连纳尔多肽通过上调细胞因子的产生并提高 CD4+、CD8+ 和 T 调节细胞的水平,减少小鼠模型中的免疫性血小板减少症。

IF 1.9 4区 医学 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
Zhaorong Yue, Fei Xie, Ruyue Wang, Xin Wang, Hongyu Li
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引用次数: 0

摘要

原发性免疫性血小板减少症(ITP)是一种以免疫介导的血小板产生不足或过度破坏为特征的疾病。本研究探讨了脾多肽注射液(Lienal polypeptide injection, LP)对抗体诱导ITP小鼠脾脏和胸腺T淋巴细胞亚群、骨髓巨核细胞计数以及与巨核细胞发育相关的细胞因子水平的影响,旨在阐明潜在的治疗机制。我们首先评估了LP对Meg-01巨核细胞增殖、凋亡和分化的影响,使用甲基噻唑基二苯基四唑溴化铵(MTT)检测、Western blot分析和流式细胞术检测细胞凋亡和CD41表达作为分化标志物。随后,以60 mg/(kg·d)的剂量给ITP小鼠腹腔注射LP,持续11天。我们量化外周血血小板和骨髓巨核细胞,测量脾脏和胸腺指数,并通过酶联免疫吸附试验(ELISA)评估血清干细胞因子(SCF)、白细胞介素-3 (IL-3)、白细胞介素-6 (IL-6)和血小板因子-4 (pf4)的水平。流式细胞术定量T辅助细胞(CD4+)、细胞毒性T细胞(CD8+)和调节性T细胞(Tregs)。LP显著诱导Meg-01细胞凋亡,但对细胞分化无明显影响。在ITP小鼠中,LP有效地阻止血小板下降,而不影响巨核细胞计数或成熟度。SCF、IL-3和IL-6水平升高以及PF-4水平降低与血小板生成增加相关。此外,CD4+/CD8+比值和Treg群体增加,有助于减少血小板破坏。综上所述,LP通过调节SCF、IL-3、IL-6和PF-4水平,恢复T细胞亚型的平衡,对ITP发挥保护作用,阐明了其治疗潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Lienal Polypeptide Decreases Immune Thrombocytopenia in a Mouse Model by Upregulating Cytokine Production and Increasing the Levels of CD4+, CD8+, and T Regulatory Cells.

Primary immune thrombocytopenia (ITP) is a condition marked by immune-mediated inadequate platelet production or excessive destruction. This study investigates the effects of Lienal polypeptide injection (LP) on T lymphocyte subgroups in the spleen and thymus, megakaryocyte counts in the bone marrow, and cytokine levels related to megakaryocyte development in mice with antibody-induced ITP, aiming to elucidate potential therapeutic mechanisms. We first assessed the effects of LP on Meg-01 megakaryocytic cells regarding proliferation, apoptosis, and differentiation using Methylthiazolyldiphenyl-tetrazolium bromide (MTT) assays, Western blot analysis, and flow cytometry for apoptosis and CD41 expression as a differentiation marker. Following this, LP was administered intraperitoneally at 60 mg/(kg·d) for 11 days to ITP mice. We quantified peripheral blood platelets and bone marrow megakaryocytes, measured spleen and thymus indices, and assessed serum levels of stem cell factor (SCF), interleukin-3 (IL-3), interleukin-6 (IL-6), and platelet factor-4 (PF-4) via enzyme-linked immunosorbent assay (ELISA). Flow cytometry quantified T-helper cells (CD4+), cytotoxic T cells (CD8+), and regulatory T cells (Tregs). LP significantly induced apoptosis in Meg-01 cells while not markedly affecting differentiation. In ITP mice, LP effectively prevented platelet decline without affecting megakaryocyte counts or maturity. Increased SCF, IL-3, and IL-6 levels, alongside decreased PF-4 levels, correlated with enhanced platelet production. Moreover, CD4+/CD8+ ratios and Treg populations increased, contributing to reduced platelet destruction. In conclusion, LP exerts a protective effect in ITP by modulating SCF, IL-3, IL-6, and PF-4 levels and restoring the balance of T cell subtypes, elucidating its therapeutic potential.

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来源期刊
CiteScore
3.80
自引率
0.00%
发文量
78
审稿时长
2.2 months
期刊介绍: Journal of Interferon & Cytokine Research (JICR) provides the latest groundbreaking research on all aspects of IFNs and cytokines. The Journal delivers current findings on emerging topics in this niche community, including the role of IFNs in the therapy of diseases such as multiple sclerosis, the understanding of the third class of IFNs, and the identification and function of IFN-inducible genes.
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