Maltol, a food flavoring agent, attenuates acute alcohol-induced oxidative damage in mice.
Nutrients. 2015 Jan 20;7(1):682-96. doi: 10.3390/nu7010682.
Han Y1, Xu Q2, Hu JN3, Han XY4, Li W5, Zhao LC6.
Author information
Abstract
The purpose of this study was to evaluate the hepatoprotective effect of maltol, a food-flavoring agent, on alcohol-induced acute oxidative damage in mice. Maltol used in this study was isolated from red ginseng (Panax ginseng C.A Meyer) and analyzed by
high performance liquid chromatography (HPLC) and mass spectrometry. For hepatoprotective activity in vivo, pretreatment with maltol (12.5, 25 and 50 mg/kg; 15 days) drastically prevented the elevated activities of aspartate transaminase (AST), alanine
transaminase (ALT), alkaline phosphatase (ALP) and triglyceride (TG) in serum and the levels of malondialdehyde (MDA), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) in liver tissue (p < 0.05). Meanwhile, the levels of hepatic antioxidant,
such as catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) were elevated by maltol pretreatment, compared to the alcohol group (p < 0.05). Histopathological examination revealed that maltol pretreatment significantly inhibited
alcohol-induced hepatocyte apoptosis and fatty degeneration. Interestingly, pretreatment of maltol effectively relieved alcohol-induced oxidative damage in a dose-dependent manner. Maltol appeared to possess promising anti-oxidative and anti-inflammatory
capacities. It was suggested that the hepatoprotective effect exhibited by maltol on alcohol-induced liver oxidative injury may be due to its potent antioxidant properties.

PMID: 25608939 PMCID: PMC4303861 DOI: 10.3390/nu7010682

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Maltol Promotes Mitophagy and Inhibits Oxidative Stress via the Nrf2/PINK1/Parkin Pathway after Spinal Cord Injury
Yuqin Mao 1, Jiqing Du 1, Xianghang Chen 1, Abdullah Al Mamun 1, Lin Cao 1, Yanhong Yang 1, Joana Mubwandarikwa 1, Muhammad Zaeem 1, Wanying Zhang 1, Yan Chen 1, Yusen Dai 1, Jian Xiao 1, Keyong Ye 1
Oxid Med Cell Longev
. 2022 Feb 1;2022:1337630. doi: 10.1155/2022/1337630. eCollection 2022.
PMID: 35154562 PMCID: PMC8826207 DOI: 10.1155/2022/1337630 https://pubmed.ncbi.nlm.nih.gov/35154562/
Abstract
Spinal cord injury (SCI), a fatal disease in the central nervous system, is characteristic of weak neuronal regeneration ability and complex pathological progress. Activation of oxidative stress (OS) and apoptosis-mediated cell death significantly
contributes to the progression of SCI. Current evidence suggests that maltol exerts natural antioxidative properties via obstructing OS and apoptosis. However, the significant effect of maltol on SCI treatment has never been evaluated yet. In our current
study, we explored maltol administration that could trigger the expression of Nrf2 and promote the retranslocation of Nrf2 from the cytosol to the nucleus, which can subsequently obstruct OS signal and apoptosis-mediated neuronal cell death after SCI.
Furthermore, we found that maltol treatment enhances PINK1/Parkin-mediated mitophagy in PC12 cells, facilitating the recovery of mitochondrial functions. Our findings propose that maltol could be a promising therapeutic candidate for the treatment and
management of SCI.

Copyright © 2022 Yuqin Mao et al.

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