Li Zuo-Tao, Li Hai-Liang, Yan Zhi-Min, Lin Jie, Chen Xiao-Yun, Liu Yan-Quan, Wang Yi-Li
Department of Intensive Medicine, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, Jiangxi Province, China.
Department of Hematology, The First Affiliated Hospital of Gannan Medical University, Ganzhou 341000, Jiangxi Province, China.
Zhongguo Shi Yan Xue Ye Xue Za Zhi. 2024 Oct;32(5):1438-1443. doi: 10.19746/j.cnki.issn.1009-2137.2024.05.021.
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.
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).
Huayu Jiedu Decoction inhibited the proliferative activity of U266 cells and induced their apoptosis in a concentration and time dependent manner ( =-0.713, =-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 and mRNA were significantly decreased, while the expression of was not significantly decreased.
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 and mRNA.
分析探讨化瘀解毒方对多发性骨髓瘤（MM）细胞恶性生物学特性的影响及其分子机制，为中医药抗MM替代疗法提供实验依据和理论依据。
采用不同浓度的化瘀解毒方干预骨髓瘤U266细胞。采用CCK-8法检测细胞增殖活性变化，采用Annexin V/PI双染流式细胞术检测细胞凋亡，采用Western blot检测凋亡及相关信号通路蛋白表达。采用实时定量PCR检测高迁移率族蛋白B1（HMGB1）、CXC趋化因子受体4（CXCR4）和白细胞介素-6（IL-6）的mRNA表达变化。
化瘀解毒方抑制U266细胞的增殖活性，并呈浓度和时间依赖性诱导其凋亡（=-0.713，=-0.827）。化瘀解毒方处理48 h后，抗凋亡蛋白Bcl-2和survivin的表达下调，而促凋亡蛋白Bax的表达上调，TLR4/NF-κB信号通路的磷酸化水平受到抑制。化瘀解毒方干预后，和mRNA的表达明显降低，而的表达无明显降低。
化瘀解毒方能够抑制U266细胞的增殖活性并诱导程序性死亡。其分子机制可能与调节凋亡蛋白表达、抑制TLR4/NF-κB通路激活及下调和mRNA表达有关。
