Senescent cells are deeply involved in the induction of tissue damage and aging-related diseases. The identification of factors that eliminate senescent cells or inhibit the senescence-associated secretory phenotype (SASP) in these cells is necessary. Here, we report an avenanthramice C (Avn C) extracted from oat as a new SASP modulator. Treatment with Avn C led to a significant reduction in the levels of markers of senescent cells, with no toxicity observed. The SASP was also inhibited by Avn C treatment, similar to non-senescent cells, and the suppression of cell division by autocrine signals associated with SASP was restored. To investigate the mechanism underlying SASP inhibition by Avn C, we analyzed the effect of Avn C in lipopolysaccharide (LPS)-induced inflammation in non-senescent cells. Avn C inhibited nuclear factor κB (NF-κB) activity and the secretion of inflammatory cytokines before or after LPS treatment. Although the activity of MAP kinases, which are NF-κB upstream signals, was inhibited by Avn C in LPS-induced inflammation, only p38 activity was specifically inhibited in senescent cells. Interestingly, the inhibition of p38 in senescent cells was observed through Avn C-induced 5′-adenosine monophosphate-activated protein kinase (AMPK) activity. Avn C-induced inhibition of the SASP is triggered by senescence-related stress.

衰老细胞与组织损伤和衰老相关疾病的诱导密切相关。有必要确定在这些细胞中消除衰老细胞或抑制衰老相关分泌表型 (SASP) 的因素。在这里，我们报告了一种从燕麦中提取的燕麦碳素 C (Avn C) 作为一种新的 SASP 调制器。Avn C 处理导致衰老细胞标志物水平显着降低，未观察到毒性。SASP 也被 Avn C 处理抑制，类似于非衰老细胞，并且恢复了与 SASP 相关的自分泌信号对细胞分裂的抑制。为了研究 Avn C 抑制 SASP 的机制，我们分析了 Avn C 在脂多糖 (LPS) 诱导的非衰老细胞炎症中的作用。Avn C 在 LPS 治疗前后抑制核因子 κB (NF-κB) 活性和炎性细胞因子的分泌。尽管作为 NF-κB 上游信号的 MAP 激酶的活性在 LPS 诱导的炎症中被 Avn C 抑制，但只有 p38 活性在衰老细胞中被特异性抑制。有趣的是，通过 Avn C 诱导的 5'-腺苷单磷酸激活蛋白激酶 (AMPK) 活性观察到衰老细胞中 p38 的抑制。Avn C 诱导的 SASP 抑制是由衰老相关的压力触发的。通过 Avn C 诱导的 5'-腺苷单磷酸激活蛋白激酶 (AMPK) 活性观察到衰老细胞中 p38 的抑制作用。Avn C 诱导的 SASP 抑制是由衰老相关的压力触发的。通过 Avn C 诱导的 5'-腺苷单磷酸激活蛋白激酶 (AMPK) 活性观察到衰老细胞中 p38 的抑制作用。Avn C 诱导的 SASP 抑制是由衰老相关的压力触发的。