JOURNAL OF SHANDONG UNIVERSITY (HEALTH SCIENCES) ›› 2009, Vol. 47 ›› Issue (9): 1-4.

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Cognition dysfunction of diabetic rats and its relation to apoptosis in the frontal lobe cortex, the hippocampus and HbA1c

CHEN Qing, ZHENG Dongmei, KONG Lei, LI Qiu, JIANG Xiuyun, GUAN Qingbo, ZHAO Jiajun    

  1. Department of Endocrinology, Shandong Provincial Hospital Affiliated to Shandong University, Jinan 250021, China
  • Received:2009-04-12 Published:2009-09-16

Abstract:

To discuss the relationship among cognition function, apoptotic status in the cortex of the frontal lobe and the hippocampus and blood glucose in diabetic rats.  MethodsLearning ability of 26 diabetic rats and 30 normal rats were measured by an electric maze after 12 weeks. Then the rats were executed to obtain the brain tissues to estimate the TUNEL (terminal deoxynucleotidyl transferasemediated dUTP nickendlabeling) positive cells and expressions of Bcl2 and Bax genes in the cortex of the frontal lobe and the hippocampus. Learning ability, the number of apoptotic cells in the frontal cortex and the hippocampus, and glycosylated hemoglobin were analyzed. ResultsLearning ability of diabetic rats was worse than that of the control group, as they needed more time to reach the learning standard(P<0.001). TUNEL positive cells in the cortex of the frontal lobe and the hippocampus were more in the diabetes group than in the control group. Expression of Bcl2 gene was reduced while that of the Bax gene was increased in diabetic rats (P<0.01). The time before the diabetic rats reached the learning standard was positively correlated with the apoptotic index of the cortex of the frontal lobe and the hippocampus (r=0.410, P<0.05), and the learning ability of diabetic rats was positively correlated with HbA1c. ConclusionIncreased apoptosis induced by expression of some regulation genes may contribute to cognition dysfunction in diabetes mellitus.

Key words: Diabetes mellitus; Apoptosis; Cognition dysfunction;Rats, Wistar

CLC Number: 

  • R318.15
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