| Description: |
Maltol is a naturally occurring organic compound that is flavour enhancer and flavouring agent. Maltol has neuroprotective effects against hypoxia-induced neuroretinal cell damage in R28 cells, and it has potential as a new neuroprotective therapeutic agent for oxidative stress-related ocular diseases, including glaucoma.Maltol exhibits hepatoprotective effect on alcohol-induced liver oxidative injury, may due to its potent antioxidant properties. |
| Targets: |
NF-kB | ERK | JNK | p38MAPK | SOD | TNF-α | IL Receptor |
| In vitro: |
| Mol Vis. 2014 Oct 17;20:1456-62. | | Neuroprotective and neurite outgrowth effects of maltol on retinal ganglion cells under oxidative stress.[Pubmed: 25352751] | To evaluate the neuroprotective and neurite outgrowth effects of Maltol, a natural aroma compound, on retinal ganglion cells (RGCs) under oxidative stress in vitro.
METHODS AND RESULTS:
Mouse primary RGCs were isolated using immunopanning-magnetic separation and exposed to H2O2 in the presence of Maltol. The cell viability and apoptosis were determined by using adenosine 5'-triphosphate (ATP) assay and terminal deoxynucleotidyl transferase (TdT)-mediated deoxyuridine triphosphate (dUTP) nick end labeling (TUNEL), respectively. Neurite outgrowth was assessed by immunofluorescence for α-tubulin. The activation of nuclear factor-κB (NF-κB) was also evaluated using immunofluorescence. When the RGCs were exposed to 20 μM of H2O2 for 16 h, their viability dropped to 40.3±3.4%. However, the Maltol treatment restored the cells in a dose-dependent manner. The viability recovered to 73.9±5.1% with 10 μM of Maltol and even reached 175.1±11.3% with 2 mM of Maltol, as measured by ATP assay. This oxidative stress significantly increased the number of TUNEL-positive RGCs, but the Maltol drastically reduced the proportion of those apoptotic cells. The oxidative stress hampered the neurite outgrowth of the RGCs, whereas Maltol restored their ability to sprout neurites. Regarding NF-κB, the active form of phosphorylated NF-κB (pNF-κB) increased the oxidative stress level but the Maltol treatment again reduced it to an unstressful level.
CONCLUSIONS:
Our data revealed that Maltol attenuated the oxidative stress-induced injury in the primary mouse RGCs. Its neuroprotective and neurite outgrowth effects seemed to be related to NF-κB signaling. Maltol has potential as a new neuroprotective therapeutic agent for oxidative stress-related ocular diseases, including glaucoma. |
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| In vivo: |
| Nutrients. 2015 Jan 20;7(1):682-96. | | Maltol, a food flavoring agent, attenuates acute alcohol-induced oxidative damage in mice.[Pubmed: 25608939] | 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.
METHODS AND RESULTS:
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.
CONCLUSIONS:
It was suggested that the hepatoprotective effect exhibited by Maltol on alcohol-induced liver oxidative injury may be due to its potent antioxidant properties. |
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Cell. 2018 Jan 11;172(1-2):249-261.e12. doi: 10.1016/j.cell.2017.12.019.IF=36.216(2019)
Cell Metab. 2020 Mar 3;31(3):534-548.e5. doi: 10.1016/j.cmet.2020.01.002.IF=22.415(2019)
Mol Cell. 2017 Nov 16;68(4):673-685.e6. doi: 10.1016/j.molcel.2017.10.022.IF=14.548(2019)
ACS Nano. 2018 Apr 24;12(4): 3385-3396. doi: 10.1021/acsnano.7b08969.IF=13.903(2019)
Nature Plants. 2016 Dec 22;3: 16206. doi: 10.1038/nplants.2016.205.IF=13.297(2019)
Sci Adv. 2018 Oct 24;4(10): eaat6994. doi: 10.1126/sciadv.aat6994.IF=12.804(2019)
