Commenced in January 2007
Frequency: Monthly
Edition: International
Paper Count: 2

liver injury Related Abstracts

2 Platelet-Derived Growth Factor-Β Receptor/P38 Pathway May Be the Potential Liver Damage Mechanisms Caused by Saikosaponin D

Authors: Li Chen, Feng Zhang, Shizhong Zheng

Abstract:

SaikosaponinD (SSD) is a major component of saikosaponins isolated from Bupleurumfalactum. Our current study was to examine the toxic effect of SSD on liver cells and explore the possible mechanism. The results demonstrated that SSD induced mouse liver injury and led to apoptosis in LO2 cells. HE staining and TUNEL analyses showed that SSD stimulated liver injury and hepatocyte apoptosis in vivo. Subsequent experiments showed that SSD down-regulated Bcl-2 but up-regulated Bax. In vitro, SSD-treated LO2 cells exhibited apparent down-regulated expression of p-p38. Moreover, PDGF-βR agonist PDGF-BB alone significantly upregulated p38 phosphorylation, while combined with SSD, p38 phosphorylation expression was reduced. Furthermore, shRNA-mediated PDGF-βR knockdown augmented the inactivation of p-p38 and Bcl2 but abrogated the activation of Bax, these results were more obvious when shRNA combined with SSD. These data indicated that SSD stimulated liver injury and apoptosis in hepatocytes and PDGF-βR /p38 pathway may be the potential mechanistic.

Keywords: apoptosis, saikosaponin D, hepatotoxicity, liver injury, platelet-derived growth factor-β receptor, p38

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1 Diallyl Trisulfide Protects the Rat Liver from CCl4-Induced Injury and Fibrogenesis by Attenuating Oxidative Stress

Authors: Liang Zhou, Xiao-Jing Zhu, Shi-Zhong Zheng

Abstract:

Various studies have shown that diallyl trisulfide (DATS) can protect the liver injury, and DATS has a strong antioxidant property. The aim of this study is to evaluate the in vivo role of DATS in protecting the liver against injury and fibrogenesis and further explores the underlying mechanisms. Our results demonstrated that DATS protected the liver from CCl4-caused injury by suppressing the elevation of ALT and AST activities, and by improving the histological architecture of the liver. Treatment with DATS or colchicine improved the liver fibrosis by sirius red staining and immunofluorescence. In addition, immunohistochemistry, western blot, and RT-PCR analyses indicated that DATS inhibited HSC activation. Furthermore, DATS attenuated oxidative stress by increasing glutathione and reducing lipid peroxides and malondialdehyde. These findings suggest that the protective effect of DATS on CCl4-caused liver injury and liver fibrogenesis was, at least partially, attributed to its antioxidant activity.

Keywords: Oxidative Stress, liver injury, DATS, liver fibrogenesis

Procedia PDF Downloads 286