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Diallyl trisulfide attenuates ethanol-induced hepatic steatosis by inhibiting oxidative stress and apoptosis.
Biomed Pharmacother 2016; 79:35-43BP

Abstract

Inhibiting the major characteristics of alcoholic fatty liver (AFL) such as lipid accumulation, oxidative stress and apoptosis is a promising strategy of treating AFL. Diallyl trisulfide (DATS) is the major constituent isolated from garlic, which shows promise in the treatment of chronic liver disease. However, the effects of DATS on ethanol-induced liver injury and the related mechanisms remain unclear. The aim of this study was to evaluate the potential protective effects of DATS on AFL and the potential mechanisms. A single intragastric dose of ethanol was given to rats in vivo, while ethanol-stimulated LO2 cells were used as an in vitro model. Our results demonstrated that DATS prevented ethanol-induced injury, as indicated by the reduced activities of aspartate transaminase (AST) and alanine aminotransferase (ALT) in the serum and culture medium, and inhibition of cell apoptosis. Furthermore, DATS reduced hepatic steatosis by up-regulating the expression of peroxisome proliferator-activated receptor-alpha (PPAR-α) and down-regulating the expression of sterolregulatory element binding protein 1c(SREBP-1c). In addition, DATS alleviated ethanol-induced oxidative stress by enhancing non-enzymatic antioxidant and enzymatic antioxidants contents and by reducing the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). These data collectively revealed that DATS protected ethanol-induced liver injury by inhibiting lipid accumulation and oxidative stress.

Authors+Show Affiliations

Departement of Pharmacy, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; National First-Class Key Discipline for Traditional Chinese Medicine of Nanjing University of Chinese Medicine, Nanjing 210023, China.Departement of Pharmacy, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; National First-Class Key Discipline for Traditional Chinese Medicine of Nanjing University of Chinese Medicine, Nanjing 210023, China.Departement of Pharmacy, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; National First-Class Key Discipline for Traditional Chinese Medicine of Nanjing University of Chinese Medicine, Nanjing 210023, China.Departement of Pharmacy, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; National First-Class Key Discipline for Traditional Chinese Medicine of Nanjing University of Chinese Medicine, Nanjing 210023, China.Departement of Pharmacy, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; National First-Class Key Discipline for Traditional Chinese Medicine of Nanjing University of Chinese Medicine, Nanjing 210023, China.Departement of Pharmacy, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; National First-Class Key Discipline for Traditional Chinese Medicine of Nanjing University of Chinese Medicine, Nanjing 210023, China.Departement of Pharmacy, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; National First-Class Key Discipline for Traditional Chinese Medicine of Nanjing University of Chinese Medicine, Nanjing 210023, China.Departement of Pharmacy, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; National First-Class Key Discipline for Traditional Chinese Medicine of Nanjing University of Chinese Medicine, Nanjing 210023, China.Departement of Pharmacy, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, China; National First-Class Key Discipline for Traditional Chinese Medicine of Nanjing University of Chinese Medicine, Nanjing 210023, China; Jiangsu Key Laboratory for Pharmacology and Safety Evaluation of Chinese Material Medical, Nanjing University of Chinese Medicine, Nanjing 210023, China. Electronic address: nytws@163.com.

Pub Type(s)

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

Language

eng

PubMed ID

27044810

Citation

Chen, Lian-Yun, et al. "Diallyl Trisulfide Attenuates Ethanol-induced Hepatic Steatosis By Inhibiting Oxidative Stress and Apoptosis." Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, vol. 79, 2016, pp. 35-43.
Chen LY, Chen Q, Cheng YF, et al. Diallyl trisulfide attenuates ethanol-induced hepatic steatosis by inhibiting oxidative stress and apoptosis. Biomed Pharmacother. 2016;79:35-43.
Chen, L. Y., Chen, Q., Cheng, Y. F., Jin, H. H., Kong, D. S., Zhang, F., ... Zheng, S. Z. (2016). Diallyl trisulfide attenuates ethanol-induced hepatic steatosis by inhibiting oxidative stress and apoptosis. Biomedicine & Pharmacotherapy = Biomedecine & Pharmacotherapie, 79, pp. 35-43. doi:10.1016/j.biopha.2016.01.009.
Chen LY, et al. Diallyl Trisulfide Attenuates Ethanol-induced Hepatic Steatosis By Inhibiting Oxidative Stress and Apoptosis. Biomed Pharmacother. 2016;79:35-43. PubMed PMID: 27044810.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Diallyl trisulfide attenuates ethanol-induced hepatic steatosis by inhibiting oxidative stress and apoptosis. AU - Chen,Lian-Yun, AU - Chen,Qin, AU - Cheng,Yi-Feng, AU - Jin,Huan-Huan, AU - Kong,De-Song, AU - Zhang,Feng, AU - Wu,Li, AU - Shao,Jiang-Juan, AU - Zheng,Shi-Zhong, Y1 - 2016/02/12/ PY - 2015/10/29/received PY - 2016/01/10/revised PY - 2016/01/13/accepted PY - 2016/4/6/entrez PY - 2016/4/6/pubmed PY - 2016/12/27/medline KW - Alcoholic fatty liver KW - Apoptosis KW - Diallyl trisulfide KW - Hepatocyte KW - Oxidative stress SP - 35 EP - 43 JF - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie JO - Biomed. Pharmacother. VL - 79 N2 - Inhibiting the major characteristics of alcoholic fatty liver (AFL) such as lipid accumulation, oxidative stress and apoptosis is a promising strategy of treating AFL. Diallyl trisulfide (DATS) is the major constituent isolated from garlic, which shows promise in the treatment of chronic liver disease. However, the effects of DATS on ethanol-induced liver injury and the related mechanisms remain unclear. The aim of this study was to evaluate the potential protective effects of DATS on AFL and the potential mechanisms. A single intragastric dose of ethanol was given to rats in vivo, while ethanol-stimulated LO2 cells were used as an in vitro model. Our results demonstrated that DATS prevented ethanol-induced injury, as indicated by the reduced activities of aspartate transaminase (AST) and alanine aminotransferase (ALT) in the serum and culture medium, and inhibition of cell apoptosis. Furthermore, DATS reduced hepatic steatosis by up-regulating the expression of peroxisome proliferator-activated receptor-alpha (PPAR-α) and down-regulating the expression of sterolregulatory element binding protein 1c(SREBP-1c). In addition, DATS alleviated ethanol-induced oxidative stress by enhancing non-enzymatic antioxidant and enzymatic antioxidants contents and by reducing the levels of reactive oxygen species (ROS) and malondialdehyde (MDA). These data collectively revealed that DATS protected ethanol-induced liver injury by inhibiting lipid accumulation and oxidative stress. SN - 1950-6007 UR - https://www.unboundmedicine.com/medline/citation/27044810/Diallyl_trisulfide_attenuates_ethanol_induced_hepatic_steatosis_by_inhibiting_oxidative_stress_and_apoptosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0753-3322(15)30330-9 DB - PRIME DP - Unbound Medicine ER -