Abstract：
OBJECTIVE: Macrophage-induced inflammation plays a key role in defense against injury and harmful pathogens. Autophagy and the inflammatory response are associated; however, the relationship between the autophagy pathway and lipopolysaccharide (LPS)- induced inflammatory responses remains unknown. We aimed to determine the effect of autophagy on the LPS-induced myeloid differentiation factor 88 (MyD88)/nuclear transcription factor kB (NF-kB) pathway-mediated inflammatory response in RAW264.7 cells.
METHODS: To determine the effect of autophagy on the LPS-induced inflammatory response, using various in vitro assays, we determined the effect of autophagy inhibitors and inducers on the inflammatory response in RAW264.7 cells.
RESULTS: Chloroquine (CQ), an autophagy inhibitor, suppressed pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor α (TNFα) in LPS-stimulated RAW264.7 cells. CQ also affected inflammatory mediators such as myeloid differentiation factor 88 and NF-kB in LPS-stimulated RAW264.7 cells.
CONCLUSIONS: This study demonstrated that CQ regulates the LPS-induced inflammatory response in RAW264.7 cells. We propose that targeting the regulation of pro-inflammatory cytokine levels and inflammatory mediators using CQ is a promising therapeutic approach for preventing inflammatory injury. CQ serves as a potential therapeutic target for treating various inflammatory diseases.
METHODS: To determine the effect of autophagy on the LPS-induced inflammatory response, using various in vitro assays, we determined the effect of autophagy inhibitors and inducers on the inflammatory response in RAW264.7 cells.
RESULTS: Chloroquine (CQ), an autophagy inhibitor, suppressed pro-inflammatory cytokines, including interleukin (IL)-1β, IL-6, and tumor necrosis factor α (TNFα) in LPS-stimulated RAW264.7 cells. CQ also affected inflammatory mediators such as myeloid differentiation factor 88 and NF-kB in LPS-stimulated RAW264.7 cells.
CONCLUSIONS: This study demonstrated that CQ regulates the LPS-induced inflammatory response in RAW264.7 cells. We propose that targeting the regulation of pro-inflammatory cytokine levels and inflammatory mediators using CQ is a promising therapeutic approach for preventing inflammatory injury. CQ serves as a potential therapeutic target for treating various inflammatory diseases.
摘要：
目的：巨噬细胞诱导的炎症在防御损伤和有害病原体中起关键作用。自噬和炎症反应是相关的;然而,自噬通路与脂多糖（LPS）诱导的炎症反应之间的关系尚不清楚。我们旨在确定自噬对LPS诱导的骨髓分化因子88（MyD88）/核转录因子kB（NF-kB）通路介导的RAW264.7细胞炎症反应的影响。
方法：为了确定自噬对LPS诱导的炎症反应的影响，使用各种体外试验，我们确定了自噬抑制剂和诱导剂对RAW264.7细胞炎症反应的影响.
结果：氯喹（CQ），自噬抑制剂，抑制促炎细胞因子，包括白细胞介素（IL）-1β，LPS刺激的RAW264.7细胞中的IL-6和肿瘤坏死因子α（TNFα）。CQ还影响LPS刺激的RAW264.7细胞中的炎症介质,如髓样分化因子88和NF-kB。
结论：本研究表明CQ调节LPS诱导的RAW264.7细胞炎症反应。我们建议使用CQ靶向调节促炎细胞因子水平和炎性介质是预防炎性损伤的有希望的治疗方法。CQ作为治疗各种炎性疾病的潜在治疗靶标。
方法：为了确定自噬对LPS诱导的炎症反应的影响，使用各种体外试验，我们确定了自噬抑制剂和诱导剂对RAW264.7细胞炎症反应的影响.
结果：氯喹（CQ），自噬抑制剂，抑制促炎细胞因子，包括白细胞介素（IL）-1β，LPS刺激的RAW264.7细胞中的IL-6和肿瘤坏死因子α（TNFα）。CQ还影响LPS刺激的RAW264.7细胞中的炎症介质,如髓样分化因子88和NF-kB。
结论：本研究表明CQ调节LPS诱导的RAW264.7细胞炎症反应。我们建议使用CQ靶向调节促炎细胞因子水平和炎性介质是预防炎性损伤的有希望的治疗方法。CQ作为治疗各种炎性疾病的潜在治疗靶标。
