<p>In traditional medicine, <i>Argemone mexicana</i> L. (Papaveraceae) is used by Indian and Bangladeshi practitioners to treat jaundice and liver ailments<i>.</i> Despite its widespread use, its hepatoprotective activity lacks scientific validation in HepG2 liver cell models. This study evaluated the protective effects of methanolic extract of <i>A. mexicana</i> (MEAM) against paracetamol-induced hepatotoxicity in HepG2 cells. Antioxidant activity were assessed via DPPH, ABTS, lipid peroxidation, and ferricyanide assays. Cytoprotective effects were evaluated using MTT, LDH, AST, ALT, and inflammatory markers (TNF-α, IL-1β), along with oxidative stress indicators (SOD, GSH, GPx, MDA). LC–MS analysis was used to identify bioactive compounds in the MEAM. In silico molecular docking studies with Schrödinger software further examined the interaction of identified bioactive compounds with PPAR-α and TGF-β1 to explore their potential hepatoprotective mechanisms. MEAM exhibited strong antioxidant activities (IC₅₀: DPPH- 92.3, ABTS- 93.7, lipid peroxidation- 43.2&#xa0;µg/mL). In the MTT assay, MEAM significantly (<i>p</i> &lt; 0.05) increased HepG2 cell viability compared to the paracetamol-treated group. It also elevated antioxidant markers (SOD, GSH, GPx) and reduced MDA levels relative to the positive control. MEAM restored cellular architecture in a dose-dependent manner, similar to silymarin. Additionally, it significantly lowered AST, ALT, TNF-α, and IL-1β levels, approaching normal control values. In silico analysis identified reticuline and oxyberberine with the highest docking scores to PPAR-α and TGF-β1. MEAM showed significant in vitro hepatoprotective activity, supporting its traditional use.</p> Graphical Abstract <p>Hepatoprotective potential of <i>Argemone mexicana</i> L. root methanol extract: LC–MS profiling, molecular docking and protection against paracetamol-induced toxicity in HepG2 cell lines.</p> <p></p>

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LC–MS-based phytochemical analysis and hepatoprotective potential of Argemone mexicana L. extract in paracetamol-treated HepG2 cells

  • Anindya Bagchi,
  • Priyanka Dash,
  • Anusree Raha,
  • Chandan Das,
  • Vineet Kumar Rai,
  • Jitu Halder,
  • Bornika Chattaraj,
  • Biswakanth Kar,
  • Debajyoti Das,
  • Goutam Ghosh,
  • Goutam Rath

摘要

In traditional medicine, Argemone mexicana L. (Papaveraceae) is used by Indian and Bangladeshi practitioners to treat jaundice and liver ailments. Despite its widespread use, its hepatoprotective activity lacks scientific validation in HepG2 liver cell models. This study evaluated the protective effects of methanolic extract of A. mexicana (MEAM) against paracetamol-induced hepatotoxicity in HepG2 cells. Antioxidant activity were assessed via DPPH, ABTS, lipid peroxidation, and ferricyanide assays. Cytoprotective effects were evaluated using MTT, LDH, AST, ALT, and inflammatory markers (TNF-α, IL-1β), along with oxidative stress indicators (SOD, GSH, GPx, MDA). LC–MS analysis was used to identify bioactive compounds in the MEAM. In silico molecular docking studies with Schrödinger software further examined the interaction of identified bioactive compounds with PPAR-α and TGF-β1 to explore their potential hepatoprotective mechanisms. MEAM exhibited strong antioxidant activities (IC₅₀: DPPH- 92.3, ABTS- 93.7, lipid peroxidation- 43.2 µg/mL). In the MTT assay, MEAM significantly (p < 0.05) increased HepG2 cell viability compared to the paracetamol-treated group. It also elevated antioxidant markers (SOD, GSH, GPx) and reduced MDA levels relative to the positive control. MEAM restored cellular architecture in a dose-dependent manner, similar to silymarin. Additionally, it significantly lowered AST, ALT, TNF-α, and IL-1β levels, approaching normal control values. In silico analysis identified reticuline and oxyberberine with the highest docking scores to PPAR-α and TGF-β1. MEAM showed significant in vitro hepatoprotective activity, supporting its traditional use.

Graphical Abstract

Hepatoprotective potential of Argemone mexicana L. root methanol extract: LC–MS profiling, molecular docking and protection against paracetamol-induced toxicity in HepG2 cell lines.