Oxaloacetate Ameliorates Chemical Liver Injury via Oxidative Stress Reduction and Enhancement of Bioenergetic Fluxes.
Oxaloacetate Ameliorates Chemical Liver Injury via Oxidative Stress Reduction and Enhancement of Bioenergetic Fluxes.
复制标题
草酰乙酸通过减少氧化应激和增强生物能通量来改善化学性肝损伤
DOI：
10.3390/ijms19061626
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发表时间：
2018-05-31
影响因子：
5.6
通讯作者：
Yang Q
中科院分区：
文献类型：
--
作者：
Kuang Y;Han X;Xu M;Wang Y;Zhao Y;Yang Q
化学性损伤部分是由于自由基脂质过氧化作用引起的氧化应激，产生大量活性氧（ROS）。草酰乙酸是三羧酸循环（TCA循环）中的重要中间体，参与代谢和能量产生。草酰乙酸（OA）能有效减轻过氧化氢（H2 O2）诱导的离体肝损伤和四氯化碳（CCl 4）诱导的肝损伤。OA能清除ROS，防止氧化损伤，维持线粒体的正常结构。我们进一步证实，OA通过促进TCA生产周期和氧化磷酸化（OXPHOS）增加三磷酸腺苷（ATP）。最后，OA通过抑制肿瘤坏死因子-α（TNF-α）抑制丝裂原活化蛋白激酶（MAPK）和凋亡途径。我们的研究结果揭示了OA改善化学性肝损伤的机制，并提出了预防化学性肝损伤的可能实施方案。
Chemical injury is partly due to free radical lipid peroxidation, which can induce oxidative stress and produce a large number of reactive oxygen species (ROS). Oxaloacetic acid is an important intermediary in the tricarboxylic acid cycle (TCA cycle) and participates in metabolism and energy production. In our study, we found that oxaloacetate (OA) effectively alleviated liver injury which was induced by hydrogen peroxide (H2O2) in vitro and carbon tetrachloride (CCl4) in vivo. OA scavenged ROS, prevented oxidative damage and maintained the normal structure of mitochondria. We further confirmed that OA increased adenosine triphosphate (ATP) by promoting the TCA production cycle and oxidative phosphorylation (OXPHOS). Finally, OA inhibited the mitogen-activated protein kinase (MAPK) and apoptotic pathways by suppressing tumor necrosis factor-α (TNF-α). Our findings reveal a mechanism for OA ameliorating chemical liver injury and suggest a possible implementation for preventing the chemical liver injury.
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影响因子：
5.6
作者：
Nascimento, Jaclyn M.;Shi, Linda Z.;Tam, James;Chandsawangbhuwana, Charlie;Durrant, Barbara;Botvinick, Elliot L.;Berns, Michael W.
通讯作者：
Berns, Michael W.
影响因子：
3.3
作者：
Felger JC;Lotrich FE
通讯作者：
Lotrich FE
影响因子：
2.4
作者：
Alempijevic T;Zec S;Milosavljevic T
通讯作者：
Milosavljevic T
影响因子：
3.8
作者：
Korzeniewski, B;Liguzinski, P
通讯作者：
Liguzinski, P
影响因子：
3.8
作者：
Chung, H;Hong, DP;Kong, G
通讯作者：
Kong, G