Entamoeba histolytica is the causative agent of
amoebic liver abscess (ALA), which course with an uncontrolled
inflammation and nitro-oxidative stresses, although it is well known that amoeba has an effective defence mechanisms against this toxic environment, the underlying molecular factors responsible for progression of tissue damage remain largely unknown. The purpose of the present study was to determine during the acute stage of ALA in hamsters, the involvement of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and
nuclear factor-kappa B (NF-κB), which are activated in response to oxidative stress. From 12 h post-
infection the ALA was visible, haematoxylin-
eosin and Masson's trichrome stains were consistent with these observations, and
alanine aminotransferase,
alkaline phosphatase and γ-
glutamyl transpeptidase serum activities were increased too. At 48 h after
infection,
liver glycogen content was significantly reduced. Western blot analyses showed that
4-Hydroxy-2-nonenal peaked at 12 h, while
glycogen synthase kinase-3β, cleaved
caspase-3, pNF-κB, interleukin-1β and tumour
necrosis factor-α were overexpressed from 12 to 48 h post-
infection. Otherwise, Nrf2 and
superoxide dismutase-1, decreased at 48 h and
catalase declined at 36 and 48 h. Furthermore,
heme oxygenase-1 was increased at 12 and 24 h and decreased to normal levels at 36 and 48 h. These findings suggest for the first time that the host
antioxidant system of Nrf2 is influenced during ALA.