Key result
20(S)-Protopanaxadiol significantly reduced aortic plaques and hepatic steatosis in HFD-fed ApoE KO mice by increasing LDLR levels and inhibiting its interaction with PCSK9.
20(S)-Protopanaxadiol reduces atherosclerosis in a preclinical model by inhibiting PCSK9-mediated LDLR degradation, suggesting potential as a lipid-lowering agent.
PPD merits human pharmacokinetic studies as a potential PCSK9 modulator; leaves open translation from ApoE KO mice to clinical atherosclerosis therapy.
saponins in the intestinal tract, can bind to the extracellular domain of LDLR and inhibit the role of Proprotein Convertase Subtilisin/Kexin Type 9 (PCSK9) in mediating LDLR degradation. The results showed that PPD significantly reduced aortic plaques and hepatic steatosis in HFD-fed ApoE KO mice. LDLR protein levels were elevated in the liver tissues isolated from PPD-treated HFD-fed ApoE KO mice and PPD-treated HepG2 cells. Our findings demonstrated that PPD significantly increased LDLR levels and reduced AS in the HFD-fed ApoE KO mice on account of LDLR degradation being inhibited by PPD inhibiting the interaction between PCSK9 and LDLR.
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Huang et al. (2022) studied Atherosclerosis. 20(S)-Protopanaxadiol (PPD) was evaluated on Aortic plaques and hepatic steatosis. 20(S)-Protopanaxadiol significantly reduced aortic plaques and hepatic steatosis in HFD-fed ApoE KO mice by increasing LDLR levels and inhibiting its interaction with PCSK9.
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