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Ocotillol-Type Pseudoginsenoside-F11 Alleviates Lipopolysaccharide-Induced Acute Kidney Injury through Regulation of Macrophage Function by Suppressing the NF-κB/NLRP3/IL-1β Signaling Pathway
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2024-09-06 , DOI: 10.1021/acs.jafc.4c05185 Yaru Wang 1 , Jinyu Zhang 1 , Zhuo Yang 2 , Changcheng Li 1 , Chenming Zhang 3 , Shengkai Sun 2 , Ziyan Jiao 2 , Guanghua Che 2 , Hang Gao 1 , Jinping Liu 4 , Jing Li 1
Journal of Agricultural and Food Chemistry ( IF 5.7 ) Pub Date : 2024-09-06 , DOI: 10.1021/acs.jafc.4c05185 Yaru Wang 1 , Jinyu Zhang 1 , Zhuo Yang 2 , Changcheng Li 1 , Chenming Zhang 3 , Shengkai Sun 2 , Ziyan Jiao 2 , Guanghua Che 2 , Hang Gao 1 , Jinping Liu 4 , Jing Li 1
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Acute kidney injury (AKI) is characterized by a sudden decline in renal function. The inflammatory response is the fundamental pathologic alteration throughout AKI, regardless of the various causal factors. Macrophages are the main immune cells involved in the inflammatory microenvironment in AKI. Consequently, targeting macrophages might become a novel strategy for the treatment of AKI. In this study, we demonstrated that pseudoginsenoside-F11 (PF11), a distinctive component of Panax quinquefolius L., regulated macrophage function and protected renal tubular epithelial cells TCMK-1 from lipopolysaccharide (LPS) in vitro. PF11 also alleviated renal injuries in an LPS-induced AKI mouse model, decreased the levels of inflammatory cytokines, reduced macrophage inflammatory infiltration, and promoted the polarization of M1 macrophages to M2c macrophages with suppression of the nuclear factor-κB/NOD-like receptor thermal protein domain-associated protein 3/interleukin-1β (NF-κB/NLRP3/IL-1β) signaling pathway. To further investigate whether this nephroprotective effect of PF11 is mediated by macrophages, we performed macrophage depletion by injection of clodronate liposomes in mice. Macrophage depletion abolished PF11’s ability to protect against LPS-induced kidney damage with downregulating the NF-κB/NLRP3/IL-1β signaling pathway. In summary, this is the first study providing data on the efficacy and mechanism of PF11 in the treatment of AKI by regulating macrophage function.
中文翻译：
Ocotillol 型伪人参皂苷-F11 通过抑制 NF-κB/NLRP3/IL-1β 信号通路调节巨噬细胞功能减轻脂多糖诱导的急性肾损伤
急性肾损伤（AKI）的特点是肾功能突然下降。无论各种致病因素如何，炎症反应是整个 AKI 的基本病理改变。巨噬细胞是参与 AKI 炎症微环境的主要免疫细胞。因此，靶向巨噬细胞可能成为治疗 AKI 的新策略。在这项研究中，我们证明了西洋参的独特成分假人参皂苷-F11 (PF11)，在体外可调节巨噬细胞功能并保护肾小管上皮细胞 TCMK-1 免受脂多糖 (LPS) 的影响。 PF11 还可以减轻 LPS 诱导的 AKI 小鼠模型中的肾损伤，降低炎症细胞因子的水平，减少巨噬细胞炎症浸润，并通过抑制核因子-κB/NOD 样受体热促进 M1 巨噬细胞极化为 M2c 巨噬细胞。蛋白结构域相关蛋白 3/IL-1β (NF-κB/NLRP3/IL-1β) 信号通路。为了进一步研究 PF11 的这种肾保护作用是否是由巨噬细胞介导的，我们通过向小鼠注射氯膦酸盐脂质体来去除巨噬细胞。巨噬细胞耗竭消除了 PF11 通过下调 NF-κB/NLRP3/IL-1β 信号通路来防止 LPS 诱导的肾脏损伤的能力。总之，这是第一项提供PF11通过调节巨噬细胞功能治疗AKI的功效和机制数据的研究。
更新日期：2024-09-06
中文翻译：
Ocotillol 型伪人参皂苷-F11 通过抑制 NF-κB/NLRP3/IL-1β 信号通路调节巨噬细胞功能减轻脂多糖诱导的急性肾损伤
急性肾损伤（AKI）的特点是肾功能突然下降。无论各种致病因素如何，炎症反应是整个 AKI 的基本病理改变。巨噬细胞是参与 AKI 炎症微环境的主要免疫细胞。因此，靶向巨噬细胞可能成为治疗 AKI 的新策略。在这项研究中，我们证明了西洋参的独特成分假人参皂苷-F11 (PF11)，在体外可调节巨噬细胞功能并保护肾小管上皮细胞 TCMK-1 免受脂多糖 (LPS) 的影响。 PF11 还可以减轻 LPS 诱导的 AKI 小鼠模型中的肾损伤，降低炎症细胞因子的水平，减少巨噬细胞炎症浸润，并通过抑制核因子-κB/NOD 样受体热促进 M1 巨噬细胞极化为 M2c 巨噬细胞。蛋白结构域相关蛋白 3/IL-1β (NF-κB/NLRP3/IL-1β) 信号通路。为了进一步研究 PF11 的这种肾保护作用是否是由巨噬细胞介导的，我们通过向小鼠注射氯膦酸盐脂质体来去除巨噬细胞。巨噬细胞耗竭消除了 PF11 通过下调 NF-κB/NLRP3/IL-1β 信号通路来防止 LPS 诱导的肾脏损伤的能力。总之，这是第一项提供PF11通过调节巨噬细胞功能治疗AKI的功效和机制数据的研究。
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