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  • 學位論文

Baicalein誘發人類前骨髓白血病細胞產生ROS之作用探討

Mechanism of Baicalein induce ROS formation in HL-60 cells

指導教授 : 周敦穗

摘要


許多的癌症常常好發在具有豐富過氧化酶的身體組織中,其內的過氧化酶會催化單電子轉移的氧化反應的進行,形成自由基中間產物。已經有許多的文獻證明了這些產物在體內會造成氧化壓力的累積,進而對細胞或組織產生危害,甚至是癌症形成的元兇之一。 本次研究的主要目的是想要利用細胞實驗探討黃芩素baicalein,在加入富含骨髓過氧化酶myeloperoxidase之HL-60人類前骨髓白血病細胞株中,是否會減少細胞因過氧化酶催化所產生的自由基帶來氧化壓力。把HL-60細胞株經培養後將之與baicalein反應後以electron spin resonance (ESR)直接分析,發現baicalein能在HL-60細胞中產生hydroxyl radical去對抗癌細胞,且hydroxyl radical的產生與細胞中MPO的活性息息相關。而baicalein也能抑制骨髓過氧化酶在HL-60細胞株中催化vitamin E analog:2,2,5,7,8-pentamethyl-6-hydroxychromane(PMC) 產生的phenoxyl radical之生成,進而減少細胞產生的氧化壓力。並且透過加入arachidonic acid而發現在HL-60細胞中,含ferryl heme的myeloperoxidase在氧化反應過程中也會造成carbon-centered radical的產生。

並列摘要


Various types of cancer occur in peroxidase-rich target tissues. Peroxidases activate most substrates by one-electron oxidation to produce radical intermediates and cause oxidative stress. The contribution of oxidative stress to the process of carcinogenesis has been well documented. In this research we used baicalein as an antioxidant and wanted to know whether baicalein can reduce HL-60 cells’ oxidative stress when MPO catalytic one-electron oxidation reaction was going on. We cultured HL-60 cells and added baicalein then used ESR directly to detect free radicals in ESR spectra. We found that baicalein can form hydroxyl radicals in HL-60 cells and MPO activity played an important roll in it. Baicalein can also reduce oxidative stress by decress MPO-catalyzed phenoxyl radical signal in ESR spectra. And we used AA to find a hemoprotein-derived carbon-centered radical, which may be formed by the oxidation of an amino acid located near the iron of the heme.

參考文獻


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