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Effect and mechanism of auricularia auriculajudae polysaccharide in hippocampus of streptozotocin‐induced diabetic cognitive impairment rats
Author(s) -
Fei Jiaqian,
Fan Ying,
Zhang Xiaoming,
Ye Tingmei,
Chen Yingying,
Shen Yueliang,
Wang Linlin
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.578.13
Subject(s) - streptozotocin , morris water navigation task , dentate gyrus , hippocampus , medicine , hippocampal formation , endocrinology , intraperitoneal injection , chemistry , diabetes mellitus
Aim To investigate the effect and mechanism of auricularia auriculajudae polysaccharide(APP) in the hippocampus of streptozotocin‐induced diabetic cognitive impairment rats. Methods APP group was treated with intragastric administration of APP (150mg/day) for 4 weeks after intraperitoneal streptozotocin(STZ) injection (60 mg/kg). Their capacity for learning and memory were detected by the Morris water maze. Microstructural and ultrastructural changes were also analysed by transmission electron microscope (TEM). Thrombospondin‐1 (TSP‐1) expression in the CA1 and dentate gyrus (DG) hippocampal area was examined by immunohistochemistry and RT‐PCR. Results Four weeks after STZ induction, the diabetic rats showed decreased capacity for learning and memory. However, the cognitive impairment was significantly less severe in APP group as indicated by decrease in the time spent in the target quadrant (P < 0.05) and the number of crossings of the previous location of the platform (P < 0.05). TEM also revealed that APP group had less swollen of mitochondria, decreased heterochromatin accumulation and increased synaptic contacts when compared with the diabetic group. Morever, TSP‐1 expressions in the CA1 and DG were significantly lower in APP group than in diabetic group. Conclusion APP could alleviate the impairment of memory and cognition in diabetic rat, which may be mediated by decreasing the expression of TSP‐1 in the hippocampus.