光明中医
光明中醫
광명중의
GUANG MING JOURNAL TRADITIONAL CHINESE MEDICINE
2015年
4期
733-736
,共4页
黄芩苷%高同型半胱氨酸%高敏C反应蛋白%肿瘤坏死因子-α%促单核细胞趋化因子-1
黃芩苷%高同型半胱氨痠%高敏C反應蛋白%腫瘤壞死因子-α%促單覈細胞趨化因子-1
황금감%고동형반광안산%고민C반응단백%종류배사인자-α%촉단핵세포추화인자-1
Baicalin%Hyperhomocysteinemia%High-sensitivity C-reactive protein%Tumor necrosis factor-α%Monocyte chemotactic protein-1
目的：研究黄芩苷对高同型半胱氨酸血症（ Hyperhomocysteinemia，HHcy） ApoE基因缺陷小鼠动脉粥样硬化发生中炎性因子表达的影响，探究黄芩苷抗动脉粥样硬化的机制。方法将30只雄性ApoE基因缺陷小鼠，随机分配到普通组（ A组）、高同型半胱氨酸血症组（B组）、黄芩苷治疗组（C组）。 A组给予普通饲料喂养；其他两组在普通饲料喂养的基础上添加2％L－蛋氨酸，喂养8周，于第4周A组和B组给予每天1次生理盐水0．4 mL灌胃，C组给予黄芩苷配置液150 mg／kg／d（稀释为0．4 mL）灌胃。实验结束后处死动物采血、取材。采用高效液相色谱法检测血清Hcy浓度；采用酶联免疫吸附法（ ELISA）检测血浆hs－CPR、TNF－α、MCP－1水平；HE染色观察形态学变化，免疫组织化学检测主动脉组织MCP－1蛋白的表达水平，采用Leica QwinV3图像分析软件。结果8周后B、C组血清Hcy、hs－CPR、TNF－α、MCP－1水平、斑块面积及主动脉组织MCP－1蛋白的表达水平较A组明显升高（ P＜0．01）；C组血清Hcy、hs－CPR、TNF－α、MCP－1水平、斑块面积及免疫组织化学MCP－1表达水平显著低于B组（ P＜0．01或P＜0．05）。结论高同型半光氨酸血症可促进动脉粥样硬化的形成，黄芩苷能通过降低血浆及动脉组织中炎性因子表达的水平，对动脉粥样硬化的形成、进展进行干预。
目的：研究黃芩苷對高同型半胱氨痠血癥（ Hyperhomocysteinemia，HHcy） ApoE基因缺陷小鼠動脈粥樣硬化髮生中炎性因子錶達的影響，探究黃芩苷抗動脈粥樣硬化的機製。方法將30隻雄性ApoE基因缺陷小鼠，隨機分配到普通組（ A組）、高同型半胱氨痠血癥組（B組）、黃芩苷治療組（C組）。 A組給予普通飼料餵養；其他兩組在普通飼料餵養的基礎上添加2％L－蛋氨痠，餵養8週，于第4週A組和B組給予每天1次生理鹽水0．4 mL灌胃，C組給予黃芩苷配置液150 mg／kg／d（稀釋為0．4 mL）灌胃。實驗結束後處死動物採血、取材。採用高效液相色譜法檢測血清Hcy濃度；採用酶聯免疫吸附法（ ELISA）檢測血漿hs－CPR、TNF－α、MCP－1水平；HE染色觀察形態學變化，免疫組織化學檢測主動脈組織MCP－1蛋白的錶達水平，採用Leica QwinV3圖像分析軟件。結果8週後B、C組血清Hcy、hs－CPR、TNF－α、MCP－1水平、斑塊麵積及主動脈組織MCP－1蛋白的錶達水平較A組明顯升高（ P＜0．01）；C組血清Hcy、hs－CPR、TNF－α、MCP－1水平、斑塊麵積及免疫組織化學MCP－1錶達水平顯著低于B組（ P＜0．01或P＜0．05）。結論高同型半光氨痠血癥可促進動脈粥樣硬化的形成，黃芩苷能通過降低血漿及動脈組織中炎性因子錶達的水平，對動脈粥樣硬化的形成、進展進行榦預。
목적：연구황금감대고동형반광안산혈증（ Hyperhomocysteinemia，HHcy） ApoE기인결함소서동맥죽양경화발생중염성인자표체적영향，탐구황금감항동맥죽양경화적궤제。방법장30지웅성ApoE기인결함소서，수궤분배도보통조（ A조）、고동형반광안산혈증조（B조）、황금감치료조（C조）。 A조급여보통사료위양；기타량조재보통사료위양적기출상첨가2％L－단안산，위양8주，우제4주A조화B조급여매천1차생리염수0．4 mL관위，C조급여황금감배치액150 mg／kg／d（희석위0．4 mL）관위。실험결속후처사동물채혈、취재。채용고효액상색보법검측혈청Hcy농도；채용매련면역흡부법（ ELISA）검측혈장hs－CPR、TNF－α、MCP－1수평；HE염색관찰형태학변화，면역조직화학검측주동맥조직MCP－1단백적표체수평，채용Leica QwinV3도상분석연건。결과8주후B、C조혈청Hcy、hs－CPR、TNF－α、MCP－1수평、반괴면적급주동맥조직MCP－1단백적표체수평교A조명현승고（ P＜0．01）；C조혈청Hcy、hs－CPR、TNF－α、MCP－1수평、반괴면적급면역조직화학MCP－1표체수평현저저우B조（ P＜0．01혹P＜0．05）。결론고동형반광안산혈증가촉진동맥죽양경화적형성，황금감능통과강저혈장급동맥조직중염성인자표체적수평，대동맥죽양경화적형성、진전진행간예。
Objective To observe the effects of baicalin on the expression of inflammatory factors in the development of atherosclerosis in apoE-/-mice with hyperhomocysteinemia, in order to ivestigate the possible mechanisms of baicalin intervention on atherosclerosis.Methods 30 male apoE-/-mices were randomly divided into 3 groups: normal control group(group A), HHcy group(group B)and baicalin dose group ( group C) .Group A was fed with normal diet, simultaneously the rest groups with the same diet based on the addition of 2%L-methionine/d/fed, feeding 8 weeks.In the fourth of the experimental period group A and group B were given normal saline 2ml 1 ig per day, at the same time group C were given baicalin 150mg/kg/d(dilution of 0.4ml),day 1.At the end of the experiment, animals were killed, serum Hcy concentration was detected by high efficiency liquid chromatography, enzyme-linked immunosorbent assay ( ELISA ) were performed to examine the protein expression levers of hs-CPR, MCP-1 and TNF-α; HE staining of aorta were used to observer the histomorphological changes and measure the size of aortic plaques, aortic MPC-1 expression was detected by immunohistochemistry ,the Leica QwinV3 image analysis software was adopted.Results Serum Hcy, hs-CPR,TNF-α,MCP-1 in plasma ,the aortic plaques area and aortic MPC-1 expression of group B and C increased obviously compared with group A(P<0.01);Hcy, hs-CPR ,TNF-α,MCP-1 in plasma, the aortic plaques area and aortic MPC-1 expression of group C was lower than that of group B obviously(P<0.01 or P<0.05).Conclusions Hyperhomocysteinemia could promote the progression of atherosclerosis.Baicalin could intervene the progress of atherosclerosis development by lowering inflammatory factors levels.
