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NARINGENIN ALLEVIATES HIGH-FAT-DIET INDUCED HEPATIC DAMAGE BY REDUCING PRO-INFLAMMATORY CYTOKINES SYSTEMICALLY AND LOCALLY
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Speaker:
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Wenfeng Zeng
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Author:
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W. Zeng*, F. Huang, C. Zhang, W. Liang
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Affiliation:
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National Laboratory of Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, China. *wfzeng1985@gmail.com
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Background and aims: Obesity is acknowledged as a risk factor for nonalcoholic fatty liver diseases (NAFLD), as well as the other chronic diseases (type 2 diabetes and atherosclerosis). Obesity induced chronic low-grade inflammation plays a pivotal role in the process of NADLD pathogenesis. Adipose tissue macrophages produce a significant proportion of the inflammatory factors induced by adipocyte. Previous studies have showed that naringenin, a natural flavonoid, exerted anti-inflammatory effect in acute inflammation animal model. Here, we determine whether naringenin enables to improve NAFLD by its anti-inflammation effect.
Methods: We established a high-fat-diet induced obesity mice model with or without naringenin supplementation for 40 weeks and the physiological status were recorded twice a week. After sacrifice serum and tissue were collected and stored in -80℃. Serum FFAs and cytokines were detected by biochemical methods and ELISA. Real-time qPCR and western blot were employed to investigate the expression of tissue related inflammatory cytokines and mediators. Finally adipose-infiltrated macrophages markers were detected by IHC.
Results: The data showed naringenin significantly alleviated obesity induced hepatic damage and effectively reduced circulating and local (hepatic and adipose) pro-inflammatory cytokines level, such as TNF-α, IL-6, MCP-1, IL-1β, Leptin and Resistin. Serum FFA levels and visceral adipose infiltrated M1 macrophages significantly reduced in the naringenin supplemented mice compared to high-fat-diet group.
Conclusions: Naringenin treatment could ameliorate high-fat-diet mediated hepatic damage through relieving the systemic and the local inflammation.
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