鹿茸干细胞的条件培养基可能通过抑制 NF-κB 信号通路有效缓解 1 型糖尿病

Dongxu Wang, Jing Ren, Jiping Li, Xiuying Li, Jinchi Ying, Tiantian Jiang, Zhen Wang, Zheng Pan, Qianqian Guo, Chunyi Li, Guokun Zhang
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摘要

背景:1 型糖尿病(T1D)严重威胁人类健康。持续的高血糖和血脂异常可导致肝功能受损,而目前尚缺乏针对这些并发症的有效干预措施。鹿茸干细胞(AnSCs)是一种新型成体干细胞,可显著减轻肝损伤,据推测这是通过旁分泌途径实现的。方法:本研究利用鹿茸干细胞条件培养基(AnSC-CM)治疗由链脲佐菌素(STZ)诱发的C57BL/6小鼠T1D症状。评估了 AnSC-CM 对 T1D 的治疗效果,并研究了其潜在机制。结果:AnSC-CM 可减轻 T1D 症状:体重下降、血糖水平升高、胰岛病变和胰岛素分泌减少。此外,AnSC-CM 还能改善 T1D 小鼠的肝功能,减轻肝损伤。令人印象深刻的是,AnSC-CM对T1D的治疗效果优于骨髓间充质干细胞-CM(BMSC-CM)。机理研究显示,AnSC-CM能显著下调胰腺和肝脏组织中的NF-κ B信号通路。结论 :AnSC-CM 对 STZ 诱导的 T1D 和肝损伤的治疗作用可能是通过靶向 NF-κ B 信号通路实现的。
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Conditioned Media from Deer Antler Stem Cells Effectively Alleviate Type 1 Diabetes Mellitus Possibly via Inhibiting the NF-κB Signaling Pathway
Background : Type 1 diabetes mellitus (T1D) represents a severe threat to human health. Persistent hyperglycemia and dyslipidemia can lead to damaged liver function, while effective interventions for these complications are currently lacking. Deer antler stem cells (AnSCs), a novel type of adult stem cells, significantly reduced liver injury, which was speculated to be achieved through the paracrine pathway. Methods : In this study, AnSC-conditioned medium (AnSC-CM) was used to treat C57BL/6 mice with T1D symptoms induced by streptozotocin (STZ). The therapeutic effects of AnSC-CM on T1D were evaluated, and the underlying mechanism was investigated. Results : It was shown that AnSC-CM alleviated the T1D symptom: decreased body weight, increased blood glucose levels and islet lesions, and reduced insulin secretion. Moreover, AnSC-CM treatment improved liver function and mitigated liver injury in T1D mice. Impressively, the therapeutic effects of AnSC-CM on T1D were better than those of bone marrow mesenchymal stem cell-CM (BMSC-CM). The mechanistic study revealed that AnSC-CM significantly downregulated the NF-κ B signaling pathway in both pancreatic and liver tissues. Conclusions : Therapeutic effects of AnSC-CM on STZ-induced T1D and liver injury may be achieved through targeting the NF-κ B signaling pathway.
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