八珍荔核抗纤方对四氯化碳诱导的肝纤维化大鼠模型的影响

廖丹丹; 吴卓檀; 龚俊文; 徐之然; 罗伟生

doi:10.12449/JCH260818

八珍荔核抗纤方对四氯化碳诱导的肝纤维化大鼠模型的影响

DOI: 10.12449/JCH260818

廖丹丹^{1, 2},
吴卓檀^{1, 2, 3},
龚俊文^{1, 2},
徐之然³,
罗伟生^{1, 2, 4, , ,}

1.
广西中医药大学研究生院，南宁 530001
2.
广西中医药防治医学分子生物重点实验室，南宁 530023
3.
广西中医药大学附属瑞康医院中西医结合转化医学中心，南宁 530011
4.
广西中医药大学附属瑞康医院肝病科，南宁 530011

基金项目:

国家自然科学基金 (82160834);

全国名老中医药专家传承工作室建设项目 (National Medical Education Letter ［2022］ No.75);

罗伟生桂派中医大师传承工作室 (Guizhong Medical Development ［2023］ No.16);

广西名中医传承工作室建设项目 (Guizhong Medical Science and Education Development ［2021］ No.6);

中西医结合广西一流学科（培育）建设项目 (Guijiao Research ［2018］ No.12)

伦理学声明：本研究方案于2025年12月24日经广西中医药大学动物伦理委员会批准通过，批号：GXTCMU-EC KS20250000-656，符合实验室动物管理与使用准则。

利益冲突声明：本文不存在任何利益冲突。

作者贡献声明：廖丹丹负责课题设计，起草论文；廖丹丹、吴卓檀和龚俊文负责实验操作，研究过程的实施；廖丹丹负责数据收集，统计学分析，绘制图表；徐之然负责论文修改；罗伟生负责指导撰写文章并最后定稿。

详细信息

通信作者:
罗伟生， 4011188@qq.com （ORCID： 0009-0005-5879-192X）

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- 文章访问数: 14
- HTML全文浏览量: 2
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- 被引次数: 0
出版历程
- 收稿日期: 2026-02-11
- 录用日期: 2026-04-13
- 出版日期: 2026-08-25

Effect of Bazhen Lihe Kangxian prescription on rats with liver fibrosis induced by carbon tetrachloride

Dandan Liao^{1, 2},
Zhuotan Wu^{1, 2, 3},
Junwen Gong^{1, 2},
Zhiran Xu³,
Weisheng Luo^{1, 2, 4
, ,
,}

1.
Graduate School，Guangxi University of Chinese Medicine，Nanning 530001，China
2.
Guangxi Key Laboratory of Molecular Biology of Traditional Chinese Medicine and Preventive Medicine，Nanning 530023，China
3.
Integrated Traditional Chinese and Western Medicine Translational Medicine Center，Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine，Nanning 530011，China
4.
Department of Hepatology，Ruikang Hospital Affiliated to Guangxi University of Chinese Medicine，Nanning 530011，China

Research funding:

National Natural Science Foundation of China (82160834);

National Famous Traditional Chinese Medicine Expert Inheritance Studio Construction Project (National Medical Education Letter ［2022］ No.75);

Luo Weisheng Guipai Traditional Chinese Medicine Master Inheritance Studio (Guizhong Medical Development ［2023］ No.16);

Construction Project of Guangxi Famous Traditional Chinese Medicine Inheritance Studio (Guizhong Medical Science and Education Development ［2021］ No.6);

Integrated Traditional Chinese and Western Medicine Guangxi First Class Discipline （Cultivation） Construction Project (Guijiao Research ［2018］ No.12)

More Information

Corresponding author: Luo Weisheng， 4011188@qq.com （ORCID： 0009-0005-5879-192X）

摘要

摘要: 目的观察八珍荔核抗纤方对四氯化碳（CCl₄）诱导的肝纤维化大鼠模型的治疗作用，探讨八珍荔核抗纤方抗肝纤维化的作用机制。方法将50只雄性SD大鼠随机分为空白组、模型组、水飞蓟宾组（43.19 mg/kg）及八珍荔核抗纤方低剂量组（7.96 g/kg）、中剂量组（15.93 g/kg）、高剂量组（31.86 g/kg），通过皮下注射40% CCl₄橄榄油混合液（每周2次，连续8周）建立肝纤维化模型。验证造模成功后，空白组及模型组予生理盐水灌胃，各治疗组予相应药物灌胃（每日1次，连续4周）。采用苏木精-伊红染色、马松染色观察大鼠肝脏组织病理学变化；采用生化仪检测血清白蛋白（Alb）、天冬氨酸氨基转移酶（AST）、丙氨酸氨基转移酶（ALT）水平；采用酶联免疫吸附测定法检测血清透明质酸（HA）、Ⅳ型胶原（Col-Ⅳ）、Ⅲ型前胶原肽（PⅢNP）、层粘连蛋白（LN）水平；采用蛋白免疫印迹法检测肝脏组织磷酸化磷脂酰肌醇3-激酶（p-PI3K）/磷脂酰肌醇3-激酶（PI3K）、磷酸化蛋白激酶B（p-Akt）/蛋白激酶B（Akt）、磷酸化雷帕霉素靶蛋白（p-mTOR）/雷帕霉素靶蛋白（mTOR）蛋白表达水平；采用逆转录荧光定量聚合酶链式反应法检测肝脏组织Ⅰ型胶原蛋白（ColⅠ）、平滑肌肌动蛋白α（α-SMA）基因表达水平。计量资料多组间比较采用单因素方差分析，进一步两两比较采用LSD-t检验。结果与空白组比较，模型组大鼠肝小叶结构破坏，肝细胞索排列紊乱，肝细胞脂肪变性，炎性细胞浸润严重，大量蓝色胶原纤维沉积，AST、ALT、HA、LN、Col-Ⅳ和PⅢNP水平均显著升高，Alb水平显著降低（P值均<0.01）；与模型组比较，水飞蓟宾组及八珍荔核抗纤方各剂量组大鼠肝脏组织炎性细胞浸润、肝细胞脂肪变性及蓝色胶原纤维沉积情况呈不同程度改善，AST、ALT、HA、LN、Col-Ⅳ和PⅢNP水平均显著降低，Alb水平显著升高（P值均<0.01）。与空白组比较，模型组大鼠肝脏组织p-PI3K/PI3K、p-Akt/Akt和p-mTOR/mTOR蛋白表达水平及ColⅠ、α-SMA基因表达水平均显著升高（P值均<0.01）；与模型组比较，水飞蓟宾组及八珍荔核抗纤方中、高剂量组大鼠肝脏组织p-PI3K/PI3K蛋白水平均显著降低（P值均<0.01），水飞蓟宾组及八珍荔核抗纤方各剂量组大鼠肝脏组织p-Akt/Akt、p-mTOR/mTOR蛋白表达水平及ColⅠ、α-SMA基因表达水平均显著降低（P值均<0.01）。结论八珍荔核抗纤方可改善CCl₄诱导的大鼠肝纤维化，减轻肝损伤，其作用机制可能与抑制PI3K/Akt/mTOR通路有关。
- 肝纤维化 /
- 八珍荔核抗纤方 /
- 信号传导 /
- 大鼠， Sprague-Dawley
Abstract: Objective To investigate the therapeutic effect of Bazhen Lihe Kangxian prescription on rats with liver fibrosis induced by carbon tetrachloride （CCl₄）， and to explore its mechanism of action against liver fibrosis. Methods A total of 50 male Sprague-Dawley rats were randomly divided into blank group， model group， silybin group （43.19 mg/kg）， and low-， middle-， and high-dose Bazhen Lihe Kangxian prescription groups （7.96， 15.93， and 31.86 g/kg， respectively）. Subcutaneous injection of 40% CCl₄-olive oil solution （twice a week for 8 consecutive weeks） was performed to establish a model of liver fibrosis. After successful modeling， the rats in the blank group and the model group were given normal saline by gavage， while those in the treatment groups were given the corresponding drug by gavage， once a day for 4 consecutive weeks. HE staining and Masson staining were used to observe liver histopathological changes； an automatic biochemical analyzer was used to measure the serum levels of albumin （Alb）， aspartate aminotransferase （AST）， and alanine aminotransferase （ALT）； ELISA was used to measure the serum levels of hyaluronic acid （HA）， collagen Ⅳ （Col-Ⅳ）， procollagen Ⅲ N-terminal peptide （PⅢNP）， and laminin （LN）； Western blotting was used to measure the protein expression levels of phosphoinositide 3-kinase （PI3K）， phosphorylated PI3K （p-PI3K）， protein kinase B （Akt）， phosphorylated Akt （p-Akt）， mammalian target of rapamycin （mTOR）， and phosphorylated mTOR （p-mTOR） in liver tissue； RT-qPCR was used to measure the mRNA expression levels of collagen Ⅰ （Col-Ⅰ） and α-smooth muscle actin （α-SMA） in liver tissue. A one-way analysis of variance was used for comparison of continuous data between multiple groups， and the least significant difference t-test was used for further comparison between two groups. Results Compared with the blank group， the model group had disrupted hepatic lobular structure， disordered arrangement of hepatic cell cords， hepatocyte fatty degeneration， severe inflammatory cell infiltration， and deposition of massive blue collagen fibers， as well as significant increases in the levels of AST， ALT， HA， LN， Col‑Ⅳ， and PⅢNP and a significant reduction in the level of Alb （all P<0.01）. Compared with the model group， the silybin group and the three Bazhen Lihe Kangxian prescription groups had varying degrees of improvement in inflammatory cell infiltration， hepatocyte fatty degeneration， and collagen deposition in liver tissue， as well as significant reductions in the levels of AST， ALT， HA， LN， Col‑Ⅳ， and PⅢNP and a significant increase in the level of Alb （all P<0.01）. Compared with the blank group， the model group had significant increases in the protein expression levels of p‑PI3K/PI3K， p-Akt/Akt， and p‑mTOR/mTOR and the mRNA expression levels of Col-I and α-SMA in liver tissue （all P<0.01）； compared with the model group， the silybin group and the high- and middle-dose Bazhen Lihe Kangxian prescription groups had significant reductions in the protein expression levels of p-PI3K/PI3K （all P<0.01）， and the silybin group and the three Bazhen Lihe Kangxian prescription groups had significant reductions in the protein expression levels of p-Akt/Akt and p-mTOR/mTOR and the mRNA expression levels of Col-Ⅰ and α-SMA in liver tissue （all P<0.01）. Conclusion Bazhen Lihe Kangxian prescription can improve CCl₄-induced liver fibrosis in rats and alleviate liver injury， possibly by inhibiting the PI3K/Akt/mTOR pathway.
- Hepatic Fibrosis /
- Bazhen Lihe Kangxian Formula /
- Signal Transduction /
- Rats， Sprague-Dawley

HTML全文

图 1 肝脏组织形态

Figure 1. Liver histomorphology

下载: 全尺寸图片幻灯片

注： HE，苏木精-伊红。

图 2 HE染色结果（×200）

Figure 2. HE staining results （×200）

下载: 全尺寸图片幻灯片

注： Masson染色，马松染色。

图 3 Masson染色结果（×200）

Figure 3. Masson staining results （×200）

下载: 全尺寸图片幻灯片

图 4 各组大鼠肝纤维化评分

Figure 4. Liver fibrosis scores of rats in each group

下载: 全尺寸图片幻灯片

注： AST，天冬氨酸氨基转移酶；ALT，丙氨酸氨基转移酶；Alb，白蛋白。

图 5 各组大鼠肝功能水平

Figure 5. Liver function levels of rats in each group

下载: 全尺寸图片幻灯片

注： HA，透明质酸；LN，层粘连蛋白；Col-Ⅳ，Ⅳ型胶原；PⅢNP，Ⅲ型前胶原肽。

图 6 各组大鼠肝纤维化四项水平

Figure 6. Liver fibrosis four-item levels in each group of rats

下载: 全尺寸图片幻灯片

注： A～F分别是空白组、模型组、水飞蓟宾组、八珍荔核抗纤方低剂量组、八珍荔核抗纤方中剂量组和八珍荔核抗纤方高剂量组。p-PI3K，磷酸化磷脂酰肌醇3-激酶；PI3K，磷脂酰肌醇3-激酶；p-Akt，磷酸化蛋白激酶B；Akt，蛋白激酶B；p-mTOR，磷酸化哺乳动物雷帕霉素靶蛋白；mTOR，哺乳动物雷帕霉素靶蛋白；GAPDH，甘油醛-3-磷酸脱氢酶。

图 7 各组大鼠肝脏组织蛋白表达水平

Figure 7. Protein expression levels in liver tissues of rats in each group

下载: 全尺寸图片幻灯片

注： ColⅠ，Ⅰ型胶原蛋白；α-SMA，平滑肌肌动蛋白α。

图 8 各组大鼠基因表达水平

Figure 8. Gene expression levels of rats in each group

下载: 全尺寸图片幻灯片

表 1 引物序列表

Table 1. List of primer sequences

名称		序列（5′-3′）
ColⅠ	上游	GATCCTGCCGATGTCGCTATCC
ColⅠ	下游	TCTTGAGGTTGCCAGTCTGTTGG
α-SMA	上游	CCCAGATTATGTTTGAGACCTTCA
α-SMA	下游	CATCTCCAGAGTCCAGCACAATAC
GAPDH	上游	GGTGCTGAGTATGTCGTGGAG
GAPDH	下游	TTGCTGACAATCTTGAGGGAG
注：Col Ⅰ，Ⅰ型胶原蛋白；α-SMA，平滑肌肌动蛋白α；GAPDH，甘油醛-3-磷酸脱氢酶。

下载: 导出CSV

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