| Objective: To explore the effects of Ghrelin on the expression of cAMP responsive element binding protein(CREB) and brain-derived neurotrophic factor(BDNF) in hippocampus of diabetic rats.Methods: 48 SD male rats were meanly divided into normal group(C group), diabetic modle group(D group), Ghrelin treatment group(T1 group),Ghrelin and D-lys3-GHRP-6 treatment group(T2 group) randomly. Streptozotocin-diabetic rats model were established, diabetic rats with depression were screened by open-field test, learning and memory behaviours were measured using a spatial version of the Morris water maze test. The protein expression of BDNF,CREB and p-CREB were examined with immunohistochemical method. The mRNA expression of BDNF, CREB was examined with RT-PCR in hippocampus.Results: All parameters tested in open-field test among the four groups were not significantly different (P>0.05).Comparing to the C group, the escape letency in D and T2 group was significantly longer and the frequency of entrance into the target zone was less(P<0.05). The escape letency was shorter in T1 group and the frequency of entrance into target zone was more than D group (P<0.05). The BDNF, CREB, p-CREB protein expression in hippocampus of D group and T1 group were decreased transparently (P<0.05), the mRNA expression of BDNF, CREB were descendent in hippocampus (P<0.05) and the protein expression of BDNF, CREB, p-CREB were also decreased than C group and T1 group (P<0.05).Conclusion:1.The diabetic rats showed cognitive dysfunction when they were 12weeks old. Ghrelin could attenuated cognitive dysfunction in STZ-induced diabetic rats.2.It's demonstrated that the changes of BDNF, CREB involve in the pathogenesis of diabetic encephalopathy.3.And Ghrelin could attenuate cognitive dysfunction in diabetic rats by improving the expression of BDNF and CREB. Objective: To explore the effects of Ghrelin on the hippocampus neuronal apoptosis and the cognitive function of diabetic rats.Methods: 48 SD male rats were meanly divided into normal group(C group), diabetic modle group(D group), Ghrelin treatment group(T1 group),Ghrelin and D-lys3-GHRP-6 treatment group(T2 group) randomly. Streptozotocin-diabetic rats model were established, diabetic rats with depression were screened by open-field test, learning and memory behaviors were measured using a spatial version of the Morris water maze test. The mRNA level of caspase-3 in hippocampus was examined by RT-PCR. The protein expression of caspase-3, BCL-xl were examined with immunohistochemical method. Meanwhile the hippocampus neuronal apoptosis were measured by TUNEL.Results: All parameters tested in open-field test among the four groups were not significantly different (P>0.05). Comparing to the C group, the escape letency in D and T2 group was significantly longer and the frequency of entrance into the target zone was less. The escape letency was shorter in T1 group and the frequency of entrance into target zone was more than D group (P<0.05). Comparing to the C group, the mRNA and protein level of caspase-3 in hippocampal neurons increased and the protein expression of BCL-xl were descendent (P<0.05), the number of neuronal apoptosis increased markedly(P<0.05)in D and T2 group . The changes of caspase-3 in hippocampus significantly reduced(P<0.05)and the expression of BCL-xl in hippocampus increased in the T1 group and the number of apoptotic neurons of the hippocampus was decreased remarkably (P<0.05).Conclusion:1.The number of apoptotic neurons was increased, accompany the cognitive dysfunction in diabetic rats. It demonstrated that neuronal apoptosis is involved in the progression of diabetic encephalopathy. 2.Ghrelin could improve cognitive ability in diabetic rats, which increased the expression of BCL-xl and decreased the expression of caspase-3 to protect hippocampus neurons. |
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