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芪胶升白胶囊通过Bcl2/Bax/CASAPSE3通路治疗白细胞减少症的机制研究

Mechanistic study of leukopenia treatment by Qijiao shengbai Capsule via the Bcl2/Bax/CASAPSE3 pathway.

作者信息

Jiang Siyue, Wang Pengjiao, Sun Xiaodong, Zhang Min, Zhang Shuo, Cao Yu, Wang Yuben, Liu Li, Gao Xiuli

机构信息

State Key Laboratory of Functions and Applications of Medicinal Plants and School of Pharmacy, Guizhou Medical University, Guiyang, China.

Center of Microbiology and Biochemical Pharmaceutical Engineering, Guizhou Medical University, Guiyang, China.

出版信息

Front Pharmacol. 2024 Sep 4;15:1451553. doi: 10.3389/fphar.2024.1451553. eCollection 2024.

DOI:10.3389/fphar.2024.1451553
PMID:39295929
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11408280/
Abstract

BACKGROUND

Leukopenia can be caused by chemotherapy, which suppresses bone marrow function and can impact the effectiveness of cancer treatment. Qijiao Shengbai Capsule (QJSB) is commonly used to treat leukopenia, but the specific bioactive components and mechanisms of action are not well understood.

OBJECTIVES AND RESULTS

This study aimed to analyze the active ingredients of QJSB and its potential targets for treating leukopenia using network pharmacology and molecular docking. Through a combination of serum pharmacochemistry, multi-omics, network pharmacology, and validation experiments in a murine leukopenia model, the researchers sought to understand how QJSB improves leukopenia. The study identified 16 key components of QJSB that act to increase the number of white blood cells in leukopenic mice. Multi-omics analysis and network pharmacology revealed that the PI3K-Akt and MAPK signaling pathways are important in the treatment of leukopenia with QJSB. Five specific targets (JUN, FOS, BCl-2, CASPAS-3) were identified as key targets.

CONCLUSION

Validation experiments confirmed that QJSB regulates genes related to cell growth and inhibits apoptosis, suggesting that apoptosis may play a crucial role in leukopenia development and that QJSB may improve immune function by regulating apoptotic proteins and increasing CD4 T cell count in leukopenic mice.

摘要

背景

白细胞减少症可由化疗引起，化疗会抑制骨髓功能，并可能影响癌症治疗的效果。芪胶升白胶囊（QJSB）常用于治疗白细胞减少症，但其具体的生物活性成分和作用机制尚不清楚。

目的与结果

本研究旨在利用网络药理学和分子对接技术分析芪胶升白胶囊的活性成分及其治疗白细胞减少症的潜在靶点。通过血清药物化学、多组学、网络药理学以及在小鼠白细胞减少模型中的验证实验相结合的方法，研究人员试图了解芪胶升白胶囊如何改善白细胞减少症。该研究确定了芪胶升白胶囊的16种关键成分，这些成分可增加白细胞减少小鼠的白细胞数量。多组学分析和网络药理学表明，PI3K-Akt和MAPK信号通路在芪胶升白胶囊治疗白细胞减少症中起重要作用。确定了五个特定靶点（JUN、FOS、BCl-2、CASPAS-3）为关键靶点。

结论

验证实验证实，芪胶升白胶囊调节与细胞生长相关的基因并抑制细胞凋亡，这表明细胞凋亡可能在白细胞减少症的发生发展中起关键作用，且芪胶升白胶囊可能通过调节凋亡蛋白和增加白细胞减少小鼠的CD4 T细胞计数来改善免疫功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/9776c4457626/fphar-15-1451553-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/914e9c5a4af6/fphar-15-1451553-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/b9ad48bcf95e/fphar-15-1451553-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/68c2d7212ec9/fphar-15-1451553-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/bd1248c65819/fphar-15-1451553-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/c4fe9e7ee77c/fphar-15-1451553-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/e8867de1fc14/fphar-15-1451553-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/15aec579aa85/fphar-15-1451553-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/84ebbbb901ee/fphar-15-1451553-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/9776c4457626/fphar-15-1451553-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/914e9c5a4af6/fphar-15-1451553-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/b9ad48bcf95e/fphar-15-1451553-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/68c2d7212ec9/fphar-15-1451553-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/bd1248c65819/fphar-15-1451553-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/c4fe9e7ee77c/fphar-15-1451553-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/e8867de1fc14/fphar-15-1451553-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/15aec579aa85/fphar-15-1451553-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/84ebbbb901ee/fphar-15-1451553-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e4fb/11408280/9776c4457626/fphar-15-1451553-g009.jpg

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