Pear Peel–Enriched Residue Extract Attenuates Ethanol‐Induced Liver Injury Through Regulation of Antioxidant Signaling and Lipid Metabolism
8 affiliations
- 1School of Food and Pharmaceutical Engineering Mokpo National University Mokpo 58554 Jeonnam South Korea mokpo.ac.kr
- 2Bio-Medicine Advanced Formulation Research Center Regional Leading Research Center Mokpo National University Mokpo 58554 Jeonnam South Korea mokpo.ac.kr
- 3College of Pharmacy and Research Institute of Life and Pharmaceutical Sciences Sunchon National University Suncheon Jeonnam-Gwangju 57922 South Korea sunchon.ac.kr
- 4Department of Natural Cosmetics Science and AI Digital Bioscience Research Institute Sunchon National University Suncheon Jeonnam-Gwangju 57922 South Korea sunchon.ac.kr
- 5AI Bio Autonomous Research Core Facility Center Sunchon National University Suncheon Jeonnam-Gwangju 57922 South Korea sunchon.ac.kr
- 6Department of Biomedicine, Health & Life Convergence Sciences BK21 Four Mokpo National University Mokpo 58554 Jeonnam South Korea mokpo.ac.kr
- 7Department of Pharmacy Mokpo National University Mokpo 58554 Jeonnam South Korea mokpo.ac.kr
- 8Good F&B Naju 58245 South Korea
Abstract
Excessive alcohol consumption induces progressive liver injury through oxidative stress, lipid accumulation, and inflammation, primarily driven by dysregulated ethanol (EtOH) metabolism. Given the growing interest in plant‐derived phytochemicals for hepatoprotection, pear (Pyrus pyrifolia) has attracted attention due to its antioxidant and lipid‐regulating properties; however, the bioactive fractions and mechanisms underlying the hepatoprotective effects of pear peel–enriched residue extracts (PPE) remain unclear. Therefore, we evaluated the hepatoprotective potential of PPE against EtOH‐induced liver injury using in vitro, in vivo, and in silico approaches. In HepG2 cells, PPE reduced oxidative stress, restored cell viability, and reduced intracellular EtOH and acetaldehyde levels more effectively than pear extract, with efficacy comparable to silymarin. In EtOH‐treated C57BL/6 mice, PPE attenuated liver injury markers, reduced hepatic lipid accumulation, and improved histopathological alterations. PPE also modulated the expression of proteins associated with oxidative stress and lipid metabolism. GNPS–FBMN analysis putatively annotated over 120 phytochemicals (or metabolites), and in silico analyses suggested potential interactions between selected metabolites and proteins involved in EtOH metabolism and lipid regulation. These findings suggest that PPE shows hepatoprotective potential and warrants further investigation as a potential candidate for the mitigation of alcohol‐associated liver disease.
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BibTeX
@article{thakuri2026pear,
title = {{Pear Peel–Enriched Residue Extract Attenuates Ethanol‐Induced Liver Injury Through Regulation of Antioxidant Signaling and Lipid Metabolism}},
author = {Laxmi Sen Thakuri and Ducdat Le and Narayan Sah Sonar and Hye Bin Park and Laxman Subedi and Ki-Sun Lee and Jeong-Ho Shon and Jin Woo Park and Mina Lee and Dong Young Rhyu},
journal = {Advances in Pharmacological and Pharmaceutical Sciences},
year = {2026},
month = nov,
doi = {10.1155/adpp/6147577},
url = {https://doi.org/10.1155/adpp/6147577},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Pear Peel–Enriched Residue Extract Attenuates Ethanol‐Induced Liver Injury Through Regulation of Antioxidant Signaling and Lipid Metabolism
AU - Laxmi Sen Thakuri
AU - Ducdat Le
AU - Narayan Sah Sonar
AU - Hye Bin Park
AU - Laxman Subedi
AU - Ki-Sun Lee
AU - Jeong-Ho Shon
AU - Jin Woo Park
AU - Mina Lee
AU - Dong Young Rhyu
PY - 2026
DA - 2026/11/04
JO - Advances in Pharmacological and Pharmaceutical Sciences
DO - 10.1155/adpp/6147577
UR - https://doi.org/10.1155/adpp/6147577
AB - Excessive alcohol consumption induces progressive liver injury through oxidative stress, lipid accumulation, and inflammation, primarily driven by dysregulated ethanol (EtOH) metabolism. Given the growing interest in plant‐derived phytochemicals for hepatoprotection, pear (Pyrus pyrifolia) has attracted attention due to its antioxidant and lipid‐regulating properties; however, the bioactive fractions and mechanisms underlying the hepatoprotective effects of pear peel–enriched residue extracts (PPE) remain unclear. Therefore, we evaluated the hepatoprotective potential of PPE against EtOH‐induced liver injury using in vitro, in vivo, and in silico approaches. In HepG2 cells, PPE reduced oxidative stress, restored cell viability, and reduced intracellular EtOH and acetaldehyde levels more effectively than pear extract, with efficacy comparable to silymarin. In EtOH‐treated C57BL/6 mice, PPE attenuated liver injury markers, reduced hepatic lipid accumulation, and improved histopathological alterations. PPE also modulated the expression of proteins associated with oxidative stress and lipid metabolism. GNPS–FBMN analysis putatively annotated over 120 phytochemicals (or metabolites), and in silico analyses suggested potential interactions between selected metabolites and proteins involved in EtOH metabolism and lipid regulation. These findings suggest that PPE shows hepatoprotective potential and warrants further investigation as a potential candidate for the mitigation of alcohol‐associated liver disease.
SN - 2633-4690
ER -