Objective To study the relationship between the changes of TRIM16 in hippocampus of type 2 diabetic rats induced by streptozotocin (STZ) and cognitive dysfunction and apoptosis of hippocampal cells.Methods The male Sprague-Dawley (SD) rats of 8 weeks old were randomly divided into diabetic group (DM group) (n=25) and normal control group (NC group) (n=15).NC group were given normal feed, DM rats were fed with high glucose and high fat diet,followed by low dose of STZ (25 mg/kg, intraperitoneal injection), induced compensatory secretion of insulin, five days after the detection of tail vein blood glucose>16.7 mmol/L, and established the STZ.Meanwhile, citric acid buffer was injected to rats in group as control.After successful modeling, the rats in the two groups were fed with 17 weeks.Morris water maze test was used to detect the cognitive function of the two groups of rats.The protein expression of TRIM16, Bax and Bcl-2 protein in fresh hippocampus tissue of DM group and NC group rats was detected using western blotting.Rats in DM group and NC group were perfused with brain, and the hippocampal tissues were stained with immunohistochemistry.TUNEL method was used to detect the apoptosis of hippocampus cells.ResultsCompared with NC group, morris water maze test showed that the escape latency of rats in DM group is longer than NC group, staying at the original platform quadrant time in DM group is less than the NC group.TUNEL assay showed that after injection of 17 weeks, hippocampal CA1 pyramidal cells in type 2 diabetic rats appeared obvious apoptosis, positive neurons in the nuclei were brown, karyopyknosis anachromasis, while control group of neurons in the nucleus without brown coloring.Compared with the NC group, hippocampus immunohistochemistry results showed that the protein of TRIM16 in hippocampus CA1 region of type 2 diabetic rats was increased, cytoplasm brown, coarse granular.Compared with the NC group, the expression of Bcl-2 had no obvious change in hippocampus of type 2 diabetic rats at 17 weeks, while the expression of TRIM16, Bax and the ratio of Bax/Bcl-2 was significantly increased (P<0.05).Conclusion The protein expression of TRIM16 using immunohistochemical and Western blotting in hippocampus of diabetic rats induced by STZ was increased.There is apoptosis in hippocampus of diabetic rats induced by STZ, the expression of Bcl-2 was not significantly changed, the expression of Bax and the ratio of Bax/Bcl-2 were significantly increased.TRIM16 is involved in diabetic cognitive dysfunction by promoting apoptosis of diabetic rat hippocampus.

Objective To explore protective effects of panaxtrial saponins (PTS) on cognition and memory of diabetic rats and to reveal its mechanism by which might involve regulating activity of astrocytes. Methods SD rats (n=24) were ran?domly assigned into control, diabetic and PTS-treated groups (n=8 in each group). Rat diabetic model was induced through streptozotocin injection intraperitoneally. Rats in control group were native rats, and rats in PTS-treated group were diabetic rats that were administered with PTS. Body weight and blood glucose were monitored through the experiments. Three months later, state of cognition was examined by methods of water maze. Hippocampal astrocyte morphology were detected by immu?nohistochemistry, and the expression of glial cell line-derived neurotrophic factor (GDNF) and glial fibrillary acidic protein (GFAP) in hippocampus were revealed by Western blot. Results Compared with control group, diabetic group showed cog?nitive dysfunction, atrophic astrocyte soma, shrinked astrocyte processes, and down-regulation of hippocampal GFAP and GDNF (P<0.05). Compared with diabetic group, PTS-treated group exhibited improved cognition and morphology of hippo?campal astrocyte, and reversed expression of GFAP and GDNF in diabetic hippocampus (P<0.05). Conclusion PTS re?versed astrocytic reactivity as well as expression of GDNF and GFAP in diabetic hippocampus and ameliorated diabetic cog?nitive dysfunction.

OBJECTIVE To clarify the influence factors of hearing impairment in mice caused by lack of folic acid and the mechanism.METHODS Mice were randomly divided into 2 groups,fed with no folic acid diet and normal diet for 10 weeks.Hearing was tested by ABR.Serum homocysteine,folic acid were detected.Immune imprint method was used to analyze the expression of related protein.Cochlear tissue was tested by histological method to observe morphological changes.At the same time using the TUNEL method was used to analyse the cochlear tissue cell apoptosis.RESULTS Analysis showed that serum folate levels in mice fed without folic acid diet dropped than that of the normal group,while homocysteine levels elevated.Through the brain stem auditory records and cochlear cell apoptosis of mice severe hearing loss was found in folate deficiency group.Western blot detection showed enzyme catalysis homocysteine products increased by 50％ in folate deficiency group than that of the normal diet group.CONCLUSION The high homocysteine levels,and folate deficiency can cause hearing loss in mice and are related with the inner ear homocysteine metabolic disorders.