甘草查尔酮A通过激活线粒体依赖性凋亡途径抑制结直肠癌HT29细胞增殖研究<sup>★</sup>

doi:10.3969/j.issn.2095-1264.2025.05.11

首页 > 过刊浏览>2025年第15卷第5期 >656-663. DOI:10.3969/j.issn.2095-1264.2025.05.11

甘草查尔酮A通过激活线粒体依赖性凋亡途径抑制结直肠癌HT29细胞增殖研究★
DOI:
                        10.3969/j.issn.2095-1264.2025.05.11
                    
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作者单位:1.内蒙古医科大学，内蒙古 呼和浩特，010000;2.北京大学肿瘤医院内蒙古医院/内蒙古医科大学附属肿瘤 医院 放疗中心，内蒙古 呼和浩特，010000;3.内蒙古医科大学放射物理与放射生物重点实验室， 内蒙古 呼和浩特，010000;4.解放军92493部队医院 核医学肿瘤科，辽宁 葫芦岛，125000
作者简介:耿宏伟，女，硕士研究生，研究方向为肿瘤放射治疗。
通讯作者:杨昊，男，医学博士，副教授，研究方向为肿瘤放射治疗。
中图分类号:R735.3
基金项目:内蒙古医科大学平台建设项目（PIKY2023030）；公立医院科研联合基金科技项目（2023GLLHO136）；自治区卫生健康委2023年首府地区公立医院高水平临床专科建设科技项目（2023SGGZ114）。

Licochalcone A inhibits proliferation of HT29 colorectal cancer cells by activating the mitochondria-dependent apoptotic pathway^★

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1.Inner Mongolia Medical University, Huhhot, 010000, Inner Mongolia, China;2.Department of Radiation Oncology, Inner Mongolia Campus of Peking University Cancer Hospital/the Affiliated Cancer Hospital of Inner Mongolia Medical University, Huhhot, 010000, Inner Mongolia, China;3.Key Laboratoy of Radiation Physics and Biology of Inner Mongolia Medical University, Inner Mongolia Autonomous Region, Huhhot, 010000, Inner Mongolia, China;4.Department of Nuclear Medicine Oncology, 92493 Troop Hospital of the People's Liberation Army, Huludao, 125000, Liaoning, China

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摘要:

目的探讨甘草查尔酮A（LCA）对人结直肠癌HT29细胞凋亡的影响及相关分子机制。方法通过CCK-8实验检测不同药物浓度处理不同时间后HT29细胞的半数抑制浓度（IC₅₀），并筛选出最佳药物浓度和时间。EdU染色法检测LCA对细胞增殖的抑制作用，流式细胞术测定LCA对细胞凋亡的影响。Western blotting检测LCA对细胞内凋亡相关蛋白Bcl-2和Bcl-2相关X蛋白（Bax）表达的影响，透射电镜观察细胞线粒体结构变化。结果 CCK-8实验结果显示，24、48、72 h后，LCA对HT29细胞的IC₅₀值分别为154.3、20.14、7.943 μmol·L^-1。筛选后分别选择0、10、20、40 μmol·L^-1作为空白对照组（NC）、LCA低（Low）、中（Middle）、高（High）浓度组，处理48 h后用于后续实验。与对照组相比，LCA组细胞EdU阳性率显著降低（P<0.001），且浓度越高抑制效果越显著。流式结果显示，随着药物浓度增加，细胞凋亡率也增加（P<0.001）。Western blotting结果显示，与对照组相比，LCA组Bcl-2蛋白表达显著降低（P<0.001），Bax蛋白表达显著升高（P<0.05），且药物浓度越高，Bcl-2、Bax蛋白水平变化越明显，Bcl-2/Bax 比值降低越显著。透射电镜观察发现，LCA组细胞线粒体变形肿胀，嵴减少。结论 LCA可通过下调Bcl-2、上调Bax蛋白诱导人结直肠癌HT29细胞凋亡，并抑制其增殖。

Abstract:

Objective To investigate the effect of licochalcone A (LCA) on apoptosis in human colorectal cancer HT29 cells and to elucidate the underlying molecular mechanisms.Methods The half-maximal inhibitory concentration (IC??) of LCA against HT29 cells at different time points (24, 48, 72 h) was determined using the CCK-8 assay. Based on these results, an optimal treatment duration of 48 h and LCA concentrations of 0, 10, 20, and 40 μmol·L^-1 were selected for subsequent experiments, designated as the blank control (NC), low-, middle-, and high-concentration groups, respectively. The inhibitory effect of LCA on cell proliferation was assessed by EdU staining. Apoptosis was measured by flow cytometry. The expression levels of apoptosis-related proteins, Bcl-2 and Bax, were analyzed by Western blotting. Morphological changes in mitochondria were observed using transmission electron microscopy.Results The IC?? values of LCA for HT29 cells were 154.3, 20.14, and 7.943 μmol·L^-1 after 24, 48, and 72 hours of treatment, respectively. Compared to the control group, LCA treatment significantly reduced the EdU-positive rate in a dose-dependent manner (P<0.001). Flow cytometry confirmed that LCA induced apoptosis in a concentration-dependent fashion (P<0.001). Western blot analysis showed that LCA significantly downregulated Bcl-2 expression (P<0.001) and upregulated Bax expression (P<0.05), leading to a marked decrease in the Bcl-2/Bax ratio in a dose-dependent manner. Furthermore, transmission electron microscopy revealed characteristic mitochondrial damage in LCA-treated cells, including swelling, deformation, and a reduction in cristae.Conclusion Licochalcone A suppresses proliferation and induces apoptosis in human colorectal cancer HT29 cells, potentially through a mitochondrial pathway involving the regulation of Bcl-2 and Bax expression.