RT Journal Article
T1 Role of Kupffer Cells in Thioacetamide-Induced Cell Cycle Dysfunction
A1 Bautista, Mirandeli
A1 Andres, David
A1 Cascales, María
A1 Morales González, José A.
A1 Sánchez Reus, María Isabel
A1 Madrigal Santillán, Eduardo
A1 Valadez Vega, Carmen
A1 Fregoso Aguilar, Tomas
A1 Mendoza Pérez, Jorge Alberto
A1 Gutiérrez Salinas, José
A1 Esquivel Soto, Jaime
AB It is well known that gadolinium chloride (GD) attenuates drug-induced hepatotoxicity by selectively inactivating Kupffer cells. In the present study the effect of GD in reference to cell cycle and postnecrotic liver regeneration induced by thioacetamide (TA) in rats was studied. Two months male rats, intraveously pretreated with a single dose of GD (0.1 mmol/Kg), were intraperitoneally injected with TA (6.6 mmol/Kg). Samples of blood and liver were obtained from rats at 0, 12, 24, 48, 72 and 96 h following TA intoxication. Parameters related to liver damage were determined in blood. In order to evaluate the mechanisms involved in the post-necrotic regenerative state, the levels of cyclin D and cyclin E as well as protein p27 and Proliferating Cell Nuclear Antigen(PCNA) were determined in liver extracts because of their roles in the control of cell cycle check-points. The results showed that GD significantly reduced the extent of necrosis. Noticeable changes were detected in the levels of cyclin D1, cyclin E, p27 and PCNA when compared to those induced by thioacetamide. Thus GD pre-treatment reduced TA-induced liver injury and accelerated the postnecrotic liver regeneration. These results demonstrate that Kupffer cells are involved in TA-induced liver and also in the postnecrotic proliferative liver states.
PB MDPI
SN 1420-3049
YR 2011
FD 2011-09-29
LK https://hdl.handle.net/20.500.14352/43341
UL https://hdl.handle.net/20.500.14352/43341
LA eng
DS Docta Complutense
RD 8 abr 2025