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Inicio Annals of Hepatology NAMPT INHIBITION AND INCREASED NAD-BIOAVAILABILITY ATENUATE LIVER DAMAGE IN CCl4...
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Vol. 27. Núm. S2.
Oral presentations at the XVI National Congress of the Mexican Association of Hepatology
(enero 2021)
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Vol. 27. Núm. S2.
Oral presentations at the XVI National Congress of the Mexican Association of Hepatology
(enero 2021)
Open Access
NAMPT INHIBITION AND INCREASED NAD-BIOAVAILABILITY ATENUATE LIVER DAMAGE IN CCl4-INDUCED MICE CHRONIC LIVER DISEASE
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J.A. Gutiérrez buendía1, R. Pérez Cabeza de Vaca3, G.A. Domínguez Pérez1, E. Vera Gomez1, A. Hernández Patricio1, K. Moreno Vega1, M. Salamanca García2, J.I. Bustamante Santillan3, P. Mondragón Terán3, R. Hernández Muñoz3, J.A. Suárez Cuenca1
1 Experimental Metabolism Laboratory. Biomedical Research Division. National Medical Center “20 de Noviembre” – ISSSTE. Anatomical Pathology Department NMC “20 de Noviembre” ISSSTE. México City, México
2 Biomedical Research Coordination NMC “20 de November” – ISSSTE. México City, México
3 Cellular Biology and Development Department – IFC – UNAM. México City, México
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Vol. 27. Núm S2

Oral presentations at the XVI National Congress of the Mexican Association of Hepatology

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Introduction and Objectives

Nicotinamide phosphoribosyltransferase (NAMPT) is the rate-limiting enzyme on the NAD+ salvage biosynthetic pathway and a cytokine regulator with an important role in inflammation and fibrogenesis modulation. Use of FK866 (NAMPT inhibitor) has been proposed as a treatment on inflammatory diseases and cancer. However, FK866-induced depletion of NAD may also cause major impairment of the redox and bioenergetics homeostasis of the cell within the liver, thus limiting a favorable outcome for Chronic Liver Disease (CLD), as low NAD levels have been associated with higher Oxidative Stress and increased metabolic risk. The aim of this study was to evaluate the effects of NAMPT inhibition and concomitant NAD restoration on experimental CLD in vivo.

Methods and Results

NAMPT inhibition was evaluated within a CCl4-induced CLD model on male BALB/c mice and a mild improved outcome was observed on the histological and biochemical features. NAD restoration strategy was accomplished by the concomitant administration of its precursor, NMN, resulting in significant improve on the histological analysis; lower inflammatory infiltrate and fibrosis were measured by image analysis on digitalized micrographies. Lower levels of Direct Bilirubin were also observed. NAMPT inhibition and adequate NAD restoration were confirmed by a colorimetric assay of NADH and NAD+ and biochemical features were measured by routinary Liver Function Tests. Silymarin was used as a hepatoprotective control.

Conclusion

This study shows that NAMPT inhibition concomitant to NAD restoration significantly attenuate experimental liver damage.

The authors declare that there is no conflict of interest.

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