ArticleCombinatorial chemistry & high throughput screening2026
Paeonol Inhibits the MAPK Signaling Pathway by Targeting SIRT1 in AGE-Induced HUVECs Injury.
Article in Combinatorial chemistry & high throughput screening, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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7 authors.
Funding
Abstract
backgroundChronic hyperglycemia in diabetes is a significant contributor to endothelial injury through the induction of oxidative stress. Paeonol is anticipated to address oxidative stress with the aim of ameliorating endothelial injury. Our study delved into the effects of paeonol on endothelial damage induced by diabetes and elucidated the underlying mechanisms.
methodsThis research presented a novel endothelial injury model employing advanced glycation end products (AGEs) in human umbilical vein endothelial cells (HUVECs). Additionally, a network analysis was carried out to pinpoint the targets influenced by paeonol, with pivotal targets substantiated via polymerase chain reaction (PCR), western blot analysis, and immunofluorescence staining. Ultimately, the introduction of small interfering RNA transfection validated the involvement of SIRT1 in AGEs-induced HUVECs injury.
resultsTwelve metabolites of paeonol were conclusively detected in vivo. Paeonol demonstrated substantial efficacy in ameliorating and diminishing levels of various cytokines and biochemical indicators, including AGEs, Col IV, ET-1, E-selectin, FN, hs-CRP, ICAM-1, MMP2, and sVCAM-1. Notably, network analysis accentuated the pivotal role of the MAPK signaling pathway. Furthermore, paeonol exhibited significantly elevated mRNA and protein levels of SIRT1 and ERK across varying dosage regimens compared to the model group while displaying relatively decreased mRNA expression levels of p38MAPK.
conclusionThis research revealed that paeonol inhibited the activation of p38 and ERK within the MAPK signaling pathway. Moreover, the regulatory influence of paeonol over p38 and ERK was compromised subsequent to the silencing of SIRT1, indicating a SIRT1-dependent suppressive action of paeonol on the MAPK pathway. The potential therapeutic utility of SIRT1 in mitigating diabetic endothelial impairment and its concomitant cardiovascular ramifications is underscored by these findings.
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