匿名使用者
匿名使用者 發問時間: 社會與文化語言 · 7 年前

請英文高手幫忙翻譯一下

Several cellular mechanisms were suggested for cocaine-induced cytotoxicity in PC12 cells. It was shown that cocaine might produce selective toxic effects which are related to the induction of apoptosis such as activation of caspase, decreased mitochondrial cytochrome c content, activation of transcription nuclear factor kappa-b and cytokine involvement. In addition, drugs of abuse have been shown to induce death of cultured PC12 cells which can be associated with an increase in dopamine turnover and oxidative cell injury. Recently, it was shown that human neuronal progenitor cells treatedwith cocaine demonstrated enlargement of cell death associated with increased markers of oxidative stress. These findings indicate that cocaine-induced oxidative damage may promote cell death, therefore exogenous antioxidant strategies may be useful in the treatment and prevention of this disorder. In order to examine antioxidant protective effects in cocaineinduced cytotoxicity associated with oxidative damage progression, we used the well established PC12 cell line as an in vitro model. We demonstrated that PC12 cells exposed to high concentrations of cocaine (1–4 mM) exhibited a significant decline of cell viability as demonstrated previously. Although cocaine physiological effects were elicited in a micromolar concentration, high concentrations were used in this study to enhance rapid cell death which can mimic the effect of chronic cocaine exposure on cell and organelle damage that results in an increased cell death. In addition to the findings that cocaine induced cell death, it was also shown that PC12 cells when exposed to cocaine exhibited amplification of oxidative stress markers such as mitochondrial superoxide radicals and peroxides.

本人用google翻譯發現很多句子都翻得很奇怪 請不要直接把google的翻譯直接貼過來 麻煩幫忙翻一下 謝謝

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  • 7 年前
    最佳解答

    幾個細胞機制建議有可卡因誘導 PC12 細胞毒性作用。它顯示了可卡因可能產生選擇性毒性作用如啟動半胱氨酸蛋白酶,減少線粒體細胞色素 c 含量,啟動的轉錄核因數 kappa b 和細胞因數參與相關的誘導凋亡的研究。此外,已表明濫用藥物誘導的培養,可以增加多巴胺營業額和細胞氧化損傷與相關聯的 PC12 細胞死亡。最近,它顯示了人類神經元祖細胞治療可卡因表明細胞死亡與氧化應激增加標記相關聯的擴大。這些研究結果表明,可卡因誘導的氧化損傷可能促進細胞死亡,因此外源性抗氧化劑戰略可能有用的治療和預防這種疾病。為了在 cocaineinduced 細胞毒性氧化損傷進展相關審查抗氧化保護作用,我們使用既定的 PC12 細胞株作為體外實驗模型。我們展示了 PC12 細胞暴露于高濃度的可卡因 (1-4 毫米) 展出的細胞活性顯著下降,以前所示。雖然可卡因的生理效應引起中 micromolar 的濃度,濃度高使用了在這項研究,加強快速細胞死亡,可以模仿的慢性可卡因曝光效果對儲存格和細胞器損傷而導致的增加的細胞死亡。除了結果那可卡因誘導細胞死亡,它還顯示了 PC12 細胞當暴露于可卡因展出擴增的氧化應激標記線粒體超氧自由基和過氧化物等。

    參考資料: 自己
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