Jianpi-Qinghua Formula alleviates liver dysfunction by suppression of HBV replication in HepG2.2.15 cells.

IF 1.8 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Jianhua Xue, Beifen Zhong, Lifeng Wan, Xiaofeng Hu, Yinhua Zhang, Minfang Zhu, Jianjie Chen, Hui Zhao, Xiangxiang Wu
{"title":"Jianpi-Qinghua Formula alleviates liver dysfunction by suppression of HBV replication in HepG2.2.15 cells.","authors":"Jianhua Xue, Beifen Zhong, Lifeng Wan, Xiaofeng Hu, Yinhua Zhang, Minfang Zhu, Jianjie Chen, Hui Zhao, Xiangxiang Wu","doi":"10.22088/IJMCM.BUMS.14.3.797","DOIUrl":null,"url":null,"abstract":"<p><p>Previous researches revealed that Jianpi-Qinghua Formula (JPQH) exhibited anti-cancer activity. However, the pharmacological effect of JPQH on HBV-positive hepatocellular carcinoma (HCC) remains unknown. Cisplatin chemotherapy serves as a major treatment for HCC. Therefore, the aim of this study was to investigate whether JPQH or in combination with cisplatin therapy could inhibit the proliferation of HepG2.2.15 cells and elucidate the underlying mechanisms associated with the effect of cisplatin on HepG2.2.15 cells. We found that JPQH alleviated carbon tetrachloride (CCl4)-induced liver fibrosis and hepatitis in vivo. In vitro expriements, cisplatin effectively enhanced the suppression of HepG2.2.15 HCC cell proliferation and decreased their migration capacity. Moreover, JPQH could reduce CCl4-induced AST and ALT levels, as well as serum markers for liver fibrosis (including PⅢNP, C-Ⅳ, LN, HA levels) and hepatitis markers (including TBIL, IL6, and IL-1β levels). JPQH also induced cellular apoptosis by downregulating the expression levels of proteins such as Bcl-2 and IL-6. Additionally, JPQH could downregulate HBV expression. These findings collectively demonstrate that JPQH may inhibit the proliferation of HepG2.2.15 cells through suppression of HBV replication.</p>","PeriodicalId":14152,"journal":{"name":"International Journal of Molecular and Cellular Medicine","volume":"14 3","pages":"797-807"},"PeriodicalIF":1.8000,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12664686/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Molecular and Cellular Medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.22088/IJMCM.BUMS.14.3.797","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2025/1/1 0:00:00","PubModel":"eCollection","JCR":"Q3","JCRName":"MEDICINE, RESEARCH & EXPERIMENTAL","Score":null,"Total":0}
引用次数: 0

Abstract

Previous researches revealed that Jianpi-Qinghua Formula (JPQH) exhibited anti-cancer activity. However, the pharmacological effect of JPQH on HBV-positive hepatocellular carcinoma (HCC) remains unknown. Cisplatin chemotherapy serves as a major treatment for HCC. Therefore, the aim of this study was to investigate whether JPQH or in combination with cisplatin therapy could inhibit the proliferation of HepG2.2.15 cells and elucidate the underlying mechanisms associated with the effect of cisplatin on HepG2.2.15 cells. We found that JPQH alleviated carbon tetrachloride (CCl4)-induced liver fibrosis and hepatitis in vivo. In vitro expriements, cisplatin effectively enhanced the suppression of HepG2.2.15 HCC cell proliferation and decreased their migration capacity. Moreover, JPQH could reduce CCl4-induced AST and ALT levels, as well as serum markers for liver fibrosis (including PⅢNP, C-Ⅳ, LN, HA levels) and hepatitis markers (including TBIL, IL6, and IL-1β levels). JPQH also induced cellular apoptosis by downregulating the expression levels of proteins such as Bcl-2 and IL-6. Additionally, JPQH could downregulate HBV expression. These findings collectively demonstrate that JPQH may inhibit the proliferation of HepG2.2.15 cells through suppression of HBV replication.

Abstract Image

Abstract Image

Abstract Image

健脾清化方通过抑制HepG2.2.15细胞HBV复制来缓解肝功能障碍。
前期研究发现健脾清化方具有抗癌活性。然而,JPQH对hbv阳性肝细胞癌(HCC)的药理作用尚不清楚。顺铂化疗是HCC的主要治疗方法。因此,本研究的目的是探讨JPQH或联合顺铂治疗是否能抑制HepG2.2.15细胞的增殖,并阐明顺铂对HepG2.2.15细胞影响的潜在机制。我们发现JPQH在体内减轻了四氯化碳(CCl4)诱导的肝纤维化和肝炎。在体外实验中,顺铂有效增强了对HepG2.2.15 HCC细胞增殖的抑制作用,降低了其迁移能力。此外,JPQH还能降低ccl4诱导的AST和ALT水平,以及肝纤维化血清标志物(包括PⅢNP、C-Ⅳ、LN、HA水平)和肝炎标志物(包括TBIL、IL6和IL-1β水平)。JPQH还通过下调Bcl-2和IL-6等蛋白的表达水平诱导细胞凋亡。此外,JPQH还能下调HBV的表达。这些结果共同表明,JPQH可能通过抑制HBV复制来抑制HepG2.2.15细胞的增殖。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
CiteScore
3.60
自引率
0.00%
发文量
0
期刊介绍: The International Journal of Molecular and Cellular Medicine (IJMCM) is a peer-reviewed, quarterly publication of Cellular and Molecular Biology Research Center (CMBRC), Babol University of Medical Sciences, Babol, Iran. The journal covers all cellular & molecular biology and medicine disciplines such as the genetic basis of disease, biomarker discovery in diagnosis and treatment, genomics and proteomics, bioinformatics, computer applications in human biology, stem cells and tissue engineering, medical biotechnology, nanomedicine, cellular processes related to growth, death and survival, clinical biochemistry, molecular & cellular immunology, molecular and cellular aspects of infectious disease and cancer research. IJMCM is a free access journal. All open access articles published in IJMCM are distributed under the terms of the Creative Commons Attribution CC BY. The journal doesn''t have any submission and article processing charges (APCs).
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书