Kushenol C (KC) is a prenylated flavonoid isolated from the roots of Sophora flavescens aiton. Little is known about its anti-inflammatory and anti-oxidative stress activities. Here, we investigated the anti-inflammatory and anti-oxidative stress effects of KC in lipopolysaccharide (LPS)-stimulated RAW264.7 macrophages, and tert-butyl hydroperoxide (tBHP)-induced oxidative stress in HaCaT cells. The results demonstrated that KC dose-dependently suppressed the production of inflammatory mediators, including NO, PGE2, IL-6, IL1β, MCP-1, and IFN-β in LPS-stimulated RAW264.7 macrophages. The study demonstrated that the inhibition of STAT1, STAT6, and NF-κB activations by KC might have been responsible for the inhibition of NO, PGE2, IL-6, IL1β, MCP-1, and IFN-β in the LPS-stimulated RAW264.7 macrophages. KC also upregulated the expression of HO-1 and its activities in the LPS-stimulated RAW264.7 macrophages. The upregulation of Nrf2 transcription activities by KC in the LPS-stimulated RAW264.7 macrophages was demonstrated to be responsible for the upregulation of HO-1 expression and its activity in LPS-stimulated RAW264.7 macrophages. In HaCaT cells, KC prevented DNA damage and cell death by upregulating the endogenous antioxidant defense system involving glutathione, superoxide dismutase, and catalase, which prevented reactive oxygen species production from tert-butyl hydroperoxide (tBHP)-induced oxidative stress in HaCaT cells. The upregulated activation of Nrf2 and Akt in the PI3K-Akt signaling pathway by KC was demonstrated to be responsible for the anti-oxidative stress activity of KC in HaCaT cells. Collectively, the study suggests that KC can be further investigated as a potential anti-inflammatory candidate for the treatment of inflammatory diseases.

中文翻译：

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苦参根中苦参酚C的体外抗炎和抗氧化应激活性

Kushenol C (KC) 是一种从苦参根中分离出来的异戊二烯化黄酮类化合物。对其抗炎和抗氧化应激活性知之甚少。在这里，我们研究了 KC 在脂多糖 (LPS) 刺激的 RAW264.7 巨噬细胞和叔丁基过氧化氢 (tBHP) 诱导的 HaCaT 细胞氧化应激中的抗炎和抗氧化应激作用。结果表明，KC 剂量依赖性地抑制了 LPS 刺激的 RAW264.7 巨噬细胞中炎症介质的产生，包括 NO、PGE2、IL-6、IL1β、MCP-1 和 IFN-β。该研究表明，KC 对 STAT1、STAT6 和 NF-κB 活化的抑制可能是抑制 LPS 刺激的 RAW264 中 NO、PGE2、IL-6、IL1β、MCP-1 和 IFN-β 的原因。 .7 巨噬细胞。KC 还上调了 HO-1 的表达及其在 LPS 刺激的 RAW264.7 巨噬细胞中的活性。KC 在 LPS 刺激的 RAW264.7 巨噬细胞中上调 Nrf2 转录活性被证明是导致 HO-1 表达上调及其在 LPS 刺激的 RAW264.7 巨噬细胞中的活性的原因。在 HaCaT 细胞中，KC 通过上调涉及谷胱甘肽、超氧化物歧化酶和过氧化氢酶的内源性抗氧化防御系统来防止 DNA 损伤和细胞死亡，这些系统阻止了 HaCaT 细胞中由叔丁基过氧化氢 (tBHP) 诱导的氧化应激产生的活性氧。KC 对 PI3K-Akt 信号通路中 Nrf2 和 Akt 的上调激活被证明是 KC 在 HaCaT 细胞中的抗氧化应激活性的原因。总的来说，