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<p>Synephrine, a protoalkaloid found in <i>Citrus aurantium</i> (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<sub>2</sub>O<sub>2</sub>, 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<sub>2</sub>O<sub>2</sub>-induced premature senescence in WI-38 cells. Synephrine significantly decreased the reactive oxygen species levels induced by H<sub>2</sub>O<sub>2</sub>, thereby reducing lipid peroxidation, and oxidative DNA damage and preventing SIPS. Additionally, synephrine inhibited mitochondrial dysfunction in H<sub>2</sub>O<sub>2</sub>-treated WI-38 cells. The expression levels of p53, p21, and p16<sup>-INK4A</sup>, 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<sub>2</sub>O<sub>2</sub>-induced oxidative stress and mitochondrial dysfunction, suppressing premature senescence by inhibiting activation of the p53–p21 and p16<sup>-INK4A</sup>–pRB pathways.</p>

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Synephrine Inhibits Oxidative Stress and H2O2-Induced Premature Senescence

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年1月20日

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  • Hiroshi Abe,
  • Hiroko P. Indo,
  • Hiromu Ito,
  • Hideyuki J. Majima,
  • Tatsuro Tanaka

摘要

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 H2O2, 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 H2O2-induced premature senescence in WI-38 cells. Synephrine significantly decreased the reactive oxygen species levels induced by H2O2, thereby reducing lipid peroxidation, and oxidative DNA damage and preventing SIPS. Additionally, synephrine inhibited mitochondrial dysfunction in H2O2-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 H2O2-induced oxidative stress and mitochondrial dysfunction, suppressing premature senescence by inhibiting activation of the p53–p21 and p16-INK4A–pRB pathways.