ArticleNaunyn-Schmiedeberg's archives of pharmacology2026
Amygdalin synergizes with the TNF-α monoclonal antibody infliximab to modulate HSP90 and related necro-inflammatory/oxidative stress pathways in a rat model of hepatic I/R.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Dynamic regulation and targeted intervention of neutrophils in hepatic ischemia‑reperfusion injury (Review).International journal of molecular medicine · 2026Review
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4 authors.
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Abstract
Hepatic ischemia/reperfusion (I/R) injury remains a major limitation in liver surgery and transplantation. Amygdalin, a natural glycoside, is known for its antioxidant, anti-inflammatory, and hepatoprotective properties, but its combination with conventional agents is not studied. Accordingly, this study explores a combinatorial approach using a small dose of amygdalin (5 mg/kg) and low-dose infliximab (1.5 mg/kg), a tumor necrosis factor (TNF)-α inhibitor, as a pre-treatment to alleviate I/R-induced liver injury. It also investigates the unexamined role of heat shock protein (HSP)-90 in the modulation of necro-inflammatory pathways during hepatic ischemia/reperfusion injury. Rats were divided into six groups: sham, I/R, infliximab (1.5 and 3 mg/kg), amygdalin (5 mg/kg), and a combination of infliximab (1.5 mg/kg) with amygdalin. Treatments were administered intraperitoneally for three days before I/R induction. Both monotherapies and the combination significantly reduced hepatic expression of HSP90, TNF-α, and phosphorylated-mixed lineage kinase domain-like protein (p-MLKL), while restoring oxidative balance as evidenced by modulation of nuclear factor erythroid 2-related factor 2 (Nrf2), malondialdehyde (MDA), and superoxide dismutase (SOD). The combination therapy additionally suppressed nuclear factor kappa B (NF-κB) in a synergistic manner and enhanced Nrf2 expression compared to amygdalin monotherapy. Correlation analysis revealed strong associations between markers of necroinflammation and oxidative stress, reinforcing the mechanistic interplay between these pathways. HSP90 emerged in the current study as an intermediate modulator linking necroinflammation to oxidative responses. Importantly, the combined therapy exerted a synergistic effect by effectively modulating HSP90 and associated signaling cascades, underscoring its potential as a superior therapeutic strategy.
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