[1]李琳婵,鱼麦侠,王松海.葛根素对肝癌小鼠肝细胞氧化应激损伤的干预机制研究[J].西部中医药,2025,38(11):8-11.[doi:10.12174/j.issn.2096-9600.2025.11.02]
　LI Linchan,YU Maixia,WANG Songhai.Study on Intervention Mechanism of Puerarin on Oxidative Stress Injury in Hepatocytes of Liver Cancer Mice[J].Western Journal of Traditional Chinese Medicine,2025,38(11):8-11.[doi:10.12174/j.issn.2096-9600.2025.11.02]
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葛根素对肝癌小鼠肝细胞氧化应激损伤的干预机制研究()

《西部中医药》[ISSN:2096-9600/CN:62-1204/R]

卷:
38
期数:
2025年11期
页码:
8-11
栏目:
基础研究
出版日期:
2025-11-15

文章信息/Info

Title:
Study on Intervention Mechanism of Puerarin on Oxidative Stress Injury in Hepatocytes of Liver Cancer Mice
作者:
李琳婵1, 鱼麦侠1, 王松海2
1.陕西省中医医院,恶性肿瘤固本培元法重点研究室，陕西 西安 710003
2.陕西省中医医院，陕西 西安 710003
Author(s):
LI Linchan1, YU Maixia1, WANG Songhai2
1.Key Research Laboratory for Fortifying the Root and Nourishing the Essence in Malignant Tumors, Shaanxi Provincial TCM Hospital, Xi’an 710003, China
2.Shaanxi Provincial TCM Hospital, Xi’an 710003, China
关键词:
肝癌; 葛根素; 氧化应激损伤; 小鼠; 实验
Keywords:
liver cancer; puerarin; oxidative stress injury; mice; experiment
分类号:
R285
DOI:
10.12174/j.issn.2096-9600.2025.11.02
文献标志码:
A
摘要:
目的探究葛根素对肝癌小鼠肝细胞氧化应激损伤的干预作用，以及对骨形态发生蛋白9（bone morphogenetic protein-9，BMP-9）、血管内皮生长因子165（vascular endothelial growth factor-165，VEGF-165）表达的调控机制。 方法将36只小鼠按照随机数字法分为空白组、模型组及实验组，每组12只。小鼠适应性饲养1周后，模型组与实验组通过左侧腋窝皮下注射人肝癌HuH-7细胞悬液建立肝癌模型，空白组不造模。造模成功后，空白组与模型组每日腹腔注射生理盐水，实验组每日腹腔注射葛根素注射液。连续干预4周后，检测各组小鼠血清活性氧（reactive oxygen species，ROS）、超氧化物歧化酶（superoxide dismutase，SOD）、血清丙二醛（malondialdehyde，MDA）及谷胱甘肽过氧化物酶（glutathione peroxidase，GSH）表达水平；苏木精-伊红染色法（hematoxylin-eosin staining，HE）观察各组小鼠肝组织病理学变化情况；通过逆转录聚合酶链式反应（reverse transcription polymerase chain reaction，RT-PCR）及蛋白免疫印迹法（western blot，WB）检测各组小鼠肝组织中BMP-9、VEGF-165 mRNA及蛋白表达情况。 结果与空白组比较，模型组小鼠肝组织细胞损伤严重，血清ROS、MDA水平升高，SOD、GSH水平降低（均P＜0.05）；肝组织BMP-9、VEGF-165的mRNA及蛋白表达升高（P＜0.05）。与模型组比较，实验组小鼠肝组织细胞形态明显改善，血清ROS、MDA水平降低，SOD、GSH水平回升（P＜0.05），肝细胞氧化应激损伤明显缓解；肝组织BMP-9、VEGF-165的mRNA及蛋白表达下调（P＜0.05）。 结论葛根素可改善肝癌小鼠肝细胞氧化应激损伤，这可能是与葛根素调控BMP-9、VEGF-165表达有关。
Abstract:
ObjectiveTo explore the intervention effects of puerarin on oxidative stress injury in hepatocytes of liver cancer mice, and its mechanism of regulating the expressions of BMP-9 and VEGF-165. MethodsA total of 36 mice were allocated to blank group, model group and experiment group with 12 in each according to random number method. After one week of adaptive feeding, the mice in the model group and the experiment group were established into liver cancer models by hypodermic injection of human hepatocellular carcinoma HuH-7 cell suspension into left armpit, and the blank group was unhandled. After successfully modeling, the blank group and the model group received peritoneal injection of physiological saline each day, and puerarin injection was given to the experiment group every day. After four consecutive weeks of the intervention, to detect the expressions of ROS, SOD, MDA and GSH in the mice of different groups; HE was used to observe pathological changes of liver tissue in the mice of different groups; RT-PCR and WB were applied to measure the levels of BMP-9, VEGF-165 mRNA and protein in different groups. ResultsCompared with the blank group, liver tissue cells were severely damaged in the model group, an increase in ROS and MDA, and a decrease in SOD and GSH were found (all P<0.05); the expressions of BMP-9, VEGF-165 mRNA and protein were elevated in liver tissue (P<0.05). Compared with the model group, the changes including significant improvement of liver tissue cell morphology, the decrease in the levels of serum ROS and MDA, and the increase in the levels of SOD and GSH were seen in the experiment group (P<0.05), oxidative stress injury of hepatic cells was relieved obviously; the expressions of BMP-9, VEGF-165 mRNA and protein were reduced in liver tissue (P<0.05). ConclusionPuerarin could improve oxidative stress injury in liver cancer mice, and it might be related to the regulation of BMP-9 and VEGF-165 expression by puerarin.

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备注/Memo

备注/Memo:
陕西省重点研发计划项目（2020SF-348）；陕西省中医药管理局中医药科研课题（2019-LC014）。李琳婵（1989—），女，硕士学位，主治医师。研究方向：恶性肿瘤的防治。
更新日期/Last Update: 2025-11-15