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Investigating The Mechanism Of Interaction Between Graphene Oxide And Reduced Graphene Oxide With Macrophage-Derived Foam Cells

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Date
2025-10
Authors
Lat, Farizah Hanim
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Research Projects
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Atherosclerosis is a chronic inflammatory disease driven by lipid accumulation and macrophage-derived foam cell formation. Graphene-based nanomaterials, including graphene oxide (go) and reduced graphene oxide (rgo), have shown potential in modulating lipid metabolism and inflammation. This study examined the effects of go and rgo on atherosclerosis-related proteins (cd36, lox1, sra1, tlr4, apob, ldlr) using computational and experimental approaches. Molecular docking and molecular dynamics simulations revealed that rgo displayed higher binding affinity for lipid-associated proteins via hydrophobic interactions, while go formed more stable complexes through hydrogen bonding and electrostatic interactions. Go and rgo were synthesised from oil palm trunk (opt) and surface functionalisation was characterised by raman spectroscopy, ftir, xrd, and afm. Go exhibited higher oxygen functionalisation and hydrophilicity, whereas rgo retained partial hydrophobicity. In vitro assays showed that go was more cytotoxic to macrophages than rgo, inducing oxidative stress in a dose- and time-dependent manner. Both inhibited oxldl-induced lipid accumulation, with go demonstrating a stronger effect. Elisa confirmed no induction of pro-inflammatory cytokines. Gene expression analysis indicated that go upregulated abca1 and downregulated multiple scavenger receptors and inflammatory genes, promoting cholesterol efflux, while rgo showed a distinct expression pattern with sra1 and il-1β upregulation.
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Investigating Mechanism Interaction Between Graphene Oxide
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