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Investigating the Protective Effects of Platycodin D on Non-Alcoholic Fatty Liver Disease in a Palmitic Acid-Induced In Vitro Model
Published on: December 2, 2022
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Procyanidin B2 Alleviates Palmitic Acid-Induced Injury in HepG2 Cells via Endoplasmic Reticulum Stress Pathway
Yi-Ming Li1, Shao-Yang Zhao1,2, Huan-Huan Zhao3
1The First School of Clinical Medicine, Guangzhou University of Chinese Medicine, Guangzhou 510000, China.
Evidence-Based Complementary and Alternative Medicine : Ecam
|December 27, 2021
Summary
Procyanidin B2 (PCB2) protects liver cells from palmitic acid (PA) damage by reducing endoplasmic reticulum stress and inhibiting the NLRP3 inflammasome pathway. This suggests PCB2
Area of Science:
- Hepatology and Molecular Biology
- Pharmacology and Toxicology
Background:
- Nonalcoholic fatty liver disease (NAFLD) affects over 25% globally, driven by metabolic syndrome and hepatic lipid accumulation.
- Current NAFLD treatments lack approved drugs, necessitating research into novel therapeutic agents.
- Procyanidin B2 (PCB2), from cinnamon, shows hepatoprotective potential, but its mechanism against NAFLD-related cellular injury is unclear.
Purpose of the Study:
- To elucidate the protective mechanism of Procyanidin B2 (PCB2) against palmitic acid (PA)-induced cellular injury in human hepatoma HepG2 cells.
- To investigate PCB2's role in modulating endoplasmic reticulum stress (ERS) and NLRP3 inflammasome activation in the context of NAFLD.
Main Methods:
- HepG2 cells were treated with PA to induce cellular injury, oxidative stress, and ERS.
- The effects of PCB2, ER stress inhibitor (4-PBA), and ER stress agonist (TG) on cell viability and key protein markers were assessed.
- Western blotting was used to analyze protein levels related to ERS, apoptosis, and the NLRP3 inflammasome pathway.
Main Results:
- PA induced oxidative stress, calcium disequilibrium, and endoplasmic reticulum stress (ERS), leading to apoptosis, evidenced by increased Bax/Bcl-2 ratio and ER stress markers (GRP78, GRP94, CHOP, p-PERK, p-IRE1α).
- PCB2 treatment restored cell viability, attenuated ERS, and reduced apoptosis in a dose-dependent manner, similar to 4-PBA and counteracting TG effects.
- PA exposure upregulated inflammatory markers (p-IKKα/β, p-NF-κB p65, NLRP3, cleaved caspase 1, IL-1β), which were significantly reduced by PCB2 intervention.
Conclusions:
- Palmitic acid induces ERS and activates the NLRP3 inflammasome pathway, leading to inflammation and apoptosis in HepG2 cells.
- Procyanidin B2 (PCB2) effectively inhibits the NLRP3/caspase 1/IL-1β pathway and mitigates ERS-induced inflammation and apoptosis.
- PCB2 demonstrates significant cell-protective effects, offering potential as a therapeutic agent for NAFLD.
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