Level D· Scientific groundwork from lab and animal studiesLaboratory StudyEurope PMCOpen access

Synephrine Inhibits Oxidative Stress and H<sub>2</sub>O<sub>2</sub>-Induced Premature Senescence

Abe H., Indo HP., Ito H., Majima HJ., Tanaka T.

Laboratory Study on Chronic Inflammation, published in Cell Biochem Biophys (2025) — summary generated from the PubMed abstract.

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Level D· Scientific groundwork from lab and animal studiesEvidence level of this study

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

  • Level A · Stronger Clinical Evidence
  • Level B · Emerging clinical evidence with positive signals
  • Level C · Early human research exploring benefits
  • Level D · Scientific groundwork from lab and animal studies
  • Emerging · Emerging topic under active research
Read the A–D evidence level guide

This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.

Study type
Laboratory Study
Journal
Cell Biochem Biophys (2025)
Reported sample size
—
Source database
Europe PMC
PMID
39832117
PMCID
PMC12089197
DOI
10.1007/s12013-025-01669-7
Citations
1

Abstract (original English)

Synephrine, a protoalkaloid found in Citrus aurantium (CA) peels, exerts lipolytic, anti-inflammatory, and vasoconstrictive effects; however, its antioxidant activity remains unclear. In this study, electron spin resonance spectroscopy revealed that synephrine scavenged both hydroxyl and superoxide anion radicals. Several external stimuli, such as H 2 O 2 , X-rays, and ultraviolet (UV) radiation, cause stress-induced premature senescence (SIPS). As oxidative stress induces SIPS, we hypothesized that synephrine, an antioxidant, would suppress H 2 O 2 -induced premature senescence in WI-38 cells. Synephrine significantly decreased the reactive oxygen species levels induced by H 2 O 2 , thereby reducing lipid peroxidation, and oxidative DNA damage and preventing SIPS. Additionally, synephrine inhibited mitochondrial dysfunction in H 2 O 2 -treated WI-38 cells. The expression levels of p53, p21, and p16 -INK4A , which are involved in the induction of cell cycle arrest in SIPS, were significantly lower in synephrine-treated cells than in untreated cells. Our results indicate that synephrine inhibits H 2 O 2 -induced oxidative stress and mitochondrial dysfunction, suppressing premature senescence by inhibiting activation of the p53-p21 and p16 -INK4A -pRB pathways.

What this study does not prove

  • • This study does not prove SVF is an approved treatment or a replacement for standard care.
  • • This is preclinical work; animal or laboratory results cannot be applied to humans.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

How we grade evidence
Cell LineMitochondriaHumansDNA DamageHydrogen PeroxideReactive Oxygen SpeciesSynephrineAntioxidantsLipid PeroxidationOxidative Stress

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