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

Document Type : Original Article

Authors
Jianhua Xue 1 , 2
Beifen Zhong 3
Lifeng Wan 4
Xiaofeng Hu 1
Yinhua Zhang 1
Minfang Zhu 5
Jianjie Chen 6
Hui Zhao 7
Xiangxiang Wu 8
1 Department of Infectious Diseases, Hospital for Infectious Diseases of Pudong District, Shanghai, 201299, P.R. China.
2 Department of Infectious Diseases, Shache County People's Hospital, Shache 844700, P.R. China.
3 Urologic Center, Shanghai General Hospital, Shanghai Jiaotong University School of Medicine, Shanghai, 200080, P.R. China.
4  Department of Infectious Diseases, Hospital for Infectious Diseases of Pudong District, Shanghai, 201299, P.R. China.
5 Pharmacy Department, Hospital for Infectious Diseases of Pudong District, Shanghai, 201299, P.R. China.
6 Department of infectious diseases, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai 201203, P.R. China.
7  Shanghai Pudong New Area Mental Health Center,Shanghai, 200124,P.R. China.
8 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.
10.22088/IJMCM.BUMS.14.3.797
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.
Keywords
mc160" class="markedContent"> Jianpi-Qinghua