Macrophages are crucial players in a variety of inflammatory responses to environmental cues. However, it has been widely reported that macrophages cause chronic inflammation and are involved in a variety of diseases, such as obesity, diabetes, metabolic syndrome, and cancer. In this study, we report the suppressive effect of 5-aminolevulinic acid (ALA), via the HO-1-related system, on the immune response of the LPS-stimulated mouse macrophage cell line RAW264.7. RAW264.7 cells were treated with LPS with or without ALA, and proinflammatory mediator expression levels and phagocytic ability were assessed. ALA treatment resulted in the attenuation of iNOS and NO expression and the downregulation of proinflammatory cytokines (TNF-α, cyclooxygenase2, IL-1β, IL-6). In addition, ALA treatment did not affect the phagocytic ability of macrophages. To our knowledge, this study is the first to investigate the effect of ALA on macrophage function. Our findings suggest that ALA may have high potential as a novel anti-inflammatory agent. In the present study, we showed that exogenous addition of ALA induces HO-1 and leads to the downregulation of NO and some proinflammatory cytokines. These findings support ALA as a promising anti-inflammatory agent.

中文翻译：

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5-氨基乙酰丙酸调节 LPS 刺激的 RAW 264.7 巨噬细胞的免疫反应


巨噬细胞在环境因素引起的各种炎症反应中发挥着重要作用。然而，据广泛报道，巨噬细胞会引起慢性炎症，并与多种疾病有关，如肥胖、糖尿病、代谢综合征和癌症。在这项研究中，我们报告了 5-氨基乙酰丙酸 (ALA) 通过 HO-1 相关系统对 LPS 刺激的小鼠巨噬细胞系 RAW264.7 的免疫反应的抑制作用。用含有或不含 ALA 的 LPS 处理 RAW264.7 细胞，并评估促炎介质表达水平和吞噬能力。 ALA 治疗导致 iNOS 和 NO 表达减弱，促炎细胞因子（TNF-α、环氧合酶 2、IL-1β、IL-6）下调。此外，ALA处理并不影响巨噬细胞的吞噬能力。据我们所知，这项研究是第一个研究 ALA 对巨噬细胞功能的影响的研究。我们的研究结果表明 ALA 可能具有作为新型抗炎剂的巨大潜力。在本研究中，我们发现外源添加 ALA 会诱导 HO-1 并导致 NO 和一些促炎细胞因子的下调。这些发现支持 ALA 作为一种有前途的抗炎剂。