Xue J, Zhong B, Wang L, Hu X, Zhang Y, Zhu M, et al . Jianpi-Qinghua Formula alleviates liver dysfunction by suppression of HBV replication in HepG2.2.15 cells. Int J Mol Cell Med 2025;
URL:
http://ijmcmed.org/article-1-2494-en.html
1- Department of Infectious Diseases, Hospital for Infectious Diseases of Pudong District, Shanghai, 201299, P.R. China.
2- Urologic Center, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200080, P.R. China.
3- Department of Infectious Diseases, Hospital for Infectious Diseases of Pudong District, Shanghai, 201299, P.R. China
4- Pharmacy Department, Hospital for Infectious Diseases of Pudong District, Shanghai, 201299, P.R. China.
5- Department of infectious diseases, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.
6- Shanghai Pudong New Area Mental Health Center,Shanghai,200124,P.R. China.
7- Department of Rheumatism and Immunology, Yueyang Hospital of Integrated Traditional Chinese and Western Medicine Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, 200437, P.R. China. , wuxiangxiang204@163.com
Abstract: (2 Views)
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.
Type of Study:
Original Article |
Subject:
Cancer Received: 2024/11/27 | Accepted: 2025/08/15 | Published: 2025/07/28