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本研究旨在探讨单核细胞趋化蛋白-1(monocyte chemotactic protein 1,MCP-1)在GK大鼠不同时期脑组织的表达以及与认知功能的关系。选取42只雄性2型糖尿病大鼠(Goto-Kakizaki rat,GK rat)为模型组(GK组)模型组随机分为12周、24周、36周组海组14只,同源性Wistar大鼠14只为对照组。应用Morris水迷宫测验(MWM)检测不同时期GK大鼠以评价大鼠的认知功能;每组选7只大鼠行光镜下HE染色来观察海马CA1和CA3区形态病理学变化;酶联免疫吸附法(enzyme-linked immunosorbent assay,ELISA)测定各组剩余大鼠脑组织匀浆MCP-1的表达量。观察GK大鼠行为学及病理学的变化,探讨MCP-1与认知功能受损之间的关系。结果显示:1与同时期对照组相比,GK各组血糖水平显著升高(p<0.01);GK大鼠24W和36W组较12W组显著升高(p<0.05),36W和24W之间无统计学差异(p>0.05);2GK组较同期对照组逃避潜伏期时间明显延长、跨过平台次数减少(p<0.05);GK 12W、24W和36W,3组间逃避潜伏期时间和跨过平台次数均有统计学差异(p<0.05);3对照组没有明显的组织病理学变化,GK组随喂养时间的延长,神经细胞逐渐排列紊乱、脱失、变形和坏死,胞质染色变浅不均,胞核固缩、破裂;4MCP-1蛋白在GK组脑组织匀浆中的表达量明显高于对照组(p<0.05),GK 12W、24W和36W,3组间MCP-1表达量均有统计学差异(p<0.05)。GK大鼠随喂养时间的延长,血糖升高至糖尿病水平从知功能逐渐下降,海马CA1和CA3区出现进展性的病理损害以及脑组织中MCP-1蛋白的高表达。MCP-1蛋白的表达量可能成为临床上判断2型糖尿病认知功能损害程度及预后的重要辅助参考指标。
The purpose of this study was to investigate the expression of monocyte chemotactic protein-1 (MCP-1) in different stages of GK rat brain and its relationship with cognitive function. Forty-two Goto-Kakizaki rats (GK group) were randomly divided into three groups: model group (GK group), model group (GK group) at 12 weeks, 24 weeks, 14 weeks at 36 weeks, 14 Wistar rats For the control group. Morris water maze test (MWM) was used to detect GK rats at different stages to evaluate the cognitive function of rats; 7 rats in each group were observed under light microscope HE staining to observe the pathological changes of hippocampal CA1 and CA3; The expression of MCP-1 in the remaining rat brain homogenates was measured by enzyme-linked immunosorbent assay (ELISA). The changes of behavior and pathology in GK rats were observed to explore the relationship between MCP-1 and impaired cognitive function. The results showed that: 1 Compared with the control group at the same period, the levels of blood glucose were significantly increased in the GK groups (p <0.01); the GW rats in the 24W and 36W groups were significantly higher than those in the 12W group (p <0.05) There was no significant difference between the two groups (p> 0.05). The evasion latency of 2GK group was significantly longer than that of the control group in the same period (p <0.05), while the evasion latency of GK 12W, 24W and 36W, (P <0.05) .3 There was no obvious histopathological changes in the control group. In the GK group, the neurons gradually became disorganized, lost, deformed and necrotic with the prolongation of feeding time, and the cytoplasmic staining became shallow (P <0.05). The expression of MCP-1 in GK group was significantly higher than that in control group (P <0.05). The expression of MCP-1 in GK 12W, 24W and 36W, There was statistical difference (p <0.05). With the prolongation of feeding time, GK rats increased their blood glucose to the level of diabetes from the decline of cognitive function, the progressive pathological damage in hippocampal CA1 and CA3 area and the high expression of MCP-1 protein in brain tissue. The expression of MCP-1 protein may become an important auxiliary reference index for judging the degree of cognitive impairment and prognosis of type 2 diabetes clinically.