Academic Journal
Evaluation of Umbelliferone Neuroprotective Effects Against Acrylamide-Induced Oxidative Stress, In Vivo and In Silico Study.
| Title: | Evaluation of Umbelliferone Neuroprotective Effects Against Acrylamide-Induced Oxidative Stress, In Vivo and In Silico Study. |
|---|---|
| Authors: | Mogadem A; Department of Chemistry, College of Science, Taibah University, Madinah, Saudi Arabia. amogadam@taibahu.edu.sa., Al-Refai HH; Department of Chemistry, College of Science in Yanbu, Taibah University, Yanbu Governorate, Saudi Arabia. |
| Source: | Journal of molecular neuroscience : MN [J Mol Neurosci] 2026 Jun 10; Vol. 76 (2). Date of Electronic Publication: 2026 Jun 10. |
| Publication Type: | Journal Article |
| Language: | English |
| Journal Info: | Publisher: Humana Press Country of Publication: United States NLM ID: 9002991 Publication Model: Electronic Cited Medium: Internet ISSN: 1559-1166 (Electronic) Linking ISSN: 08958696 NLM ISO Abbreviation: J Mol Neurosci Subsets: MEDLINE |
| Imprint Name(s): | Publication: Totowa, NJ : Humana Press Original Publication: Boston : Birkhäuser [i.e. Cambridge, MA : Birkhäuser Boston, c1989- |
| MeSH Terms: | Umbelliferones*/pharmacology , Umbelliferones*/therapeutic use , Acrylamide*/toxicity , Neuroprotective Agents*/pharmacology , Neuroprotective Agents*/therapeutic use , Antioxidants*/pharmacology , Antioxidants*/therapeutic use , Oxidative Stress*, Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Liver/drug effects ; Liver/metabolism ; Heme Oxygenase-1/metabolism ; Heme Oxygenase-1/genetics ; Caspase 3/metabolism ; Caspase 3/genetics ; Brain/metabolism ; Brain/drug effects ; Alanine Transaminase/metabolism ; Animals ; Mice ; Male ; Molecular Docking Simulation ; Lipid Peroxidation |
| Abstract: | Acrylamide (ACR) is a heat-generated carcinogen, one of the most common toxins, with various effects on the biological system, including oxidative stress and related disorders. Umbelliferone (UMB) is a naturally occurring coumarin derivative that is present in edible fruits, known as an antioxidant, and reported for many other therapeutic effects. In the current study, UMB was evaluated for neuro- and hepatoprotective activity against oxidative stress toxicity induced by a 40 mg/kg daily dose of ACR in a mouse model over 15 days. Also, UMB was used as a ligand for the first time to predict its affinity for the most important proteins involved in neuronal failure. The UMB administration significantly improves liver enzyme elevations, alanine transaminase (ALT) and aspartate transaminase (AST), following ACR injection. Also, UMB treatment reduced elevated total protein (TP) and albumin (ALB) serum levels. In addition, lipid peroxidation levels were significantly reduced by UMB (expressed as malondialdehyde MDA levels), and the levels of total non-enzymatic antioxidant capacity (TAC) were increased in brain tissue homogenate in comparison with brain injury in the ACR group. Furthermore, UMB downregulated the expression of tumor necrosis factor-alpha (TNF-α), an inflammatory marker and caspase-3, an apoptotic marker, while upregulating heme oxygenase-1 (HO-1), an antioxidant enzyme, in both liver and brain tissues. Molecular docking analysis revealed that the compound could form H-bonds and hydrophobic interactions with the target receptors. Results of this study conclude that UMB may be considered a potential pharmaceutical agent to ameliorate ACR-induced toxicity in the liver and brain, due to its anti-inflammatory, antioxidant, and antiapoptotic mechanisms, as well as its moderate affinity for neuronal disease-targeted proteins. (© 2026. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.) |
| Competing Interests: | Declarations. Competing interests: The authors declare no competing interests. |
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| Contributed Indexing: | Keywords: Acrylamide; Caspase-3; Hemeoxygenase-1; Hepatoprotective; Molecular docking; Neuroprotective; Oxidative stress; Umbelliferone |
| Substance Nomenclature: | 0 (Umbelliferones) 20R035KLCI (Acrylamide) 0 (Neuroprotective Agents) 60Z60NTL4G (7-hydroxycoumarin) 0 (Tumor Necrosis Factor-alpha) 0 (Antioxidants) EC 1.14.14.18 (Heme Oxygenase-1) EC 3.4.22.- (Caspase 3) EC 2.6.1.2 (Alanine Transaminase) |
| Entry Date(s): | Date Created: 20260610 Date Completed: 20260612 Latest Revision: 20260706 |
| Update Code: | 20260706 |
| DOI: | 10.1007/s12031-026-02555-4 |
| PMID: | 42268355 |
| Database: | MEDLINE |
| FullText | Links: – Type: other Url: https://resolver.ebsco.com:443/public/rma-ftfapi/ejs/direct?AccessToken=409B93844BF16687F9B5&Show=Object Text: Availability: 0 CustomLinks: – Url: https://dx.doi.org/doi:10.1007/s12031-026-02555-4 Name: EDS - Springer Nature Journals (s7799221) Category: fullText Text: View record at Springer |
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| Header | DbId: cmedm DbLabel: MEDLINE An: 42268355 AccessLevel: 3 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: Evaluation of Umbelliferone Neuroprotective Effects Against Acrylamide-Induced Oxidative Stress, In Vivo and In Silico Study. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AU" term="%22Mogadem+A%22">Mogadem A</searchLink>; Department of Chemistry, College of Science, Taibah University, Madinah, Saudi Arabia. amogadam@taibahu.edu.sa.<br /><searchLink fieldCode="AU" term="%22Al-Refai+HH%22">Al-Refai HH</searchLink>; Department of Chemistry, College of Science in Yanbu, Taibah University, Yanbu Governorate, Saudi Arabia. – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%229002991%22">Journal of molecular neuroscience : MN</searchLink> [J Mol Neurosci] 2026 Jun 10; Vol. 76 (2). <i>Date of Electronic Publication: </i>2026 Jun 10. – Name: TypePub Label: Publication Type Group: TypPub Data: Journal Article – Name: Language Label: Language Group: Lang Data: English – Name: TitleSource Label: Journal Info Group: Src Data: <i>Publisher: </i><searchLink fieldCode="PB" term="%22Humana+Press%22">Humana Press </searchLink><i>Country of Publication: </i>United States <i>NLM ID: </i>9002991 <i>Publication Model: </i>Electronic <i>Cited Medium: </i>Internet <i>ISSN: </i>1559-1166 (Electronic) <i>Linking ISSN: </i><searchLink fieldCode="IS" term="%2208958696%22">08958696 </searchLink><i>NLM ISO Abbreviation: </i>J Mol Neurosci <i>Subsets: </i>MEDLINE – Name: PublisherInfo Label: Imprint Name(s) Group: PubInfo Data: <i>Publication</i>: Totowa, NJ : Humana Press<br /><i>Original Publication</i>: Boston : Birkhäuser [i.e. Cambridge, MA : Birkhäuser Boston, c1989- – Name: SubjectMESH Label: MeSH Terms Group: Su Data: <searchLink fieldCode="MM" term="%22Umbelliferones%22">Umbelliferones*</searchLink>/<searchLink fieldCode="MM" term="%22Umbelliferones+pharmacology%22">pharmacology</searchLink> <br /><searchLink fieldCode="MM" term="%22Umbelliferones%22">Umbelliferones*</searchLink>/<searchLink fieldCode="MM" term="%22Umbelliferones+therapeutic+use%22">therapeutic use</searchLink> <br /><searchLink fieldCode="MM" term="%22Acrylamide%22">Acrylamide*</searchLink>/<searchLink fieldCode="MM" term="%22Acrylamide+toxicity%22">toxicity</searchLink> <br /><searchLink fieldCode="MM" term="%22Neuroprotective+Agents%22">Neuroprotective Agents*</searchLink>/<searchLink fieldCode="MM" term="%22Neuroprotective+Agents+pharmacology%22">pharmacology</searchLink> <br /><searchLink fieldCode="MM" term="%22Neuroprotective+Agents%22">Neuroprotective Agents*</searchLink>/<searchLink fieldCode="MM" term="%22Neuroprotective+Agents+therapeutic+use%22">therapeutic use</searchLink> <br /><searchLink fieldCode="MM" term="%22Antioxidants%22">Antioxidants*</searchLink>/<searchLink fieldCode="MM" term="%22Antioxidants+pharmacology%22">pharmacology</searchLink> <br /><searchLink fieldCode="MM" term="%22Antioxidants%22">Antioxidants*</searchLink>/<searchLink fieldCode="MM" term="%22Antioxidants+therapeutic+use%22">therapeutic use</searchLink> <br /><searchLink fieldCode="MM" term="%22Oxidative+Stress%22">Oxidative Stress*</searchLink><br /><searchLink fieldCode="MH" term="%22Tumor+Necrosis+Factor-alpha%22">Tumor Necrosis Factor-alpha</searchLink>/<searchLink fieldCode="MH" term="%22Tumor+Necrosis+Factor-alpha+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Tumor+Necrosis+Factor-alpha%22">Tumor Necrosis Factor-alpha</searchLink>/<searchLink fieldCode="MH" term="%22Tumor+Necrosis+Factor-alpha+genetics%22">genetics</searchLink> ; <searchLink fieldCode="MH" term="%22Liver%22">Liver</searchLink>/<searchLink fieldCode="MH" term="%22Liver+drug+effects%22">drug effects</searchLink> ; <searchLink fieldCode="MH" term="%22Liver%22">Liver</searchLink>/<searchLink fieldCode="MH" term="%22Liver+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Heme+Oxygenase-1%22">Heme Oxygenase-1</searchLink>/<searchLink fieldCode="MH" term="%22Heme+Oxygenase-1+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Heme+Oxygenase-1%22">Heme Oxygenase-1</searchLink>/<searchLink fieldCode="MH" term="%22Heme+Oxygenase-1+genetics%22">genetics</searchLink> ; <searchLink fieldCode="MH" term="%22Caspase+3%22">Caspase 3</searchLink>/<searchLink fieldCode="MH" term="%22Caspase+3+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Caspase+3%22">Caspase 3</searchLink>/<searchLink fieldCode="MH" term="%22Caspase+3+genetics%22">genetics</searchLink> ; <searchLink fieldCode="MH" term="%22Brain%22">Brain</searchLink>/<searchLink fieldCode="MH" term="%22Brain+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Brain%22">Brain</searchLink>/<searchLink fieldCode="MH" term="%22Brain+drug+effects%22">drug effects</searchLink> ; <searchLink fieldCode="MH" term="%22Alanine+Transaminase%22">Alanine Transaminase</searchLink>/<searchLink fieldCode="MH" term="%22Alanine+Transaminase+metabolism%22">metabolism</searchLink> ; <searchLink fieldCode="MH" term="%22Animals%22">Animals</searchLink> ; <searchLink fieldCode="MH" term="%22Mice%22">Mice</searchLink> ; <searchLink fieldCode="MH" term="%22Male%22">Male</searchLink> ; <searchLink fieldCode="MH" term="%22Molecular+Docking+Simulation%22">Molecular Docking Simulation</searchLink> ; <searchLink fieldCode="MH" term="%22Lipid+Peroxidation%22">Lipid Peroxidation</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: Acrylamide (ACR) is a heat-generated carcinogen, one of the most common toxins, with various effects on the biological system, including oxidative stress and related disorders. Umbelliferone (UMB) is a naturally occurring coumarin derivative that is present in edible fruits, known as an antioxidant, and reported for many other therapeutic effects. In the current study, UMB was evaluated for neuro- and hepatoprotective activity against oxidative stress toxicity induced by a 40 mg/kg daily dose of ACR in a mouse model over 15 days. Also, UMB was used as a ligand for the first time to predict its affinity for the most important proteins involved in neuronal failure. The UMB administration significantly improves liver enzyme elevations, alanine transaminase (ALT) and aspartate transaminase (AST), following ACR injection. Also, UMB treatment reduced elevated total protein (TP) and albumin (ALB) serum levels. In addition, lipid peroxidation levels were significantly reduced by UMB (expressed as malondialdehyde MDA levels), and the levels of total non-enzymatic antioxidant capacity (TAC) were increased in brain tissue homogenate in comparison with brain injury in the ACR group. Furthermore, UMB downregulated the expression of tumor necrosis factor-alpha (TNF-α), an inflammatory marker and caspase-3, an apoptotic marker, while upregulating heme oxygenase-1 (HO-1), an antioxidant enzyme, in both liver and brain tissues. Molecular docking analysis revealed that the compound could form H-bonds and hydrophobic interactions with the target receptors. Results of this study conclude that UMB may be considered a potential pharmaceutical agent to ameliorate ACR-induced toxicity in the liver and brain, due to its anti-inflammatory, antioxidant, and antiapoptotic mechanisms, as well as its moderate affinity for neuronal disease-targeted proteins.<br /> (© 2026. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.) – Name: Abstract Label: Competing Interests Group: Ab Data: Declarations. Competing interests: The authors declare no competing interests. – Name: Ref Label: References Group: RefInfo Data: Adams LS, Seeram NP, Aggarwal BB, Takada Y, Sand D, Heber D (2006) Pomegranate juice, total pomegranate ellagitannins, and punicalagin suppress inflammatory cell signaling in colon cancer cells. J Agric Food Chem 54(3):980–985. (PMID: <searchLink fieldCode="PM" term="%221644821210%2E1021%2Fjf052005r%22">1644821210.1021/jf052005r)</searchLink><br />Ageena SA, Bakr AG, Mokhlis HA, Abd-Ellah MF (2025) Renoprotective effects of apocynin and/or umbelliferone against acrylamide-induced acute kidney injury in rats: role of the NLRP3 inflammasome and Nrf-2/HO-1 signaling pathways. Naunyn Schmiedebergs Arch Pharmacol 398(1):569–580. 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(PMID: <searchLink fieldCode="PM" term="%2220129494508410910%2E1016%2Fj%2Enurt%2E2009%2E10%2E016%22">20129494508410910.1016/j.nurt.2009.10.016)</searchLink> – Name: SubjectMinor Label: Contributed Indexing Group: Data: <i>Keywords: </i>Acrylamide; Caspase-3; Hemeoxygenase-1; Hepatoprotective; Molecular docking; Neuroprotective; Oxidative stress; Umbelliferone – Name: NumberCAS Label: Substance Nomenclature Group: ID Data: 0 (Umbelliferones)<br />20R035KLCI (Acrylamide)<br />0 (Neuroprotective Agents)<br />60Z60NTL4G (7-hydroxycoumarin)<br />0 (Tumor Necrosis Factor-alpha)<br />0 (Antioxidants)<br />EC 1.14.14.18 (Heme Oxygenase-1)<br />EC 3.4.22.- (Caspase 3)<br />EC 2.6.1.2 (Alanine Transaminase) – Name: DateEntry Label: Entry Date(s) Group: Date Data: <i>Date Created: </i>20260610 <i>Date Completed: </i>20260612 <i>Latest Revision: </i>20260706 – Name: DateUpdate Label: Update Code Group: Date Data: 20260706 – Name: DOI Label: DOI Group: ID Data: 10.1007/s12031-026-02555-4 – Name: AN Label: PMID Group: ID Data: 42268355 |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1007/s12031-026-02555-4 Languages: – Code: eng Text: English Subjects: – SubjectFull: Tumor Necrosis Factor-alpha metabolism Type: general – SubjectFull: Tumor Necrosis Factor-alpha genetics Type: general – SubjectFull: Liver drug effects Type: general – SubjectFull: Liver metabolism Type: general – SubjectFull: Heme Oxygenase-1 metabolism Type: general – SubjectFull: Heme Oxygenase-1 genetics Type: general – SubjectFull: Caspase 3 metabolism Type: general – SubjectFull: Caspase 3 genetics Type: general – SubjectFull: Brain metabolism Type: general – SubjectFull: Brain drug effects Type: general – SubjectFull: Alanine Transaminase metabolism Type: general – SubjectFull: Animals Type: general – SubjectFull: Mice Type: general – SubjectFull: Male Type: general – SubjectFull: Molecular Docking Simulation Type: general – SubjectFull: Lipid Peroxidation Type: general – SubjectFull: Umbelliferones pharmacology Type: general – SubjectFull: Umbelliferones therapeutic use Type: general – SubjectFull: Acrylamide toxicity Type: general – SubjectFull: Neuroprotective Agents pharmacology Type: general – SubjectFull: Neuroprotective Agents therapeutic use Type: general – SubjectFull: Antioxidants pharmacology Type: general – SubjectFull: Antioxidants therapeutic use Type: general – SubjectFull: Oxidative Stress Type: general Titles: – TitleFull: Evaluation of Umbelliferone Neuroprotective Effects Against Acrylamide-Induced Oxidative Stress, In Vivo and In Silico Study. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Mogadem A – PersonEntity: Name: NameFull: Al-Refai HH IsPartOfRelationships: – BibEntity: Dates: – D: 10 M: 06 Text: 2026 Jun 10 Type: published Y: 2026 Identifiers: – Type: issn-electronic Value: 1559-1166 Numbering: – Type: volume Value: 76 – Type: issue Value: 2 Titles: – TitleFull: Journal of molecular neuroscience : MN Type: main |
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