Objective To explore the effects of sodium aminosalicylate (PAS-Na) on basal forebrain choline acetyltransferase (ChAT) neurons of rats induced by sub-chronic Mn exposure.
Methods Forty-eight male SD rats were randomly assigned into 6 groups: control group I and Ⅱ, Mn-exposed group I and Ⅱ, PAS-Na prevention (PAS-P) group, and PAS-Na treatment (PAS-T) group, 8 rats for each group. The Mn-exposed group, the PAS-P group, and the PAS-T group received intraperitoneal injection (ip) of MnCl2O& #183;4H2O 15 mg/kg, the control group received ip of physiological saline at the same dose, and the PAS-P group received back subcutaneous injection (sc) of PAS-Na 200 mg/kg, all procedures were performed 5 days a week for 12 weeks. Then, the rats in the PAS-T group received back sc of PAS-Na 200 mg/kg, while the rats in the Mn-exposed group II and the control group II received back sc of physiological saline at the same volume once a day, for 6 weeks. Morris water maze was utilized to probe rats learning and memory capacity. Morphological change and ChAT positive neuron count in basal forebrain were recorded under microscope after immunohistochemistry staining, and ChAT protein activity was also detected.
Results After 12 weeks, the escape latency and the swimming distance obviously increased in the Mn-exposed group I when compared with those of the control group I, but the treatment in the PAS-P group reversed the escape latency and swimming distance induced by Mn exposure (P < 0.05). The ChAT positive neuron count of basal forebrain vertical limb of diagonal band (vDB)/horizontal limb of diagonal band (hDB) and ChAT protein activity in the Mn-exposed group I were lower than those in the control group I, the treatment in the PAS-P group reversed distinctly vDB/hDB ChAT positive count and ChAT protein activity induced by Mn (P < 0.05). After 18 weeks, the escape latency and the swimming distance obviously increased in the Mn-exposed group Ⅱ when compared with those of the control group Ⅱ , but the treatment in the PAS-T group reversed the escape latency and the swimming distance induced by Mn (P < 0.05). The ChAT positive neuron count of basal forebrain vDB/hDB in the Mn-exposed group Ⅱwas lower than that in the control group Ⅱ, the treatment of the PAS-T group reversed distinctly vDB ChAT positive count induced by Mn (P < 0.05).
Conclusion PAS-Na may reverse the number of ChAT positive neurons and ChAT protein activity reduced by manganese exposure. Therefore, it may have an interventive effect on learning capacity and memory impairment by manganese exposure.
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