统计学意义.说明“软脉1号”制剂对超生理剂量维生素D 3联合高脂乳剂造成的小鼠血管钙化具有预防作用.
배경:원인다철대인기동맥개화적양화응격、염증、개리자실형등궤제유작용,유생소E대인기동맥개화양화응격、면역문란、염증、혈지이상등궤제야유작용,“연맥1호”제제유원인다철여유생소E량약조성.목적:용초생리제량유생소D 3연합고지유제건립소서동맥개화모형,탐토“연맥1호”제제대소서동맥개화적예방작용.방법:청길급KM소서40지,수궤모구법균분위정상대조조、모형조、보벌타정납조화“연맥1호”제제조,후3조건립소서동맥개화모형,연후분별급약간예.실험6주후안구취혈처사소서,제작흉주동맥소목정-이홍염색병리절편,관찰흉주동맥、혈지、홍세포화혈홍단백적변화.결과여결론:모형조가견흉주동맥유대량흑색개질침적우중층탄성섬유중,파랑상적탄성섬유이무법변청,간거확대심지단렬,부분평활기세포배사소실,내외탄성막결구불완정,혈청총담고순、고밀도지단백승고(P <0.05),혈홍단백、평균홍세포혈홍단백함량강저(P <0.05).보벌타정납조흉주동맥혈관병변무명현개선,총담고순、저밀도지단백、고밀도지단백、혈홍단백、평균홍세포혈홍단백、홍세포수교모형조균무현저성의의.“연맥1호”제제조소서흉주동맥혈관병변명현감경,흑색개질재탄성섬유중침적교소,내탄성막여중층탄성섬유균정분염、청석,탄성섬유간거감소,가견정파랑상적탄성섬유,내외탄성막적결구비교완정.여모형조비교,“연맥1호”제제조총담고순하강(P <0.05),혈홍단백、평균홍세포혈홍단백함량승고(P <0.05),기타지표균무통계학의의.설명“연맥1호”제제대초생리제량유생소D 3연합고지유제조성적소서혈관개화구유예방작용.
@@@@BACKGROUND: Protocatechuic aldehyde treats oxidative stress, inflammation, and calcium imbalance, which cause arterial calcification, while vitamin E functions at oxidative stress, inflammation, immune disorders, and abnormal blood lipid, which also cause arterial calcification. Ruanmai preparation is composed of protocatechuic aldehyde and vitamin E. OBJECTIVE: To establish arterial calcification model of mice with super-physiological dose Vitamin D3 and hyperlipidemia, and to investigate the preventive effect of Ruanmai preparation on arterial calcification in mice. METHODS: Forty clean mice of Kunming species were randomly divided into four groups: normal control group, model group, Pravastatin group and Ruanmai preparation group. Each group contained 10 mice. Except the normal control group, arterial calcification model was established in the other three groups, which was then given drug administrations. Six weeks later, mice were kil ed to col ect blood sample from the eyebal s. Then hematoxylin-eosin staining sections of thoracic aortas were made, to observe the changes of thoracic aortas, blood lipids, red blood cel s and hemoglobin. RESULTS AND CONCLUSION: In the model group, a large number of calcium deposits were seen in the middle elastic fibers of thoracic aorta, wavy elastic fibers were difficult to be distinguished, with expanding space and even fracture, part of smooth muscle cel s were necrotic and disappeared. The structure of internal and external elastic membrane was incomplete. Serum total cholesterol and high-density lipoprotein levels increased (P < 0.05), while hemoglobin and mean corpuscular hemoglobin decreased (P < 0.05). The vascular lesions of thoracic aorta in the Pravastatin group showed no significant improvement. There were no significant differences in the total cholesterol, low-density lipoprotein, high-density lipoprotein, hemoglobin, mean corpuscular hemoglobin and red blood cel s compared with model group. In the Ruanmai preparation group, the vascular lesions of thoracic aorta al eviated significantly. There was a little calcium deposition in elastic fibers, the internal elastic membrane and the middle elastic fibers showed a pink dye and clearness, elastic fiber spacing reduced and wavy elastic fibers were visible. The structure of internal and external elastic membrane was complete. Compared with model group, serum total cholesterol decreased (P < 0.05), while hemoglobin and mean corpuscular hemoglobin increased in the Ruanmai preparation group (P < 0.05). Other indicators had no statistical y significant difference. Experimental findings indicate that Ruanmai preparation has a preventive effect on vascular calcification of mice caused by super-physiological dose Vitamin D3 and hyperlipidemia.