RESUMEN
<p><b>OBJECTIVE</b>To observe the effects of electroacupuncture (EA) on postoperative cognitive dysfunction (POCD) and AngⅡ/AT1R in the hippocampus in D-galactose-induced aging rats which received hepalobectomy, and to explore the possible mechanism of EA on POCD.</p><p><b>METHODS</b>Eighty male Sprague-Dawley rats were randomly divided into a young control group (10 rats), a D-Galactose-induced aged (Da) group (10 rats), a Da+hepatolobectomy group (30 rats) and an EA group (30 rats). The rats in the Da+hepatolobectomy group and EA group were further randomly divided into a 1 d subgroup, 3 d subgroup and a 7 d subgroup, 10 rats in each subgroup. The rats in the EA group were treated with EA at "Baihui" (GV 20) and "Dazhui" (GV 14) with continuous wave (15 Hz in frequency and 1 mA in intensity), and rats in each subgroup were treated for 1 d, 3 d and 7 d, respectively. The rats in the remaining groups were treated with immobilization, once a day. The Y-maze was used to observe the behavior change of rats, and ELISA was applied to measure the level of hippocampal AngⅡ, and RT-PCR and immunohistochemistry method were performed to detect AT1R mRNA expressions and AT1R positive expression in the hippocampus.</p><p><b>RESULTS</b>The number of rat initiative avoidance in the Da group was significantly less than that in the young control group (<0.05), and the mRNA expression and positive percentage of AT1R in the hippocampus in the Da group were significantly higher than those in the young control group (both<0.01). Compared with the Da group, the number of rat initiative avoidance in each subgroup of Da+hepatolobectomy group and EA group were significantly reduced (all<0.01), and the expression of AngⅡ, AT1R mRNA and AT1R positive cells percentage in the hippocampus were significantly increased (<0.05,<0.01). The number of rat initiative avoidance in each subgroup of EA group was higher than that in the subgroup of Da+hepatolobectomy group (<0.05,<0.01); and the expression of AngⅡ, AT1R mRNA, and AT1R positive percentage in the EA group were significantly less than that in the Da+hepatolobectomy group (<0.05,<0.01).</p><p><b>CONCLUSIONS</b>EA at "Baihui" (GV 20) and "Dazhui" (GV 14) could improve POCD in D-galactose-induced aging rats which received hepalobectomy, and it is likely to be related with the inhibition of AngⅡ, AT1R positive expression and AT1R mRNA in the hippocampus.</p>
RESUMEN
<p><b>OBJECTIVE</b>To investigate the effects of nano-lead exposure on learning and memory and iron homeostasis in the brain of the offspring rats on postnatal day 21 (PND21) and postnatal day 42 (PND42).</p><p><b>METHODS</b>Twenty adult pregnant female Sprague-Dawley rats were randomly divided into control group and nano-lead group. Rats in the nano-lead group were orally administrated 10 mg/kg nano-lead, while rats in the control group were administrated an equal volume of normal saline until PND21. On PND21, the offspring rats were weaned and given the same treatment as the pregnant rats until 42 days after birth. The learning and memory ability of offspring rats on PND21 and PND42 was evaluated by Morris water maze test. The hippocampus and cortex s amples of offspring rats on PND21 and PND42 were collected to determine iron and lead levels in the hippocampus and cortex by inductively coupled plasma-mass spectrometry. The distributions of iron in the hippocampus and cortex were observed by Perl's iron staining. The expression levels of ferritin, ferroportin 1 (FPN1), hephaestin (HP), and ceruloplasmin (CP) were measured by enzyme-linked immunosorbent assay.</p><p><b>RESULTS</b>After nano-lead exposure, the iron content in the cortex of offspring rats on PND21 and PND42 in the nano-lead group was significantly higher than those in the control group (32.63 ± 6.03 µg/g vs 27.04 ± 5.82 µg/g, P<0.05; 46.20 ±10.60 µg/g vs 36.61 ± 10.2µg/g, P<0.05). The iron content in the hippocampus of offspring rats on PND42 in the nano-lead group was significantly higher than that in the control group (56.9 ± 4.37µg/g vs 37.71 ± 6.92µg/g, P<0.05). The Perl's staining showed massive iron deposition in the cortex and hippocampus in the nano-lead group. FPNl level in the cotfex of offspring rats on PND21 in the nano-lead group was significantly lower than that in the control group (3.64 ± 0.23 ng/g vs 4.99 ± 0.95 ng/g, P<0.05). FPN1 level in the hippocampus of offspring rats on PND42 in the nano-lead group was significantly lower than that in the control group (2.28 ± 0.51 ng/g vs 3.69 ± 0.69 ng/g, P<0.05). The escape latencies of offspring rats on PND21 and PND42 in the nano-lead group were longer than those in the control group (15.54 ± 2.89 s vs 9.01 ± 4.66 s; 6.16 ± 1.42 s vs 4.26 ± 1.51 s). The numbers of platform crossings of offspring rats on PND21 and PND42 in the nano- lead group were significantly lower than those in the control group (7.77 ± 2.16 times vs 11.2 ± 1.61 times, P<0.05; 8.12 ± 1.51 times vs 13.0 ± 2.21 times, P<0.05).</p><p><b>ONCLUSION</b>n Nano-lead exposure can result in iron homeostasis disorders in the hippocampus and cortex of offspring rats and affect their learning and memory ability.</p>