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5-氨基酮戊酸/血卟啉单甲醚通过 MAPK/Nrf2 抗氧化通路增强 HO-1 表达，减轻小鼠肾小管上皮细胞凋亡。

5-ALA/SFC enhances HO-1 expression through the MAPK/Nrf2 antioxidant pathway and attenuates murine tubular epithelial cell apoptosis.

机构信息

Division of Transplantation Immunology, National Research Institute for Child Health and Development, Tokyo, Japan.

AIDS Research Center, National Institute of Infectious Diseases, Tokyo, Japan.

出版信息

FEBS Open Bio. 2019 Nov;9(11):1928-1938. doi: 10.1002/2211-5463.12729. Epub 2019 Sep 30.

DOI:10.1002/2211-5463.12729
PMID:31495071
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6823284/
Abstract

Cyclosporin A (CsA) is a common immunosuppressant, but its use is limited as it can cause chronic kidney injury. Oxidative stress and apoptosis play a key role in CsA-induced nephrotoxicity. This study investigated the protective effect of 5-aminolevulinic acid and iron (5-ALA/SFC) on CsA-induced injury in murine proximal tubular epithelial cells (mProx24). 5-ALA/SFC significantly inhibited apoptosis in CsA-treated mProx24 cells with increases in heme oxygenase (HO)-1, nuclear factor E2-related factor 2 (Nrf2), and p38, and Erk-1/2 phosphorylation. Moreover, 5-ALA/SFC suppressed production of reactive oxygen species in CsA-exposed cells and inhibition of HO-1 suppressed the protective effects of 5-ALA/SFC. In summary, 5-ALA/SFC may have potential for development into a treatment for the anti-nephrotoxic/apoptotic effects of CsA.

摘要

环孢素 A（CsA）是一种常用的免疫抑制剂，但由于其会导致慢性肾损伤，其应用受到限制。氧化应激和细胞凋亡在 CsA 诱导的肾毒性中起关键作用。本研究探讨了 5-氨基酮戊酸和铁（5-ALA/SFC）对 CsA 诱导的鼠近端肾小管上皮细胞（mProx24）损伤的保护作用。5-ALA/SFC 显著抑制 CsA 处理的 mProx24 细胞凋亡，同时增加血红素加氧酶 1（HO-1）、核因子 E2 相关因子 2（Nrf2）和 p38、Erk-1/2 的磷酸化。此外，5-ALA/SFC 抑制 CsA 暴露细胞中活性氧的产生，而 HO-1 的抑制则抑制了 5-ALA/SFC 的保护作用。总之，5-ALA/SFC 可能具有开发为 CsA 抗肾毒性/抗凋亡作用的治疗方法的潜力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ae/6823284/323945590fae/FEB4-9-1928-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ae/6823284/64d579979c13/FEB4-9-1928-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ae/6823284/c3710581fe7f/FEB4-9-1928-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ae/6823284/64aba77934d3/FEB4-9-1928-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ae/6823284/323945590fae/FEB4-9-1928-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ae/6823284/64d579979c13/FEB4-9-1928-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ae/6823284/c3710581fe7f/FEB4-9-1928-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ae/6823284/64aba77934d3/FEB4-9-1928-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d5ae/6823284/323945590fae/FEB4-9-1928-g004.jpg

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