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落羽0401

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虫号: 15702199
注册: 2019-07-23
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专业: 水产生物免疫学与病害控制

[求助] 关于刃天青和糖酵解的问题。已有1人参与

文中说hif-1α 敲除后，小鼠无法在髓系细胞中进行有氧糖酵解。
作者评估了用 β-葡聚糖刺激野生型和 hif-1a ko 巨噬细胞的代谢活性。
hif-1a ko 巨噬细胞显示代谢指示剂刃天青的化学还原增加（图 4g），这与 hif-1a 诱导有氧糖酵解以响应 β-葡聚糖的假设一致。
那么我想问，刃天青的吸光度减少，是不是就是代表刃天青的化学还原增加？这能够说明糖酵解的什么问题呢？
没有这方面的背景知识，希望有大佬可以讲解一下。

文献原话：we assessed whether the effects of mtor were mediated at the level of innate immunity but not at the level of adaptive t and b cell immunity elicited during vaccination. an exper-imental model of b-glucan╟induced protection against s. aureus sepsis can be observed in myeloid cell╟specific hif-1a conditional knock-out mice (mhif-1a ko) (30). these mice are unable to mount glycolysis specifically in cells of the myeloid lineage. we assessed the metabolic activity ofwild-type and mhif-1a ko macrophages when stimulated with b-glucan. mhif-1a ko macrophages shwed increased chemical reduction of the metabolic indicator resazurin (fig.4g), consistent with the hypothesis that hif-1a induces the switch to aerobic glycolysis in response to b-glucan.
原文献：cheng, shih-chin et al. “mtor- and hif-1α-mediated aerobic glycolysis as metabolic basis for trained immunity.” science (new york, n.y.) vol. 345,6204 (2014): 1250684. doi:10.1126/science.1250684

图4 g.png

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