雷公藤红素对肝癌细胞氧化应激和衰老的调控作用

doi:10.11958/20260496

天津医药 ›› 2026, Vol. 54 ›› Issue (7): 681-686.doi: 10.11958/20260496

雷公藤红素对肝癌细胞氧化应激和衰老的调控作用

付楠楠¹^,²(), 刘涛³, 李娟¹^,², 赵煜¹^,²^,^△()

¹ 天津大学儿童医院（天津市儿童医院）消化科（邮编300134）
² 天津市儿童出生缺陷防治重点实验室（邮编300134）
³ 天津市第一中心医院国家卫生健康委员会危重病急救医学重点实验室

收稿日期:2026-02-24 修回日期:2026-04-15 出版日期:2026-07-15 发布日期:2026-07-13
通讯作者: ^△E-mail：zhaoyu1617@126.com
作者简介:付楠楠（1988），女，主治医师，主要从事消化系统疾病的细胞生物学方面研究。E-mail：funannan8802@126.com
基金资助:
天津市医学重点学科建设项目(TJYXZDXK-3-016B)

Regulative effect of tripterine on oxidative stress and senescence in hepatocellular carcinoma cells

FU Nannan¹^,²(), LIU Tao³, LI Juan¹^,², ZHAO Yu¹^,²^,^△()

¹ Gastroenterology Department, Children’s Hospital, Tianjin University (Tianjin Children’s Hospital), Tianjin 300134, China
² Tianjin Key Laboratory of Birth Defects for Prevention and Treatment, Children’s Hospital, Tianjin University (Tianjin Children’s Hospital), Tianjin 300134, China
³ National Health Commission’s Key Laboratory of Critical Care Medicine,Tianjin First Central Hospital

Received:2026-02-24 Revised:2026-04-15 Published:2026-07-15 Online:2026-07-13
Contact: ^△E-mail：zhaoyu1617@126.com

付楠楠, 刘涛, 李娟, 赵煜. 雷公藤红素对肝癌细胞氧化应激和衰老的调控作用[J]. 天津医药, 2026, 54(7): 681-686.

FU Nannan, LIU Tao, LI Juan, ZHAO Yu. Regulative effect of tripterine on oxidative stress and senescence in hepatocellular carcinoma cells[J]. Tianjin Medical Journal, 2026, 54(7): 681-686.

摘要/Abstract

摘要：

目的探讨雷公藤红素对氧化应激和衰老状态下肝细胞癌（HCC）细胞的调控作用。方法体外常规培养Huh-7人HCC细胞系，用梯度浓度（0、0.25、0.5、1、2、4 μmol/L）的雷公藤红素处理细胞，CCK-8细胞活性实验确定不影响细胞活性的最高药物浓度。实验分为对照组、H₂O₂组、H₂O₂+DMSO组、H₂O₂+雷公藤红素组。β-半乳糖苷酶染色实验检测细胞衰老程度，DCFH-DA荧光探针法检测细胞内的活性氧（ROS）水平，萤光素酶催化法检测细胞内腺苷三磷酸（ATP）的水平，MitoSO Red荧光探针法检测细胞线粒体内超氧化物的含量，JC-1荧光探针法检测细胞线粒体内的膜电位水平。结果雷公藤红素的浓度为0.5 μmol/L时，是不影响HCC细胞系Huh-7活性的最高药物浓度，用于后续实验。与对照组相比，H₂O₂组细胞衰老程度增加，细胞内ROS水平升高，ATP水平降低，细胞线粒体内超氧化物水平增加，线粒体膜电位降低（均P<0.05）。与H₂O₂+DMSO组相比，H₂O₂+雷公藤红素组细胞衰老程度减轻，细胞内ROS水平降低，ATP水平升高，细胞线粒体内超氧化物水平降低，线粒体膜电位升高（均P<0.05）。结论雷公藤红素能减轻HCC细胞的氧化应激及其诱导的细胞衰老，并减轻线粒体损伤。

关键词: 雷公藤红素, 癌, 肝细胞, 细胞衰老, 氧化性应激, 活性氧, 线粒体功能障碍

Abstract:

Objective To investigate the regulatory effect of tripterine on hepatocellular carcinoma (HCC) cells under oxidative stress and senescence conditions. Methods The Huh-7 human HCC cell line was routinely cultured in vitro. The cells were treated with different concentrations (0, 0.25, 0.5, 1, 2 and 4 μmol/L) of tripterine. The highest drug concentration that did not affect cell viability was determined by CCK-8 cell viability assay. The experiment was divided into four groups: the control group, the H₂O₂ group, the H₂O₂ + DMSO group and the H₂O₂ + tripterine group. The degree of cell senescence was assessed by β-galactosidase staining. The intracellular reactive oxygen species (ROS) level was detected by the DCFH-DA fluorescence probe method. The intracellular ATP level was detected by the luciferase catalysis method. The superoxide level in mitochondria was detected by the MitoSO Red fluorescence probe method. The mitochondrial membrane potential level was assessed by the JC-1 fluorescence probe method. Results The highest drug concentration of tripterine that did not affect the viability of the HCC cell line Huh-7 was 0.5 μmol/L, and this optimal drug concentration was used for the subsequent experiments. Compared with the control group, the cell senescence was enhanced in the H₂O₂ group, intracellular reactive oxygen species (ROS) level was increased, ATP level decreased, mitochondrial superoxide level increased and mitochondrial membrane potential level decreased (all P<0.05). Compared with the H₂O₂ + DMSO group, the H₂O₂ + tripterine group showed alleviated cell senescence, decreased intracellular ROS level, increased ATP level, decreased mitochondrial superoxide level and elevated mitochondrial membrane potential level (all P<0.05). Conclusion Tripterine can alleviate oxidative stress and subsequent senescence and mitigate mitochondrial damage in HCC cells.

Key words: celastrol, carcinoma, hepatocellular, cellular senescence, oxidative stress, reactive oxygen species, mitochondrial dysfunction

中图分类号:

R285.5

图/表 7

图1 雷公藤红素最适浓度的确定＊＊P<0.01；a与不含H2O2的0 μmol/L组比较，b与含H2O2的0 μmol/L组比较，P<0.05。

Fig.1 Confirmation of the optimal concentration of tripterine

图2 各组细胞衰老程度检测（β-半乳糖苷酶染色，×200）

Fig.2 Detection of cell senescence in each group (β-galactosidase staining，×200)

表1 各组细胞衰老程度和ATP水平比较

Tab.1 Comparison of senescence degree and intracellular ATP level between the four groups （n=3，$\stackrel{-}{x}\pm s$）

组别	衰老程度	ATP（μmol/L）
对照组	3.72±1.31	2.94±0.10
H₂O₂组	13.19±4.25^a	2.46±0.06^a
H₂O₂+DMSO组	16.15±2.45	2.76±0.00
H₂O₂+雷公藤红素组	8.25±2.40^b	3.39±0.01^b
F	11.430^＊＊	131.300^＊＊

表2 各组细胞内ROS水平、线粒体超氧化物水平和MMP比较

Tab.2 Comparison of intracellular ROS level, superoxide level in mitochondria and MMP level between the four groups （n=4，$\stackrel{-}{x}\pm s$）

组别	ROS	线粒体超氧化物	MMP（R/G值）
对照组	1.00±0.03	96.25±16.84	1.02±0.09
H₂O₂组	1.33±0.09^a	127.50±8.50^a	0.83±0.07^a
H₂O₂+DMSO组	1.07±0.05	124.00±14.57	0.77±0.07
H₂O₂+雷公藤红素组	0.77±0.05^b	89.00±9.29^b	0.95±0.09^b
F	63.100^＊＊	9.207^＊＊	8.111^＊＊

图3 各组细胞内ROS水平检测（荧光检测，×200）

Fig.3 Detection of intracellular ROS level in each group (fluorescence detection, ×200)

图4 各组细胞线粒体内超氧化物水平检测（荧光检测，×200）

Fig.4 Detection of superoxide level in mitochondria in each group (fluorescence detection, ×200)

图5 各组细胞MMP水平检测（荧光检测，×200）

Fig.5 Detection of MMP level in each group (fluorescence detection, ×200)

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雷公藤红素对肝癌细胞氧化应激和衰老的调控作用

Regulative effect of tripterine on oxidative stress and senescence in hepatocellular carcinoma cells

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