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Purpose <p>The present study demonstrates the hepatoprotective effects of Caffeic Acid (CA), a natural phenolic compound, in modulating systemic toxin Lipopolysaccharide (LPS)-induced inflammation of the liver. LPS can impair hepatic function eliciting inflammation, oxidative stress, apoptosis, and lipid dysregulation.</p> Method <p>Female Swiss Albino mice (age: 60 days) were divided into four groups (<i>n</i> = 6/group): Group I: Control; Groups II and III were exposed to LPS (1&#xa0;mg/kg BW; intraperitoneally) for 5 days. CA was administered to Groups III and IV (20&#xa0;mg/kg BW; intraperitoneally) from day 6 to next 28 days. LPS-induced liver toxicity was investigated by analyzing oxidative stress modulation, lipid metabolism, and apoptotic signalling. Biochemical assays were performed to evaluate oxidative stress markers, serum-lipid profiles (cholesterol, triglycerides), and plasma levels of apoptotic-proteins B-cell lymphoma 2 (BCL-2), Caspase-3. Additionally, complementary in silico molecular docking was conducted to assess CA’s binding affinity and interactions with TLR4-MD2-LPS complex, BCL-2 and Caspase-3.</p> Results <p>CA administration significantly attenuated hepatic oxidative stress and improved lipid profiles by decreasing serum-lipid levels by 50–55%. Apoptotic signalling was modulated, as evidenced by reduced Caspase-3 and upregulated BCL-2 expression around three-folds. In silico analyses revealed strong binding affinities of CA with target proteins, suggesting a possible mechanistic basis for its anti-apoptotic effects.</p> Conclusion <p>CA exhibits potent hepatoprotective properties through antioxidant, anti-apoptotic, anti-inflammatory, and lipid-regulating mechanisms. This investigation uniquely integrates both in vivo plasma-level findings and receptor-level in silico interaction analysis in an LPS-induced inflammatory model, underscoring CA’s dual regulatory potential and therapeutic promise for managing liver-inflammation.</p>

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Validating hepatoprotective potency of caffeic acid targeting BCL-2/Caspase-3 axis against endotoxin-driven liver toxicity: an in vivo and in silico approach

  • 期刊论文

  • 发表日期：

    2025年11月26日

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  • Anjali Yadav,
  • Banalata Mohanty

摘要

Purpose

The present study demonstrates the hepatoprotective effects of Caffeic Acid (CA), a natural phenolic compound, in modulating systemic toxin Lipopolysaccharide (LPS)-induced inflammation of the liver. LPS can impair hepatic function eliciting inflammation, oxidative stress, apoptosis, and lipid dysregulation.

Method

Female Swiss Albino mice (age: 60 days) were divided into four groups (n = 6/group): Group I: Control; Groups II and III were exposed to LPS (1 mg/kg BW; intraperitoneally) for 5 days. CA was administered to Groups III and IV (20 mg/kg BW; intraperitoneally) from day 6 to next 28 days. LPS-induced liver toxicity was investigated by analyzing oxidative stress modulation, lipid metabolism, and apoptotic signalling. Biochemical assays were performed to evaluate oxidative stress markers, serum-lipid profiles (cholesterol, triglycerides), and plasma levels of apoptotic-proteins B-cell lymphoma 2 (BCL-2), Caspase-3. Additionally, complementary in silico molecular docking was conducted to assess CA’s binding affinity and interactions with TLR4-MD2-LPS complex, BCL-2 and Caspase-3.

Results

CA administration significantly attenuated hepatic oxidative stress and improved lipid profiles by decreasing serum-lipid levels by 50–55%. Apoptotic signalling was modulated, as evidenced by reduced Caspase-3 and upregulated BCL-2 expression around three-folds. In silico analyses revealed strong binding affinities of CA with target proteins, suggesting a possible mechanistic basis for its anti-apoptotic effects.

Conclusion

CA exhibits potent hepatoprotective properties through antioxidant, anti-apoptotic, anti-inflammatory, and lipid-regulating mechanisms. This investigation uniquely integrates both in vivo plasma-level findings and receptor-level in silico interaction analysis in an LPS-induced inflammatory model, underscoring CA’s dual regulatory potential and therapeutic promise for managing liver-inflammation.