Relationship between the changes of cognitive function and the expression of tumor necrosis factor alpha, interleukin 10 in hippocampus of diabetic rats
Ting He, Ya Miao, Yitong Zhu, Wei Li
Abstract
Ting He, Ya Miao, Yitong Zhu, Wei Li
Abstract
Objective To observe changes of cognitive function and the expression of tumor necrosis factor alpha(TNF-α), interleukin 10(IL-10) in hippocampus of diabetic rats, and assess the role of inflammation in the possible pathogenesis of diabetic encephalopathy(DE). Methods 30 male SD rats were randomly divided into control group and diabetes mellitus group. After 4 weeks of feeding high fat diet, diabetes mellitus group according to 30mg/kg injected with streptozotocin to establish type 2 diabetic rat model. At the end of the experiment, cognition were evaluated using water maze test. The concentration of beta-amyloid(Aβ) in hippocampus of diabetic rats were detected through enzyme linked immunosorbent assay, and the expression of TNF-α, IL-10 were detected by Western blotting. The expression of Aβ, TNF-α, IL-10 were observed through immunohistochemistry. Results Time spent in the target quadrant in diabetes mellitus group was shorter than that in control group((38.21±3.68)s vs(42.10±2.62)s, t=3.105, P<0.01). The frequency of crossing original platform site was less than that in control group((2.62±0.77) vs(3.69±0.95), t=3.184, P<0.01). Compared with control group the expression of Aβ, TNF-α were higher(BothP<0.01), and IL-10 were lower(P<0.01)in diabetes mellitus group. The positive expression of Aβ, TNF-α were obviously and IL-10 were less obviously observed in diabetes mellitus group according to immunohistochemistry. Conclusion The cognitive decline in diabetic rats is possibly related to inflammatory cytokines expressing out of balance. Key words: Diabetes mellitus; Cognition disorder; Tumor necrosis factor alpha; Interleukin 10
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Objective To observe changes of cognitive function and the expression of tumor necrosis factor alpha(TNF-α), interleukin 10(IL-10) in hippocampus of diabetic rats, and assess the role of inflammation in the possible pathogenesis of diabetic encephalopathy(DE). Methods 30 male SD rats were randomly divided into control group and diabetes mellitus group. After 4 weeks of feeding high fat diet, diabetes mellitus group according to 30mg/kg injected with streptozotocin to establish type 2 diabetic rat model. At the end of the experiment, cognition were evaluated using water maze test. The concentration of beta-amyloid(Aβ) in hippocampus of diabetic rats were detected through enzyme linked immunosorbent assay, and the expression of TNF-α, IL-10 were detected by Western blotting. The expression of Aβ, TNF-α, IL-10 were observed through immunohistochemistry. Results Time spent in the target quadrant in diabetes mellitus group was shorter than that in control group((38.21±3.68)s vs(42.10±2.62)s, t=3.105, P<0.01). The frequency of crossing original platform site was less than that in control group((2.62±0.77) vs(3.69±0.95), t=3.184, P<0.01). Compared with control group the expression of Aβ, TNF-α were higher(BothP<0.01), and IL-10 were lower(P<0.01)in diabetes mellitus group. The positive expression of Aβ, TNF-α were obviously and IL-10 were less obviously observed in diabetes mellitus group according to immunohistochemistry. Conclusion The cognitive decline in diabetic rats is possibly related to inflammatory cytokines expressing out of balance. Key words: Diabetes mellitus; Cognition disorder; Tumor necrosis factor alpha; Interleukin 10
Key concepts: Internal medicine, Diabetes mellitus, Endocrinology, Streptozotocin, Medicine, Tumor necrosis factor alpha, Hippocampus, Immunohistochemistry