ABSTRACT
Objective To explore the protective effect of selenium, an antioxidant, on fluoride-induced renal injury in rats and find out the optimal level of selenium against fluoride toxicity and its valid molecular target.Methods All 80 male weanling SD rats were randomly divided into 8 groups by body weight as follows: normal control group(drinking tap water), fluoride exposed group (drinking water containing 50 mg/L of NaF), low, middle,high selenium exposed groups(drinking water containing 0.375, 0.750, 1.500 mg/L of Na2SeO3) and low, middle,high Se-fluoride groups (drinking water containing both 50 mg/L NaF and three doses of Na2SeO3 as abovementioned, respectively). After 6 months, the rats were killed then the oxidation level and nuclear factor κB(NF-κB)expression level in kidney were measured. Results The weight of the fluoride exposed group[(695.95 ± 55.89 )g]was significantly deceased than the controls[(782.69 ± 56.12)g, P ＜ 0.01]. Glutathione peroxidase(GSH-Px)activity of fluoride exposed group[(55.86 ± 5.09)U/mgprot] was not significantly different but decreased. Tatal antioxidant capacity (T-AOC) activity in fluoride exposed group [(7.54 ± 1.35)U/mgprot] significantly decreased than the controls[(9.03 ± 0.37 )U/mgprot, P ＜ 0.05]. In addition, a significant increase of malondialdehyde ( MDA )in fluoride exposed group[(3.86 ± 0.31 )mnol/mgprot, P ＜ 0.05] was observed than the controls[(3.14 ± 0.32)nmol/mgprot, P ＜ 0.05]. GSH-Px activity of high Se-fluoride group[(74.99 ± 8.41 )U/mgprot] was significantly higher than the fluoride exposed group[(55.86 ± 5.09)U/mgprot, P ＜ 0.05] and its MDA level[(3.17 ± 0.20)nmol/mgprot] was lower than the fluoride exposed group[(3.86 ± 0.31 ) nmol/mgprot, P ＜ 0.05]. NF-κB expression levels of fluoride group, high selenium group and low Se-fluoride group(0.360 ± 0.015,0.367 ± 0.007,0.376 ± 0.006,respecyively) were obviously increased compared with the controls(0.312 ± 0.022, P ＜ 0.05); it was significantly lower in high Se-fluoride group(0.312 ± 0.005) than in fluoride exposed group(0.360 ± 0.015, P ＜ 0.05). Conclusions Na2SeO3 of 1.5 mg/L is the optimal dose against chronic fluorosis on kidney injury under this experimental condition.NF-κB is likely to be a target molecule of the selenium as an antagonist on fluorosis.
ABSTRACT
<p><b>AIM</b>To study the effects of puerarin on learning-memory behavior of aging mice induced by D-galactose and its possible mechanism of action.</p><p><b>METHODS</b>The aging mice were induced by s.c. 0.12 g.kg-1 D-galactose for 6 weeks. The aging mice were treated with three doses of puerarin once a day for 5 weeks. The spontaneous behavior and the learning memory behavior were tested in the aging mice using open field and Y-maze at the next day after the last treatment. The structure of Gray I synaptic interface in the CA3 area of the hippocampus was quantitatively analyzed by electronic microscope and computer image processing appliance.</p><p><b>RESULTS</b>Compared with the D-galactose control group, puerarin (60 mg.kg-1) was shown to increase significantly the spontaneous behavior and explorative response in the open field, and improve remarkablely the learning and memory ability of the aging mice induced by D-galactose. Meanwhile, the thickness of post-synaptic density (PSD) was increased, and the width of the synaptic cleft in the hippocampus CA3 area was shortened.</p><p><b>CONCLUSION</b>Puerarin showed an improvement effect against the memory impairment in the modelling aging-mice induced by D-galactose. A pathological alteration of synaptic interface structure in hippocampus of the mice may be involved in the effect.</p>