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首页> 外文期刊>Neurochemistry International: The International Journal for the Rapid Publication of Critical Reviews, Preliminary and Original Research Communications in Neurochemistry >Hydrogen sulfide mitigates matrix metalloproteinase-9 activity and neurovascular permeability in hyperhomocysteinemic mice.
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Hydrogen sulfide mitigates matrix metalloproteinase-9 activity and neurovascular permeability in hyperhomocysteinemic mice.

机译：硫化氢减轻高同型半胱氨酸血症小鼠的基质金属蛋白酶9活性和神经血管通透性。

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An elevated level of homocysteine (Hcy), known as hyperhomocysteinemia (HHcy), was associated with neurovascular diseases. At physiological levels, hydrogen sulfide (H(2)S) protected the neurovascular system. Because Hcy was also a precursor of hydrogen sulfide (H(2)S), we sought to test whether the H(2)S protected the brain during HHcy. Cystathionine-beta-synthase heterozygous (CBS+/-) and wild type (WT) mice were supplemented with or without NaHS (30 microM/L, H(2)S donor) in drinking water. Blood flow and cerebral microvascular permeability in pial vessels were measured by intravital microscopy in WT, WT+NaHS, CBS-/+ and (CBS-/+)+NaHS-treated mice. The brain tissues were analyzed for matrix metalloproteinase (MMP) and tissue inhibitor of metalloproteinase (TIMP) by Western blot and RT-PCR. The mRNA levels of CBS and cystathionine gamma lyase (CSE, enzyme responsible for conversion of Hcy to H(2)S) genes were measured by RT-PCR. The results showed a significant increase in MMP-2, MMP-9, TIMP-3 protein and mRNA in CBS (-/+) mice, while H(2)S treatment mitigated this increase. Interstitial localization of MMPs was also apparent through immunohistochemistry. A decrease in protein and mRNA expression of TIMP-4 was observed in CBS (-/+) mice. Microscopy data revealed increase in permeability in CBS (-/+) mice. These effects were ameliorated by H(2)S and suggested that physiological levels of H(2)S supplementation may have therapeutic potential against HHcy-induced microvascular permeability, in part, by normalizing the MMP/TIMP ratio in the brain.
机译：高半胱氨酸（Hcy）水平升高，称为高同型半胱氨酸血症（HHcy），与神经血管疾病有关。在生理水平，硫化氢（H（2）S）保护神经血管系统。因为Hcy也是硫化氢（H（2）S）的前体，所以我们试图测试H（2）S是否在HHcy期间保护大脑。胱硫醚-β-合酶杂合子（CBS +/-）和野生型（WT）小鼠在饮用水中添加或不添加NaHS（30 microM / L，H（2）S供体）。在WT，WT + NaHS，CBS-/ +和（CBS-/ +）+ NaHS处理的小鼠中，通过活体显微镜测量了脉管中的血流量和脑微血管通透性。通过蛋白质印迹和RT-PCR分析脑组织中的基质金属蛋白酶（MMP）和金属蛋白酶组织抑制剂（TIMP）。通过RT-PCR测量CBS和胱硫醚γ裂解酶（CSE，负责将Hcy转化为H（2）S的酶）基因的mRNA水平。结果显示CBS（-/ +）小鼠中MMP-2，MMP-9，TIMP-3蛋白和mRNA的显着增加，而H（2）S处理则减轻了这种增加。通过免疫组织化学，MMP的间质定位也很明显。在CBS（-/ +）小鼠中观察到TIMP-4的蛋白质和mRNA表达下降。显微镜数据显示CBS（-/ +）小鼠的通透性增加。 H（2）S改善了这些影响，并暗示生理水平的H（2）S补充可能对HHcy诱导的微血管通透性具有治疗潜力，部分是通过使脑中MMP / TIMP比值正常化来实现的。

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