Tags

Type your tag names separated by a space and hit enter

Diallyl trisulfide attenuates carbon tetrachloride-caused liver injury and fibrogenesis and reduces hepatic oxidative stress in rats.
Naunyn Schmiedebergs Arch Pharmacol. 2014 May; 387(5):445-55.NS

Abstract

Liver fibrosis represents a frequent event following chronic insult to trigger wound healing reactions with accumulation of extracellular matrix (ECM) components in the liver. Activation of hepatic stellate cells (HSCs) is the pivotal event during liver fibrogenesis. The process of HSC activation is accompanied by enhanced expression of a series of marker proteins and pro-fibrogenic signal molecules. Natural products have been an important source of antifibrotic remedies. The present study aims to evaluate the in vivo effects of diallyl trisulfide (DATS), the primary component derived from garlic, on carbon tetrachloride (CCl4)-induced injury and fibrosis in rats. Our results showed that DATS improved liver histological architecture and decreased hepatic enzyme levels, but did not significantly affect cytochrome P450 2E1 activity in vivo. DATS also attenuated collagen deposition and inhibited HSC activation in the rat fibrotic liver demonstrated by reduced expression of α-smooth muscle actin, α1(I) procollagen, and fibronectin-three key markers of HSC activation-and by downregulation of transforming growth factor-β receptor 1, platelet-derived growth factor-β receptor, and epidermal growth factor receptor-three key receptors transmitting pro-fibrogenic pathways. In addition, DATS ameliorated hepatic oxidative stress by diminishing the levels of lipid peroxides and malondialdehyde and enhancing glutathione content. These data collectively revealed that DATS protected the rat liver from CCl4-caused injury and fibrogenesis in vivo, which was associated with inhibition of HSC activation and attenuation of oxidative stress. Our results suggested DATS as a promising antifibrogenic candidate for the prevention and treatment of liver fibrosis.

Authors+Show Affiliations

Department of Pharmacology, College of Pharmacy, Nanjing University of Chinese Medicine, 138 Xianlin Avenue, Nanjing, 210023, Jiangsu, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

24557053

Citation

Zhu, Xiaojing, et al. "Diallyl Trisulfide Attenuates Carbon Tetrachloride-caused Liver Injury and Fibrogenesis and Reduces Hepatic Oxidative Stress in Rats." Naunyn-Schmiedeberg's Archives of Pharmacology, vol. 387, no. 5, 2014, pp. 445-55.
Zhu X, Zhang F, Zhou L, et al. Diallyl trisulfide attenuates carbon tetrachloride-caused liver injury and fibrogenesis and reduces hepatic oxidative stress in rats. Naunyn Schmiedebergs Arch Pharmacol. 2014;387(5):445-55.
Zhu, X., Zhang, F., Zhou, L., Kong, D., Chen, L., Lu, Y., & Zheng, S. (2014). Diallyl trisulfide attenuates carbon tetrachloride-caused liver injury and fibrogenesis and reduces hepatic oxidative stress in rats. Naunyn-Schmiedeberg's Archives of Pharmacology, 387(5), 445-55. https://doi.org/10.1007/s00210-014-0959-3
Zhu X, et al. Diallyl Trisulfide Attenuates Carbon Tetrachloride-caused Liver Injury and Fibrogenesis and Reduces Hepatic Oxidative Stress in Rats. Naunyn Schmiedebergs Arch Pharmacol. 2014;387(5):445-55. PubMed PMID: 24557053.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diallyl trisulfide attenuates carbon tetrachloride-caused liver injury and fibrogenesis and reduces hepatic oxidative stress in rats. AU - Zhu,Xiaojing, AU - Zhang,Feng, AU - Zhou,Liang, AU - Kong,Desong, AU - Chen,Li, AU - Lu,Yin, AU - Zheng,Shizhong, Y1 - 2014/02/21/ PY - 2013/12/19/received PY - 2014/01/30/accepted PY - 2014/2/22/entrez PY - 2014/2/22/pubmed PY - 2015/1/3/medline SP - 445 EP - 55 JF - Naunyn-Schmiedeberg's archives of pharmacology JO - Naunyn Schmiedebergs Arch. Pharmacol. VL - 387 IS - 5 N2 - Liver fibrosis represents a frequent event following chronic insult to trigger wound healing reactions with accumulation of extracellular matrix (ECM) components in the liver. Activation of hepatic stellate cells (HSCs) is the pivotal event during liver fibrogenesis. The process of HSC activation is accompanied by enhanced expression of a series of marker proteins and pro-fibrogenic signal molecules. Natural products have been an important source of antifibrotic remedies. The present study aims to evaluate the in vivo effects of diallyl trisulfide (DATS), the primary component derived from garlic, on carbon tetrachloride (CCl4)-induced injury and fibrosis in rats. Our results showed that DATS improved liver histological architecture and decreased hepatic enzyme levels, but did not significantly affect cytochrome P450 2E1 activity in vivo. DATS also attenuated collagen deposition and inhibited HSC activation in the rat fibrotic liver demonstrated by reduced expression of α-smooth muscle actin, α1(I) procollagen, and fibronectin-three key markers of HSC activation-and by downregulation of transforming growth factor-β receptor 1, platelet-derived growth factor-β receptor, and epidermal growth factor receptor-three key receptors transmitting pro-fibrogenic pathways. In addition, DATS ameliorated hepatic oxidative stress by diminishing the levels of lipid peroxides and malondialdehyde and enhancing glutathione content. These data collectively revealed that DATS protected the rat liver from CCl4-caused injury and fibrogenesis in vivo, which was associated with inhibition of HSC activation and attenuation of oxidative stress. Our results suggested DATS as a promising antifibrogenic candidate for the prevention and treatment of liver fibrosis. SN - 1432-1912 UR - https://www.unboundmedicine.com/medline/citation/24557053/Diallyl_trisulfide_attenuates_carbon_tetrachloride_caused_liver_injury_and_fibrogenesis_and_reduces_hepatic_oxidative_stress_in_rats_ L2 - https://dx.doi.org/10.1007/s00210-014-0959-3 DB - PRIME DP - Unbound Medicine ER -