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探讨 改善再生障碍性贫血造血功能的机制。

Exploring the mechanism by which improves haematopoietic function in aplastic anaemia.

机构信息

Department of Gerontology, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250014, China.

Department of Acupuncture, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250014, China.

出版信息

Aging (Albany NY). 2024 Jun 26;16(15):11535-11552. doi: 10.18632/aging.205971.

DOI:10.18632/aging.205971
PMID:39103204
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11346780/
Abstract

(AS) can improve the haematopoietic function, but the treatment mechanism is unknown. Transfusion dependency was estimated by Kaplan-Meier survival analyses and Cox proportional-hazard model in AS treated apalstic anemia (AA) patients. After that, the AA GEO database was analysed, the up differentially expressed genes (DEGs) of AA were combined with AS targets for the intersection of targets. After the AA mouse model was established, the effect of AS was confirmed by haematopoietic function tests. The same experiment plus mitochondrial apoptotic pathway tests were performed in polysaccharide (ASP)-treated mice, the key ingredient in AS. For experiment, bone marrow nucleated cells (BMNCs) were tested. Clinical data confirmed that the level of transfusion dependency and IL17A were lower in AS-users compared to non-AS users ( < 0.001). The intersection of targets between AA and AS most concentrated on inflammation and apoptosis. Then, the same effect was found in AS treated AA mice model. In both and tests, ASP demonstrated the ability to mitigate P38/MAPK-induced Bax-associated mitochondrial apoptosis, while also reducing the levels of activated Th17 cells and alleviating abnormal cytokine levels. So, the protective effect of AS and ASP on hematopoietic function lies in their ability to prevent apoptosis.

摘要

(AS) 可以改善造血功能,但治疗机制尚不清楚。通过 Kaplan-Meier 生存分析和 Cox 比例风险模型估计输血依赖在 AS 治疗再生障碍性贫血 (AA) 患者中的作用。然后,分析了 AA GEO 数据库,将 AA 的上调差异表达基因 (DEGs) 与 AS 靶点结合,寻找靶点的交集。在建立 AA 小鼠模型后,通过造血功能测试来验证 AS 的作用。在多糖 (ASP) 处理的小鼠中进行了相同的实验加线粒体凋亡途径测试,ASP 是 AS 的关键成分。对于实验,测试了骨髓有核细胞 (BMNCs)。临床数据证实,与非 AS 使用者相比,AS 使用者的输血依赖性和 IL17A 水平较低(<0.001)。AA 和 AS 之间的靶点交集最集中在炎症和凋亡上。然后,在 AS 治疗 AA 小鼠模型中也发现了相同的效果。在 和 测试中,ASP 证明了其减轻 P38/MAPK 诱导的 Bax 相关线粒体凋亡的能力,同时还降低了活化 Th17 细胞的水平并减轻了异常细胞因子水平。因此,AS 和 ASP 对造血功能的保护作用在于其预防凋亡的能力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/66683ba02ded/aging-16-205971-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/522f7ee1e743/aging-16-205971-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/281fc924321b/aging-16-205971-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/7261196dd232/aging-16-205971-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/f26a351a6285/aging-16-205971-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/deb813e936ea/aging-16-205971-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/f5e62b80e11d/aging-16-205971-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/47007037adba/aging-16-205971-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/66683ba02ded/aging-16-205971-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/522f7ee1e743/aging-16-205971-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/281fc924321b/aging-16-205971-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/7261196dd232/aging-16-205971-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/a4167934e156/aging-16-205971-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/f26a351a6285/aging-16-205971-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/deb813e936ea/aging-16-205971-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/f5e62b80e11d/aging-16-205971-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/47007037adba/aging-16-205971-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fea2/11346780/66683ba02ded/aging-16-205971-g009.jpg

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