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负电荷刺激通过减少一氧化氮来预防 LPS 诱导的肝损伤。

Minus charge stimulation prevents LPS-induced liver injury by reduction of nitric oxide.

机构信息

ITO Co., LTD., 3-3-3, Toyotama-Minami, Nerima-ku, Tokyo 176-8605, Japan.

出版信息

J Clin Biochem Nutr. 2008 May;42(3):222-7. doi: 10.3164/jcbn.2008032.

DOI:10.3164/jcbn.2008032
PMID:18545644
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2386525/
Abstract

The liver is one of the major target organs affected in sepsis that are usually accompanied with free radical formation. The use of minus charge for the prevention and cure of various radical related diseases is gaining wide importance in the medicinal field. Here, we investigate whether minus charge stimulation (MCS) inhibits nitric oxide (NO) production induced by lipopolysaccharide (LPS) in the mice liver. The survival rate was compared in LPS-treated group with MCS group. The liver NO radical was measured using electron spin resonance technique. Serum alanine transaminase (ALT) was estimated for liver injury. MCS significantly improved the survival rate of LPS-treated mice and inhibited increase of ALT in serum levels. MCS also reduced NO radical production significantly in the LPS-treated mice liver tissue. In conclusion, our results indicate that MCS prevents LPS-induced liver injury, which may be through the inhibition of liver NO radical production.

摘要

肝脏是脓毒症中受影响的主要靶器官之一，通常伴随着自由基的形成。在医学领域，利用负电荷来预防和治疗各种自由基相关疾病正受到越来越多的关注。在这里，我们研究了负电荷刺激（MCS）是否抑制脂多糖（LPS）诱导的小鼠肝脏中一氧化氮（NO）的产生。比较了 LPS 处理组和 MCS 组的存活率。采用电子自旋共振技术测量肝 NO 自由基。估计血清丙氨酸转氨酶（ALT）以评估肝损伤。MCS 显著提高了 LPS 处理小鼠的存活率，并抑制了血清 ALT 水平的升高。MCS 还显著减少了 LPS 处理小鼠肝组织中 NO 自由基的产生。总之，我们的结果表明，MCS 可预防 LPS 诱导的肝损伤，这可能是通过抑制肝 NO 自由基的产生。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/bfe5e7d7a8fb/jcbn2008032f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/21b4c0bc8cf7/jcbn2008032f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/7af065f6c040/jcbn2008032f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/e4abdcaf4383/jcbn2008032f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/2a7fd099f5e2/jcbn2008032f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/01f49001ea83/jcbn2008032f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/bfe5e7d7a8fb/jcbn2008032f06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/21b4c0bc8cf7/jcbn2008032f01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/7af065f6c040/jcbn2008032f02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/e4abdcaf4383/jcbn2008032f03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/2a7fd099f5e2/jcbn2008032f04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/01f49001ea83/jcbn2008032f05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a908/2386525/bfe5e7d7a8fb/jcbn2008032f06.jpg

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