Jieduquyuziyin Prescription Suppresses Inflammatory Activity of MRL/lpr Mice and Their Bone Marrow-Derived Macrophages via Inhibiting Expression of IRAK1-NF-κB Signaling Pathway
Jieduquyuziyin Prescription Suppresses Inflammatory Activity of MRL/lpr Mice and Their Bone Marrow-Derived Macrophages via Inhibiting Expression of IRAK1-NF-κB Signaling Pathway
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解毒祛瘀滋饮方通过抑制IRAK1-NF-kappa B信号通路表达抑制MRL/lpr小鼠及其骨髓源性巨噬细胞炎症活性
DOI：
10.3389/fphar.2020.01049
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发表时间：
2020-07-14
影响因子：
5.6
通讯作者：
Li, Rongqun
中科院分区：
文献类型：
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作者：
Ji, Lina;Fan, Xuemin;Li, Rongqun
解毒祛瘀子饮方用于治疗系统性红斑狼疮(SLE)。虽然JP治疗SLE的有效性已被临床证实，但其潜在的机制尚未完全清楚。我们观察了JP对MRL/LPR小鼠及其骨髓源性巨噬细胞(BMDM)的治疗作用，并探讨了其抑制炎症活性的可能机制。为评价JP的抗炎作用，用JP治疗MRL/LPR和MRL/MP小鼠的BMDM，并用JP治疗MRL/LPR小鼠8周。其中，JP及其处理血清进行了质量控制，并对BMDM进行了分离和鉴定。结果表明，在脂多糖(LPS)刺激的MRL/LPR小鼠BMDM的JP组，IL-6和肿瘤坏死因子-α(TNF-α)的分泌减少，IL-1受体相关激酶1(IRAK1)及其下游核因子-kappaB(NF-kappa B)途径的表达减少。同时，通过减轻肾脏病理损害，降低尿蛋白和血清抗dsDNA含量，抑制肿瘤坏死因子-α水平，进而抑制脾、肾组织中IRAK1-NF-kappaB的炎症信号，证实了JP的治疗作用。结果表明，JP可通过抑制IRAK1-NF-kappa B信号通路的激活，抑制MRL/LPR小鼠及其BMDM的炎症活动，有望成为治疗SLE的良好选择。
Jieduquyuziyin prescription (JP) has been used to treat systemic lupus erythematosus (SLE). Although the effectiveness of JP in the treatment of SLE has been clinically proven, the underlying mechanisms have yet to be completely understood. We observed the therapeutic actions of JP in MRL/lpr mice and their bone marrow-derived macrophages (BMDMs) and the potential mechanism of their inhibition of inflammatory activity. To estimate the effect of JP on suppressing inflammatory activity, BMDMs of MRL/lpr and MRL/MP mice were treated with JP-treated serum, and MRL/lpr mice were treated by JP for 8 weeks. Among them, JP and its treated serum were subjected to quality control, and BMDMs were separated and identified. The results showed that in the JP group of BMDMs stimulated by Lipopolysaccharide (LPS) in MRL/lpr mice, the secretion of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) reduced, and the expressions of Interleukin-1 receptor-associated kinase 1 (IRAK1) and its downstream nuclear factor kappa B (NF-kappa B) pathway decreased. Meanwhile, the alleviation of renal pathological damage, the decrease of urinary protein and serum anti-dsDNA contents, the inhibition of TNF-alpha level, and then the suppression of the IRAK1-NF-kappa B inflammatory signaling in the spleen and kidney, confirmed that the therapeutic effect of JP. These results demonstrated that JP could inhibit the inflammatory activity of MRL/lpr mice and their BMDMs by suppressing the activation of IRAK1-NF-kappa B signaling and was supposed to be a good choice for the treatment of SLE.