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Int J Biol Macromol. 2014 Aug;69:73-8. doi: 10.1016/j.ijbiomac.2014.05.034. Epub 2014 May 22.

Lycium barbarum polysaccharide attenuates alcoholic cellular injury through TXNIP-NLRP3 inflammasome pathway.

Author information

  • 1Department of Immunobiology, Institute of Tissue Transplantation and Immunology, Jinan University, Guangzhou 510632, China; Department of Anatomy, The University of Hong Kong, Hong Kong, China; Department of Infectious Diseases, Shenzhen Third People's Hospital, Shenzhen 518112, China.
  • 2Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Guangzhou, China.
  • 3Department of Infectious Diseases, Shenzhen Third People's Hospital, Shenzhen 518112, China.
  • 4Department of Anatomy, The University of Hong Kong, Hong Kong, China.
  • 5Department of Immunobiology, Institute of Tissue Transplantation and Immunology, Jinan University, Guangzhou 510632, China. Electronic address: tfyxing@jnu.edu.cn.
  • 6GMH Institute of CNS Regeneration, Guangdong Medical Key Laboratory of Brain Function and Diseases, Jinan University, Guangzhou, China; Department of Ophthalmology, The University of Hong Kong, Hong Kong, China. Electronic address: hrmaskf@hku.hk.

Abstract

Lycium barbarum has been used as a traditional Chinese medicine to nourish liver, kidneys and the eyes. However, the underlying mechanisms of its hepatic-protective properties remain uncertain. In this study, we aimed to investigate whether thioredoxin-interacting protein (TXNIP) and NOD-like receptor 3 (NLRP3) inflammasome mediated the attenuation of ethanol-induced hepatic injury by Lycium barbarum polysaccharide (LBP). Rat normal hepatocyte line BRL-3A was pre-treated with LBP prior to ethanol incubation. Hepatic damages, including apoptosis, inflammation, and oxidative stress, were measured. Then the inhibition of endogenous TXNIP expression was achieved by using its specific siRNA to test its possible involvement in the injury attenuation. We found that 50μg/ml LBP pre-treatment significantly alleviated 24-h ethanol exposure-induced overexpression of TXNIP, increased cellular apoptosis, secretion of inflammatory cytokines, activation of NLRP3 inflammasome, production of ROS, and reduced antioxidant enzyme expression. Silence of TXNIP suppressed the activated NLRP3 inflammasome, increased oxidative stress and worsened apoptosis in the cells. Further addition of LBP did not influence the effects of TXNIP inhibition on the cells. In conclusion, inhibition of hepatic TXNIP by LBP contributes to the reduction of cellular apoptosis, oxidative stress and NLRP3 inflammasome-mediated inflammation.

Copyright © 2014 Elsevier B.V. All rights reserved.

KEYWORDS:

LBP; NLRP3 inflammasome; TXNIP

PMID:
24858535
[PubMed - in process]
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