Paeoniflorin mitigates insulin-like growth factor 1-induced lipogenesis and inflammation in human sebocytes by inhibiting the PI3K/Akt/FoxO1 and JAK2/STAT3 signaling pathways

IF 4.8 3区化学 Q1 CHEMISTRY, MEDICINAL Natural Products and Bioprospecting Pub Date : 2024-10-01 DOI:10.1007/s13659-024-00478-4

Chuanchuan Cai, Si Liu, Yufeng Liu, Shaobin Huang, Shiya Lu, Fang Liu, Xiaohua Luo, Christos C. Zouboulis, Ge Shi

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Abstract

Insulin-like growth factor-1 (IGF-1) is considered as a pathogenic factor contributing to sebaceous gland dysfunction, which leads to acne vulgaris. Paeoniflorin (Pae), a bioactive monomer derived from total glycosides of paeony, has shown potential in treating various diseases. However, its anti-acne effects on human sebocytes are not well understood. In this study, we investigated the effects of Pae on acne development induced by IGF-1 in SZ95 sebocytes. Following IGF-1 stimulation, SZ95 sebocytes were exposed to Pae and then determined for proliferation, cell cycle, apoptosis, lipogenesis and pro-inflammatory cytokine secretion. We also analyzed the expression of proteins involved in the PI3K/Akt/FoxO1 and JAK2/STAT3 pathways. In vitro experiments demonstrated that Pae significantly inhibited colony formation, induced G1/S cell cycle arrest, promoted apoptosis, inhibited lipogenesis and cytokine synthesis in IGF-1-treated SZ95 sebocytes. Furthermore, Pae suppressed the phosphorylation of Akt, FoxO1, JAK2, and STAT3. Importantly, the sebo-suppressive and anti-inflammatory effects of Pae were enhanced by blocking PI3K and JAK2. In summary, our findings suggest that Pae has potent anti-proliferative and pro-apoptotic effects in SZ95 sebocytes. Additionally, Pae effectively protects against IGF-1-induced lipogenesis and inflammation by targeting the PI3K/Akt/FoxO1 and JAK2/STAT3 signaling pathways.

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芍药苷通过抑制PI3K/Akt/FoxO1和JAK2/STAT3信号通路，减轻胰岛素样生长因子1诱导的人皮脂细胞脂肪生成和炎症。

胰岛素样生长因子-1（IGF-1）被认为是导致皮脂腺功能障碍的致病因素，而皮脂腺功能障碍又会导致寻常痤疮。芍药苷（Pae）是从芍药总苷中提取的一种生物活性单体，已显示出治疗多种疾病的潜力。然而，芍药苷对人体皮脂细胞的抗痤疮作用还不甚了解。在这项研究中，我们研究了芍药对 IGF-1 诱导的 SZ95 皮脂细胞痤疮发展的影响。在 IGF-1 刺激下，SZ95 皮脂腺细胞暴露于 Pae，然后测定其增殖、细胞周期、细胞凋亡、脂肪生成和促炎细胞因子分泌。我们还分析了参与 PI3K/Akt/FoxO1 和 JAK2/STAT3 通路的蛋白质的表达。体外实验表明，Pae能明显抑制IGF-1处理的SZ95皮脂腺细胞的集落形成、诱导G1/S细胞周期停滞、促进细胞凋亡、抑制脂肪生成和细胞因子合成。此外，Pae 还能抑制 Akt、FoxO1、JAK2 和 STAT3 的磷酸化。重要的是，阻断 PI3K 和 JAK2 可增强 Pae 的皮脂抑制和抗炎作用。总之，我们的研究结果表明，Pae 在 SZ95 皮脂腺细胞中具有强大的抗增殖和促凋亡作用。此外，Pae 还能通过靶向 PI3K/Akt/FoxO1 和 JAK2/STAT3 信号通路，有效防止 IGF-1 诱导的脂肪生成和炎症。

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