Role of nitric oxide increase on induced programmed cell death during early stages of rat liver regeneration

24Citations
Citations of this article
14Readers
Mendeley users who have this article in their library.

Abstract

We analysed the possible cellular mechanism involved in the NO action in the balance between apoptosis and cell proliferation in liver regeneration process. We determined p53, proapoptotic protein Bax, antiapoptotic Bcl-x L, proliferating cell nuclear antigen (PCNA) and apoptotic index at the early stages of regenerative process after NO increase by lipopolysaccharide-induction (LPS) of inducible-type nitric oxide synthase (iNOS) and by direct NO donor (sodium nitroprusside, SNP). Male Wistar rats were randomised in four experimental groups: sham operated control (Sh), partial hepatectomised control (PH-C), partial hepatectomised pretreated with LPS (2 mg/kg body weight, i.p.) (PH-LPS), and partial hepatectomised pretreated with SNP (2.5 mg/kg body weight, i.v. at a rate of 1 ml/h) (PH-SNP). Animals were killed 5 h post-surgery. Hepatic cytosolic iNOS showed an increase of 34% in PH-C animals with respect to Sh, and LPS-treatment increased iNOS protein levels 30% compared with PH-C. Bax and p53 protein levels showed significant increases in LPS- and SNP-treated hepatectomised rats with respect to PH-C. The apoptotic indexes were increased 75% in both, PH-LPS and PH-SNP rats versus PH-C. The increase of NO did not show any change in the proliferation process. These results suggest that NO is involved in apoptosis via p53 and Bax proteins after PH, showing a tightly regulated growth process in liver regeneration. © 2004 Elsevier B.V. All rights reserved.

Cite

CITATION STYLE

APA

Ronco, M. T., Alvarez, M. D. L., Monti, J. A., Carrillo, M. C., Pisani, G. B., Lugano, M. C., & Carnovale, C. E. (2004). Role of nitric oxide increase on induced programmed cell death during early stages of rat liver regeneration. Biochimica et Biophysica Acta - Molecular Basis of Disease, 1690(1), 70–76. https://doi.org/10.1016/j.bbadis.2004.05.004

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free