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  • 學位論文

龍葵萃取物抑制動脈硬化形成機轉之探討

Study of Solanum nigrum Extracts on the mecharisms of atherosclerosis

指導教授 : 李彗禎
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摘要


氧化型低密度脂蛋白在動脈粥狀硬化形成過程中起著十分重要的作用,可透過致血管內皮的損傷、促進泡沫細胞的形成及血管平滑肌細胞的增殖、影響多種原素促使血栓的形成,從而加速動脈粥狀硬化的發生和發展。在先前的研究中發現龍葵水萃物(Solanum nigrum water extract, SNWE)含有多酚化合物,並且有抗氧化的功效,因此本研究一開始以龍葵萃取物作為抗氧化劑,並以銅離子誘導LDL 氧化的模式進行體外抗氧化實驗。藉由ApoB 蛋白斷裂現象及LDL 蛋白表面電荷改變的程度與脂質過氧化產物MDA 及diene 的生成量來判斷抗氧化的活性。結果證明, SNWE與龍葵多酚萃取物 (Solanum nigrum polyphenol extract, SNPE)具有抑制氧化型低密度脂蛋白形成之能力並有dose-dependent 的現象;接下來進一步以高脂質飲食模式(膽固醇1.3%和猪油3%)誘導紐西蘭大白兔動脈硬化,結果發現SNWE具有降低動脈中動脈粥狀硬化的損傷面積,且在血清脂蛋白的表現中也發現SNWE可提高HDL(86%)、降低triglyceride(23%),進而去抑制動脈粥狀硬化之形成。最後在細胞實驗中,透過Wound healing 及 Gelatin Zymography 的實驗發現,SNWE與SNPE具有抑制由PDGF所誘導的細胞遷移作用。 由上述的結果顯示,SNWE以及SNPE具有抗氧化活性並且能抑制LDL 的氧化,而阻斷血管平滑肌細胞的遷移的機制,抑制動脈粥狀硬化的生成。綜合以上結果,我們認為龍葵萃取物具有預防動脈粥狀硬化的作用。

關鍵字

龍葵 動脈硬化

並列摘要


Oxidative LDL was known a major factor to cause atherosclersis. In previous study, Solanum nigrum water extract (SNWE) was proved to contain polyphenols and possess antioxidative ability. This study aimed to detect the effect of SNWE on atherosclerosis. Firstly, LDL was oxidized with copper ion accompanied with SNWEE or Solanum nigrum polyphenol extract (SNPE) treatment. In electrophoretic mobility, ApoB fragmentation, diene conjugation, and TBARS assay, the results showed that both SNWE and SNPE have the inhibitory effect on oxidative LDL in a dose-dependent manner. Second, in in vivo assay, New Zealand White (NZW) rabbits were fed with high fat diet (cholesterol 1.3% and lard oil 3%) to induce atherosclerosis. 0.25%, 0.5% or 1% of SNWE was co-treated to observe the effect on anti-atherosclerosis. The results showed that SNWE could reduce atherosclerosis lesion, lower the serum level of triglyceride to 23 % and increase the level of HDL-C to 86% significantly. Finally, wound healing and MMP activity assay were carried out to prove that SNWE and SNPE could suppress the smooth muscle cell migtation. In conclusion, SNWE and SNPE possess strong antioxidative ability to inhibit LDL oxidation and further to inhibit atherosclerosis. One of the possible mechanisms was that SNWE SNPE could regulate signal pathway of cytoskeleton to suppress smooth mucsle cell migration.

參考文獻


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