| Objectives: To make brain damage of intrauterine growth retardation (IUGR) ratmodel by feeding pregnant rats6%low protein diet. To observe expressive changes ofneuropsin in hippocampus, assess learning and memory ability of offspring rats. To discussthe mechanism of brain damage of IUGRMethods: Twenty-eight healthy three-month Sprague-Dawley rats were enrolled inthe study. Male and female rats were put into a cage at the proportion of1:1. The pregnantrats were divided into two groups: the control group and IUGR group. The rats of controlgroup were fed by21%normal protein diet and the rats of IUGR group were fed by6%low protein diet to the pregnant rats. During the loctation of21d for offspring rats of twogroups, all the female rats were fed by21%normal protein diet and running water. After21d, the offspring rats of the two groups were separated from female rats, given21%normal protein diet and running water until32d. We chose1d,5d,10d and21d as for4different time points. In every time point, there were six rats in each group, we observe theoffspring body weight, crown-rump length, brain weight and take hippocampus for study,hippocampus structure was observed with HE stain method in1d and21d, the expressionof neuropsin in hippocampus was observed with Western blot method. Morris water mazetest was performed to assess learning and memory ability of offspring rats from26d to32d.Results:1. The dynamic comparison of physique growth and brain weight of theoffspring rats in two groups: At1d, the IUGR rats were thinner and shorter, and their bodyweight, crown-rump and brain weight was lower than controls(P＜0.05); At5d and10d,body weight, crown-rump and the brain weight of the IUGR rats were still lower thancontrols(P＜0.05); After catch-up growing, at21d, body weight, crown-rump of the twogroups had no differences(P＞0.05), but the brain weight of them were still lower thancontrols(P＜0.05) 2. The changes of HE stain in the hippocampus of the offspring rats in two groups: At1d, the neurons in the hippocampus of IUGR rats arranged raritas and disorder, someneurons were dropsy, chromatospherite pyknosis cell appeared, there were more apoptosiscell and the numbers of neurons decreased compared with normal group.21d the dropsy ofthe neurons in IUGR group alomst disappeared, but the arrange of neurons was stilldisorder and there was no obviously increase of the numbers of neurons.3.The expression of neuropsin in hippocampus of the offspring rats in two groups:for4time points of two groups, at1d the expression of neuropsin was low, at5d theexpression of neuropsin increased, at10d and21d the expression of neuropsin was a steepincrease. For controls, the expression of neuropsin of IUGR group was lower than theexpression of control group (P＜0.05) for4time points.4.Morris water test:(1)The average latencies of all rats were reduced by degree fromD1to D5.The escape latency was longer in rats of IUGR group than that of control atD5(P<0.05).(2) As far as search strategy is concerned, rats of IUGR group performedworse than those in control group at D5,with statistically significant difference.(3)Thefrequency of passing through the platform quadrant in rats had no significant difference inthe two groups (P>0.05).Conclusions:1.Feeding6%low protein diet can make model of brain damage ofIUGR rats.2. IUGR rats were thinner and shorter; the brain weight was lower; the numbers of theneurons in the hippocampus were less. By feeding normal protein diet, IUGR rats couldachieve the catch-up growth, but the brain weight and the numbers of neurons failed. Andthe learning and memory ability of IUGR rats decreased.3. The expression of neuropsin in hippocampus of IUGR rats was lower than theexpression of normal rats from birth to21d, the reduced expression of neuropsin isprobably one of the important neural mechanisms of brain damage of IUGR. |
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