Objective To investigate the prevalence rate of senile insomnia and revealing the characteristics of its pathogenesis. Methods On the basic study of senile insomnia clinical literature, the questionnaire was made and followed by epidemiological investigation. The database was set up for statistical analysis with SPSS13.0. Results Prevalence rate of senile insomnia in Wuchang District of Wuhan City was 36.47%. There were significant difference in sleep time, the length of sleep at night, sleep continuity especially mental state during the day between insomnia group and the normal group (P

Objective To observe the effects of wild jujube seed decoction (WJSD) on learning memory and the levels of malondialdehyde (MDA) and the activities of supemxide dismutase (SOD) and nitric oxide synthase (NOS) in the brain of the pathogeny model rats with sleep deprivation (SD). Methods Levels of learning memory and MDA, and activities of SOD and NOS in rats' brain were assayed after SD induced by made-self multiple platform method ( MMPM), senescence induced by D-galactose, and Yin and blood-deficiency induced by eyclophosphamide and hydrocortisonum. Results After 48 h SD, the levels of learning memory was lower in the model group( ( 108.9 ± 12.5 ) s, ( 89 ± 11.5 ) s, ( 0 ) ) than those in the environmental control group ( ( 47.3 ±4.6)s,(9±1.4)s,(6.5 ±1.2))(( t=4.36,3.18,2.07, P＜0.01＝＝. While MDA, and activities of SOD and NO in rats'brain higher in the model group( (3.8 ±0.6) ,(3.0 ±0.5)nmol · mgprot-1 ,(229.7 ±25.8) ,(236.3± 25.2 ) U · mgprot - 1, ( 5.7 ± 0. 8 ), ( 5.4 ± 0.9 ) U · mgprot - 1 ) than those in the environmental control group ( (2. 1 ±0.4) ,(1.6 ±0.4)nmol · mgprot-1 ,(155.5 ±10.6) ,( 147.2 ±26.1 )U · mgprot-1 ,(2.8 ±0.7),(2.9 ± 0.5 ) U · mgprot -1 ) ( t = 2.89,3.01,6.78,5.94,3.10,3.46, P ＜ 0.05 ＝. However, the observation of the groups treated with WJSD, the levels of learning memory showed a tendency in returning to normal level (P ＜ 0.05 ＝ ,and MDA, and activities of SOD and NO of the high dose of WJSD showed a tendency in returning to normal leve1 (P ＜ 0.05 ＝ ,and the low dose of WJSD showed a tendency in returning to normal level too(P ＜ 0.05 ＝. Conclusion WJSD can improve the disability of learning and memory of the pathogeny rats model, and its one of mechanism maybe involve the reduction of neural cell damage with free radical and NO.

Objective To observe the effects of wild jujube seed decoction(WJSD) on ultrastructure and astrocytes expression in the brain cortex of old model rats with blood-deficiency and Yin and sleep deprivation(SD)after SD. Methods Ultrastructural changes in cortical parts of the experiment rat were observed by transmission electron microscopy , immunohistochemical staining was used to detect star-shaped glial cells marker-glial fibrillary acidic protein(GFAP) expression after SD induced by made-self multiple platform method (MMPM), senescence induced by D-galactose, and Yin and blood-deficiency induced by cyclophosphamide and hydrocortisonum. Results Compared to environmental control group((9.8 ± 2.5), (0.11 ± 0.02) ) , syndrome model group (( 20.4 ±4.4), (0.20 ±0.011) ) rats had obvious ultrastructural changes and stronger expression of GFAP in cortical parts (t = 7.63,3.18, P ＜ 0. 01), while those of W J SD of high and low dose group ((14.4 ± 3.9), (15.5 ± 6.4),(0.14 ±0.02)(0.14±0.02)) rats showed weaker(t=6.32,5.24,2.31,2.45, P＜0.05). Conclusion WJSD of large and small lose group could improve the rats neurons pathological changes,WJSD downward adjusting the expression of GFAP may be one of the mechanisms of treatment on insomnia with blood-deficiency and Yin in the old.

ObjectiveTo investigate the effects of jujuboside A （JuA） on the learning and memory abilities and histopathological changes in the rat model of vascular cognitive impairment （VCI） and explore the potential mechanisms by which JuA treats VCI. MethodsA total of 50 male SPF-grade SD rats were randomized into a sham operation group （n=10）， a blank control group （n=10）， and a modeling group （n=30）. The rats in the modeling group underwent bilateral carotid artery ligation （2-VO） for the modeling of VCI. After stabilization， the VCI rats were randomized into model， JuA （20 mg·kg^-¹）， and donepezil （0.45 mg·kg^-¹） groups. After 4 weeks of gavage， the novel object recognition and Morris water maze tests were conducted to evaluate the learning and memory abilities of rats. Nissl staining was employed to evaluate the morphology and number of hippocampal neurons. Real-time PCR was employed to measure the mRNA levels of glycogen synthase kinase-3β （GSK-3β）， cAMP response element-binding protein （CREB）， B cell lymphoma-2 （Bcl-2）， phosphatidylinositol 3-kinase （PI3K）， and protein kinase B （Akt） in the hippocampal tissue. Western blot was employed to quantify the protein levels of GSK-3β， p-GSK-3β， p-CREB， Bcl-2， PI3K， p-PI3K， Akt， and p-Akt in the hippocampal tissue. ResultCompared with the sham operation group， the model group exhibited declines in the learning and memory abilities （P<0.01）， neuronal damage and decreased neurons in the hippocampal CA1 region （P<0.01）， up-regulation in the mRNA level of GSK-3β （P<0.01）， and down-regulation in the mRNA levels of PI3K， Akt， CREB， and Bcl-2， as well as the protein levels of p-PI3K， p-Akt， p-GSK-3β， p-CREB， and Bcl-2 （P<0.01）. In comparison to the model group， both the JuA and donepezil groups demonstrated improvements in the learning and memory abilities （P<0.05， P<0.01）， with reduced neuronal damage and increased neurons （P<0.05， P<0.01）. In addition， the two groups showed down-regulation in the mRNA level of GSK-3β （P<0.01） and up-regulation in the mRNA levels of PI3K， Akt， CREB， and Bcl-2 and the protein levels of p-PI3K， p-Akt， p-GSK-3β， p-CREB， and Bcl-2 （P<0.05， P<0.01）. There were no statistically significant differences between the blank control and sham operation groups in terms of the learning and memory abilities， neuron count， and mRNA and protein levels of PI3K/Akt/GSK-3β pathway-related factors. ConclusionJuA can ameliorate the cognitive impairment in the rat model of VCI by activating the PI3K/Akt signaling pathway， reducing the apoptosis of hippocampal neurons， and alleviating the hippocampal neuronal damage.