ABSTRACT
La esteatosis hepática es el acúmulo de grasa en los hepatocitos, que puede ser la consecuencia del proceso de regeneración hepática o de procesos patológicos como la enfermedad del hígado graso alcohólica y no-alcohólica. A pesar de su importancia, en ambos casos el mecanismo exacto en que la esteatosis influye en la regeneración hepática es escasamente comprendido. Estudios previos han demostrado que los pacientes que presentan hígado graso expresan una regeneración hepática dispar, posiblemente debido a la acumulación de especies reactivas de oxígeno generada por procesos inflamatorios ocasionados por activación de las células de Kupffer. En este artículo se revisan distintos factores que afectan la regeneración hepática, tratando de comprender el mecanismo involucrado en la regeneración dispar en hígados con esteatosis ocasionada por una enfermedad de hígado graso no-alcohólica.
Steatosis is the accumulation of fat in hepatocytes, which may be the result of liver regeneration or pathological processes such as alcoholic and nonalcoholic fatty liver disease. Despite its importance, in both cases the exact mechanism that prevails in fatty liver regeneration is poorly understood. Previous studies have shown that patients with fatty liver express dispar regeneration, possibly due to the accumulation of reactive oxygen species generated by inflammatory processes caused by activation of Kupffer cells. In this article we review several factors that affect liver regeneration, trying to understand the underlying mechanism of dispar regeneration in fatty liver as a consequence of nonalcoholic fatty liver disease.
Subject(s)
Humans , Fatty Liver/etiology , Kupffer Cells/physiology , Liver Regeneration/physiology , Cytokines , Reactive Oxygen SpeciesABSTRACT
Although hepatic stellate cells, which are liver specific pericytes, have been recognized within the vasculature of the sinusoid for more than one hundred years, the biology and function of these cells is unclear. Recent studies have highlighted the key role of stellate cells in a number of fundamental processes that include wound healing/fibrosis, vasoregulation, and vascular remodeling/angiogenesis. In the liver, these processes are particularly important in the development of cirrhosis, portal hypertension and cancer. This article highlights the recent advances in our understanding of the biology of hepatic stellate cells and discusses some of the recently-ascribed functions that are relevant to liver fibrosis, portal hypertension and cancer angiogenesis.
Subject(s)
Humans , Cell Communication/physiology , Hypertension, Portal/etiology , Kupffer Cells/physiology , Liver Cirrhosis/etiology , Liver Neoplasms/blood supply , Neovascularization, Pathologic/etiology , Pericytes/physiologyABSTRACT
Kupffer cells are major determinants of outcome of liver injury. Their activity was therefore studied in a model of chronic liver disease. The effect of Tinospora cordifolia, an indigenous agent with proven hepatoprotective activity, was evaluated on Kupffer cell function, using carbon clearance test as a parameter. Rats were divided into two major groups. In Gp I which served as normal control t1/2 of carbon was 9.48 +/- 4.14 min. GpII received horse-serum in a dose of 0.5 ml/100 gm b.w. i.p. for a period of 12 weeks and was divided into three sub-groups. In Gp IIA at the end of 12 weeks half-life of carbon was found to be significantly increased to 19.86 +/- 7.95 min (p < 0.01). Indicating suppressed Kupffer cell function in chronic liver damage. In Gp IIB treated with vehicle for 4 more weeks there was significant prolongation of half-life to 38.32 +/- 10.61 min (p < 0.01), indicating perpetuation of damage in absence of damaging agent. Whereas in Gp IIc, treated with Tinospora cordifolia t 1/2 was decreased to 14.24 7.74 min (p < .01), as compared to vehicle control indicating a significant improvement in Kupffer cell function and a trend towards normalization.
Subject(s)
Analysis of Variance , Animals , Carbon/pharmacokinetics , Disease Models, Animal , Female , Kupffer Cells/physiology , Liver Failure/metabolism , Male , Metabolic Clearance Rate , Plants, Medicinal , RatsABSTRACT
Ricin, a highly toxic protein from castor beans was administered (ip) to rats in a dose of 1.25 micrograms/100 g to selectively deplete at least 60-70% of Kupffer cells. This dose spared hepatocytes. This rat model was used to study acute phase protein synthesis and the role of Kupffer cells in acute phase response (APR). Ricin itself induced an APR, similar in pattern but of lower magnitude, than that induced by turpentine. However, the effect of combination of ricin and turpentine on APR was not additive. Kupffer cells appear to play permissive role in APR through mediators like hepatocytes stimulating factors.