Consumption of anti-inflammatory nutraceuticals may help treat or prevent inflammation-related illnesses such as diabetes, cardiovascular disease, and cancer. This study evaluated the effect of Croton hirtus L'Hér extract (CHE) on lipopolysaccharide (LPS)-induced nitric oxide (NO) production and nuclear factor kappa-B (NF-κB) signaling cascades. CHE significantly suppressed LPS-induced NO production and inducible nitric oxide synthase (iNOS) expression in RAW264.7 macrophages, although cyclooxygenase (COX)-2 expression was not affected. CHE also suppressed LPS-induced IκB kinase (IKK), IκB, and p65 phosphorylation in RAW264.7 cells. Western blot and immunofluorescence assays of cytosol and nuclear p65 and the catalytic subunit of NF-κB showed that CHE suppressed LPS-induced p65 translocation from the cytosol to the nucleus. CHE also suppressed LPS-induced Interleukin (IL)-6 and tumor necrosis factor (TNF)-α production in RAW264.7 cells. These results suggest that CHE prevents NO-mediated inflammation by suppressing NF-κB and inflammatory cytokines.

中文翻译：

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Croton hirtus L'Hér 提取物通过抑制 NF-κB 信号通路预防 RAW264.7 巨噬细胞的炎症。

服用抗炎营养品可能有助于治疗或预防与炎症相关的疾病，例如糖尿病、心血管疾病和癌症。本研究评估了Croton hirtus L'Hér的效果提取物 (CHE) 对脂多糖 (LPS) 诱导的一氧化氮 (NO) 产生和核因子 kappa-B (NF-κB) 信号级联反应的影响。CHE 显着抑制 RAW264.7 巨噬细胞中 LPS 诱导的 NO 产生和诱导型一氧化氮合酶 (iNOS) 表达，尽管环氧合酶 (COX)-2 表达不受影响。CHE 还抑制 RAW264.7 细胞中 LPS 诱导的 IκB 激酶 (IKK)、IκB 和 p65 磷酸化。细胞质和细胞核 p65 以及 NF-κB 催化亚基的蛋白质印迹和免疫荧光分析表明，CHE 抑制了 LPS 诱导的 p65 从细胞质到细胞核的易位。CHE 还抑制 RAW264.7 细胞中 LPS 诱导的白细胞介素 (IL)-6 和肿瘤坏死因子 (TNF)-α 的产生。这些结果表明，CHE 通过抑制 NF-κB 和炎性细胞因子来预防 NO 介导的炎症。