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首页> 外文OA文献 >Metallothionein (MT) -I and MT-II expression are induced and cause zinc sequestration in the liver after brain injury
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Metallothionein (MT) -I and MT-II expression are induced and cause zinc sequestration in the liver after brain injury

机译：诱导金属硫蛋白（MT）-I和MT-II的表达并在脑损伤后引起肝脏中的锌螯合

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Experiments with transgenic over-expressing, and null mutant mice have determined that metallothionein-I and -II (MT-I/II) are protective after brain injury. MT-I/II is primarily a zinc-binding protein and it is not known how it provides neuroprotection to the injured brain or where MT-I/II acts to have its effects. MT-I/II is often expressed in the liver under stressful conditions but to date, measurement of MT-I/II expression after brain injury has focused primarily on the injured brain itself. In the present study we measured MT-I/II expression in the liver of mice after cryolesion brain injury by quantitative reverse-transcriptase PCR (RT-PCR) and enzyme-linked immunosorbent assay (ELISA) with the UC1MT antibody. Displacement curves constructed using MT-I/II knockout (MT-I/II -/-) mouse tissues were used to validate the ELISA. Hepatic MT-I and MT-II mRNA levels were significantly increased within 24 hours of brain injury but hepatic MT-I/II protein levels were not significantly increased until 3 days post injury (DPI) and were maximal at the end of the experimental period, 7 DPI. Hepatic zinc content was measured by atomic absorption spectroscopy and was found to decrease at 1 and 3 DPI but returned to normal by 7DPI. Zinc in the livers of MT-I/II -/- mice did not show a return to normal at 7 DPI which suggests that after brain injury, MT-I/II is responsible for sequestering elevated levels of zinc to the liver. Conclusion: MT-I/II is up-regulated in the liver after brain injury and modulates the amount of zinc that is sequestered to the liver.
机译：转基因过表达和无效突变小鼠的实验已经确定，金属硫蛋白-I和-II（MT-I / II）在脑损伤后具有保护作用。 MT-I / II主要是锌结合蛋白，尚不知道它如何为受伤的大脑提供神经保护作用，或MT-I / II在何处发挥作用。 MT-I / II通常在压力条件下在肝脏中表达，但迄今为止，脑损伤后MT-I / II表达的测量主要集中在受伤的大脑本身。在本研究中，我们通过定量逆转录酶PCR（RT-PCR）和酶联免疫吸附测定（ELISA）和UC1MT抗体，测量了冷冻性脑损伤后小鼠肝脏中MT-I / II的表达。使用MT-I / II基因敲除（MT-I / II-/-）小鼠组织构建的位移曲线用于验证ELISA。肝MT-I和MT-II mRNA水平在脑损伤后24小时内显着增加，但是直到损伤后3天（DPI），肝MT-I / II蛋白水平才显着升高，并且在实验期结束时达到最高水平，7 DPI。肝锌含量通过原子吸收光谱法测量，发现在DPI为1和3时降低，但7DPI恢复为正常。 MT-I / II-/-小鼠肝脏中的锌在7 DPI时未显示恢复正常，这表明在脑损伤后，MT-I / II负责将升高水平的锌螯合到肝脏中。结论：脑损伤后肝脏中MT-I / II的表达上调，并调节了螯合到肝脏中的锌的含量。

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