Comparative proteome analysis of splenic lymphocytes in long-term high-fat diet and dietary supplement with lipoic acid mice.

Cell Immunol

State Key Laboratory of Food Science and Technology, School of Food Science and Technology, Jiangnan University, Wuxi 214122, China.

Published: October 2010

AI Article Synopsis

  • A study looked at how a high-fat diet (HFD) affected cells called splenic lymphocytes in mice, causing stress and cell death.
  • Researchers found changes in the proteins of these cells that are related to their health and function.
  • They discovered that adding a supplement called lipoic acid (LA) helped protect these lymphocytes from damage caused by the high-fat diet.

Article Abstract

The objective of this investigation was to explore possible molecular changes for role of a high-fat diet (HFD)-induced oxidative stress in splenic lymphocytes, and whether a dietary lipoic acid (LA) supplement could attenuate these changes. Male C57BL/6 mice were fed one of three diets 10 weeks and outcome measures centered on parameters of oxidative stress and lymphocytes apoptosis in spleen. Two-dimensional gel electrophoresis was used to compare the proteomes of splenic lymphocytes with three dietary groups. Differentially expressed spots whose expression altered over three fold were identified by MALDI-TOF MS. In this study, HFD resulted in oxidative stress in mice spleen, and significantly increased apoptotic percentage of splenic lymphocytes. Bioinformatic evaluation results of MALDI-TOF MS showed that 20 differentially expressed protein spots were known to be involved in many processes associated with cell function, such as cytoskeleton, energy metabolism and oxidative stress, signal transduction and cell defense. In conclusion, these results indicate that HFD-induced oxidative stress could lead to the functional decline of splenic lymphocytes, and LA supplement attenuates the alterations of protein expression to maintain the basic biological processes.

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Source
http://dx.doi.org/10.1016/j.cellimm.2010.06.002DOI Listing

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