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Acta Physiologica Congress

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Acta Physiologica 2012; Volume 206, Supplement 693
Joint FEPS and Spanish Physiological Society Scientific Congress 2012
9/8/2012-9/11/2012
Santiago de Compostela, Spain


POSSIBLE PROTECTIVE EFFECT OF XANTHOHUMOL AGAINST LIVER DAMAGE SECONDARY TO AGING
Abstract number: P14

Cuesta1 S, Kireev1 R, Rancan2 L, Borras3 C, Garcia2 C, Vina3 J, Vara2 E, AF Tresguerres1 J

1Physiology, UCM,
2Biochemistry and Molecular Biology III, UCM,
3Physiology, UV

Objectives: 

Recent studies suggested xanthohumol (XANT) is a promising agent for preventing inflammatory and oxidative stress secondary to aging. However, the mechanism related to the possible protective role of XANT preventing liver injury loss is not well understood. The aim of the present study was investigated the effect of aging on different parameters related to inflammation and oxidative stress in liver from two types of male mice models: SAMP8 and SAMR1, and the influence of XANT administration on old SAMP8 mice.

Materials: 

Protein (western) and mRNA expression (RT-PCR) of tumor necrosis factor-alpha, interleukin-1, interleukin 10, heme oxygenases1 and 2, endothelial and inducible nitric oxide synthases, carbonylated proteins and MDA levels were determined. In addition, the apoptotic mediators BAD, BAX and AIF were also determined. Results were submitted to a two way ANOVA statistical evaluation using the Statgraphics program, following for a Fisher test.

Results: 

Inflammation, as well as, oxidative stress and apoptosis markers were increased in the liver of old SAMP8 males, as compared to young controls (p<0.05) and this situation was not observed in the old SAMR1 mice. Exogenous XANT administration partially reverted the effect of aging in the described parameters of old SAMP8 mice (p<0.05).

Conclusions: 

In conclusion, our results suggest that apoptosis secondary to inflammation and oxidative stress could play an important role in the observed liver injury secondary to aging of SAMP8 mice and that XANT may play a potential protective against these age-induced effects.

To cite this abstract, please use the following information:
Acta Physiologica 2012; Volume 206, Supplement 693 :P14

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