To explore the
role of
nitric oxide (NO) in the pathogenesis and effect on
regulation of
iron metabolism in
anemia of
chronic disease (ACD) and provide experimental evidence for prevention and
treatment of ACD. On the basis of traditional
animal model of
rheumatoid arthritis, an ACD
rat model was established by repeated
injection of Freund's complete adjuvant. The relationship between NO concentration and
iron metabolism was observed in ACD
rats with and without
NO synthase inhibitor,
L-NAME, (
N omega-nitro-L-arginine methyl ester L-NAME). The results showed that
anemia was induced in the
rat model. In the ACD group, NO concentration and
NO synthase activity in
serum increased;
iron, total
iron binding capacity (TIBC) and
transferrin saturation (TS) in
serum and
ferritin in
erythrocytes (rFn) decreased;
transferrin receptor (TfR) and
iron in
bone marrow cells decreased;
ferritin in
serum and
iron in
liver increased and meanwhile the acotinase activity in
liver decreased. After
administration of
L-NAME,
anemia was improved, when NO, NO-synthase activity,
liver iron and
serum ferritin decreased, but
serum iron, TS, TIBC, rFn, TfR,
iron in
marrow cells and
liver acotinase activity elevated. The levels of
parameters for
iron metabolism in ACD +
L-NAME group were situated between ACD and
control groups. It is concluded that NO
plays an important
role in pathogenesis of ACD and influences the
regulation of
iron in ACD. Decrease of NO level as early as possible
will benefit to block the development of
anemia, that
will provide a new strategy of
therapy for ACD.