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Immunoenhancing Effects of Cyclina sinensis Pentadecapeptide through Modulation of Signaling Pathways in Mice with Cyclophosphamide-Induced Immunosuppression

机译:Cyclina sinensis Pentadecapeptide 通过调节环磷酰胺诱导的免疫抑制小鼠信号通路的免疫增强作用

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摘要

Our study aimed to investigate the immune-enhancing mechanism of the pentadecapeptide (RVAPEEHPVEGRYLV) from Cyclina sinensis (SCSP) in a cyclophosphamide (CTX)-induced murine model of immunosuppression. Our results showed that SCSP treatment significantly increased mouse body weight, immune organ indices, and the production of serum IL-6, IL-1β, and tumor necrosis factor (TNF)-α in CTX-treated mice. In addition, SCSP treatment enhanced the proliferation of splenic lymphocytes and peritoneal macrophages, as well as phagocytosis of the latter in a dose-dependent manner. Moreover, SCSP elevated the phosphorylation levels of p38, ERK, JNK, PI3K and Akt, and up-regulated IKKα, IKKβ, p50 NF-κB and p65 NF-κB protein levels, while down-regulating IκBα protein levels. Our results indicate that SCSP has immune-enhancing activities, and that it can activate the MAPK/NF-κB and PI3K/Akt pathways to enhance immunity in CTX-induced immunosuppressed mice.
机译:本研究旨在探讨环磷酰胺 (CTX) 诱导的免疫抑制小鼠模型中 Cyclina sinensis (SCSP) 的十五肽 (RVAPEEHPVEGRYLV) 的免疫增强机制。我们的结果表明,SCSP 处理显着增加了小鼠体重、免疫器官指数以及 CTX 处理小鼠血清 IL-6 、 IL-1β 和肿瘤坏死因子 (TNF) -α 的产生。此外,SCSP 处理以剂量依赖性方式增强了脾淋巴细胞和腹膜巨噬细胞的增殖以及后者的吞噬作用。此外,SCSP 提高了 p38 、 ERK 、 JNK 、 PI3K 和 Akt 的磷酸化水平,上调了 IKKα 、 IKKβ 、 p50 NF-κB 和 p65 NF-κB 蛋白水平,同时下调了 IκBα 蛋白水平。我们的结果表明,SCSP 具有免疫增强活性,它可以激活 MAPK/NF-κB 和 PI3K/Akt 通路以增强 CTX 诱导的免疫抑制小鼠的免疫力。

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