Mechanism of Huayu Jiedu Decoction in Inhibiting Malignant Biological Characteristics of Multiple Myeloma
10.19746/j.cnki.issn1009-2137.2024.05.021
- VernacularTitle:化瘀解毒汤抑制多发性骨髓瘤恶性生物学特性的作用机制
- Author:
Zuo-Tao LI
1
;
Hai-Liang LI
;
Zhi-Min YAN
;
Jie LIN
;
Xiao-Yun CHEN
;
Yan-Quan LIU
;
Yi-Li WANG
Author Information
1. 赣南医科大学第一附属医院重症医学科,江西赣州 341000
- Keywords:
Huayu Jiedu decoction;
multiple myeloma;
malignant biological characteristics;
anticancer mechanism
- From:
Journal of Experimental Hematology
2024;32(5):1438-1443
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To analyze and explore the effects of Huayu Jiedu Decoction on the malignant biological characteristics of multiple myeloma(MM)cells and its molecular mechanism,so as to provide experimental basis and theoretical basis for the alternative therapy of anti-MM in traditional Chinese medicine.Methods:Different concentrations of Huayu Jiedu Decoction were used to intervene myeloma U266 cells.The changes of cell proliferation activity were detected by CCK-8 assay,apoptosis was detected by Annexin V/PI double staining flow cytometry,and apoptosis and protein expression of related signaling pathways were detected by Western blot.Real-time quantitative PCR was used to detect mRNA expression changes of high mobility group protein B1(HMGB1),CXC chemokine receptor 4(CXCR4)and interleukin-6(IL-6).Results:Huayu Jiedu Decoction inhibited the proliferative activity of U266 cells and induced their apoptosis in a concentration and time dependent manner(r=-0.713,r=-0.827).After treatment with Huayu Jiedu Decoction for 48 h,the expressions of anti-apoptotic protein Bcl-2 and survivin were down-regulated,while the expression of pro-apoptotic protein Bax was up-regulated,and the phosphorylation level of TLR4/NF-κB signaling pathway was inhibited.After intervention of Huayu Jiedu decoction,the expressions of HMGB1 and IL-6 mRNA were significantly decreased,while the expression of CXCR4 was not significantly decreased.Conclusion:Huayu Jiedu Decoction can inhibit the proliferative activity of U266 cells and induce programmed death.Its molecular mechanism may be related to regulating the expression of apoptotic proteins,inhibiting the activation of TLR4/NF-κB pathway and down-regulating the expression of HMGB1 and IL-6 mRNA.
