Dahuang Zhechong Pill Alleviates Liver Fibrosis Progression by Regulating p38 MAPK/NF-κ B/TGF-β1 Pathway.
10.1007/s11655-024-3801-x
- Author:
Xiao-Yan HE
1
;
Xiao-Jiao XIONG
2
;
Mei-Jun LIU
2
;
Jing-Tao LIANG
2
;
Fu-You LIU
2
;
Jing-Yi XIAO
1
;
Li-Juan WU
3
Author Information
1. School of Public Health, Chengdu University of Traditional Chinese Medicine, Chengdu, 610036, China.
2. Department of Neurology, Hospital of Chengdu University of Traditional Chinese Medicine, Chengdu, 610072, China.
3. School of Public Health, Chengdu University of Traditional Chinese Medicine, Chengdu, 610036, China. wulijuan@cdutcm.edu.cn.
- Publication Type:Journal Article
- Keywords:
Chinese medicine;
Dahuang Zhechong Pill;
inflammation;
liver fibrosis;
p38 mitogen-activated protein kinase/nuclear factor kappa B/transforming growth factor-β1 pathway
- MeSH:
Animals;
Liver Cirrhosis/pathology*;
Drugs, Chinese Herbal/therapeutic use*;
p38 Mitogen-Activated Protein Kinases/metabolism*;
NF-kappa B/metabolism*;
Transforming Growth Factor beta1/metabolism*;
Male;
Signal Transduction/drug effects*;
Rats;
Disease Progression;
Cell Line;
Hepatic Stellate Cells/pathology*;
Rats, Sprague-Dawley
- From:
Chinese journal of integrative medicine
2024;30(12):1113-1120
- CountryChina
- Language:English
-
Abstract:
OBJECTIVE:To explore the effect and mechanism of Dahuang Zhechong Pill (DHZCP) on liver fibrosis.
METHODS:Liver fibrosis cell model was induced by transforming growth factor-β (TGF-β) in hepatic stellate cells (HSC-T6). DHZCP medicated serum (DMS) was prepared in rats. HSC-T6 cells were divided into the control (15% normal blank serum culture), TGF-β (15% normal blank serum + 5 ng/mL TGF-β), DHZCP (15% DMS + 5 ng/mL TGF-β), DHZCP+PDTC [15% DMS + 4 mmol/L ammonium pyrrolidine dithiocarbamate (PDTC)+ 5 ng/mL TGF-β], and PDTC groups (4 mmol/L PDTC + 5 ng/mL TGF-β). Cell activity was detected by cell counting kit 8 and levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β, IL-6, aspartate aminotransferase (AST) and alanine aminotransferase (ALT) in the cell supernatant were determined by enzyme-linked immunosorbnent assay. Western blot was used to measure the expressions of p38 mitogen-activated protein kinase/nuclear factor kappa B/transforming growth factor-β1 (p38 MAPK/NF-κ B/TGF-β1) pathway related proteins, and the localization and expressions of these proteins were observed by immunofluorescence staining.
RESULTS:DHZCP improves the viability of cells damaged by TGF-β and reduces inflammatory cytokines and ALT and AST levels in the supernatant of HSC-T6 cells induced with TGF-β (P<0.05 or P<0.01). Compared with the TGF-β group, NF-κ B p65 levels in the DHZCP group were decreased (P<0.05). p38 MAPK and NF-κ B p65 levels in the DHZCP+PDTC were also reduced (P<0.01). Compared with the TGF-β group, the protein expression of Smad2 showed a downward trend in the DHZCP, DHZCP+PDTC, and PDTC groups (all P<0.01), and the decreasing trend of Samd3 was statistically significant only in DHZCP+PDTC group (P<0.01), whereas Smad7 was increased (P<0.05 or P<0.01).
CONCLUSION:DHZCP can inhibit the process of HSC-T6 cell fibrosis by down-regulating the expression of p38 MAPK/NF-κ B/TGF-β1 pathway.
