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ORIGINAL ARTICLE
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Quercetin-3-O-β-D-glucuronide inhibits mitochondria pathway-mediated platelet apoptosis via the phosphatidylinositol-3-kinase/AKT pathway in immunological bone marrow failure


1 Department of Hematology, Jing' an District Centre Hospital of Shanghai (Jing' an Branch, Huashan Hospital, Fudan University); Department of Hematology, Shanghai Bao' shan Hospital of Integrated Traditional Chinese and Western Medicine (Bao' shan Branch of Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine), Shanghai, China
2 Department of Hematology, Shanghai Bao' shan Hospital of Integrated Traditional Chinese and Western Medicine (Bao' shan Branch of Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine), Shanghai, China
3 Department of Hematology, Jing' an District Centre Hospital of Shanghai (Jing' an Branch, Huashan Hospital, Fudan University), Shanghai, China
4 Department of Hematology Laboratory, Singapore General Hospital, Singapore

Correspondence Address:
He-Ping Yu,
Department of Hematology, Jing' an District Centre Hospital of Shanghai (Jing' an Branch, Huashan Hospital, Fudan University), Shanghai 200040
China
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/wjtcm.wjtcm_44_21

Objective: Quercetin-3-O-β-D-glucuronide (QG) can alleviate immunological bone marrow failure (BMF) by increasing platelet counts. However, the principal mechanism is less known. This study aimed at deciphering the possible underlying mechanism of QG that is indicated in thrombocytopenic purpura. Methods: In vitro and in vivo experiments were carried out for investigating the mechanism behind QG-facilitated inhibition of mitochondrial pathway-mediated excessive apoptosis of platelets through the phosphatidylinositol-3-kinase (PI3K)/AKT pathway. Results: Our results revealed that QG, the main effective ingredient of Herba Sarcandrae, increases the number of platelets and decreases the expression of Bax, Bad, Bid, and caspase-9 in immunological BMF, indicating the inhibition of mitochondrial pathway-mediated apoptosis. Moreover, we found that the protein and mRNA expressions, as well as the phosphorylated levels of PI3K and AKT, were increased significantly by QG, suggesting the activation of the PI3K/AKT pathway. Furthermore, the inhibition of the PI3K/AKT pathway by LY294002 antagonizes the effects of QG on platelet counts and mitochondrial pathway-mediated apoptosis. Conclusion: We demonstrate that QG inhibits the mitochondria pathway-mediated platelet apoptosis via the PI3K/AKT pathway in immunological BMF. This study thus sheds light on exploring the possible regulatory mechanism of traditional Chinese medicine in the treatment of thrombocytopenia induced by BMF.


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