Flos Albiziae aqueous extract and its active constituent quercetin potentiate the hypnotic effect of pentobarbital via the serotonergic system.

Flos albiziae (FA) is reportedly used for treatment of insomnia and anxiety in traditional medicine. The hypnotic effect of an extract of FA (FAE) and its constituent quercetin [2-(3,4-dihydroxyphenyl)-3,5,7-trihydroxy-4H-chromen-4-one, QR] was examined in mice. QR is a widely distributed natural flavonoid abundant in FA flowers and other tissues. The possible mechanisms underlying the hypnotic effects of FAE and QR were investigated using behavioral pharmacology. FAE and QR significantly potentiated pentobarbital-induced [50 mg/kg, intraperitoneal (ip)] sleep (prolonged sleeping time; shortened sleep latency) in a dose-dependent manner, and these effects were augmented by administration of 5-hydroxytryptophan (5-HTP), a precursor of 5-hydroxytryptamine. With a sub-hypnotic dose of pentobarbital (28 mg/kg, ip), FAE and QR significantly increased the rate of sleep onset and were synergistic with 5-HTP (2.5 mg/kg, ip). Pretreatment with p-chlorophenylalanine, an inhibitor of tryptophan hydroxylase, significantly decreased sleeping time and prolonged sleep latency in pentobarbital-treated mice, whereas FAE and QR significantly reversed this effect. Data show that FAE and QR have hypnotic activity, possibly mediated by the serotonergic system. The present study offers a rationale for the use of FA in treating sleep disorders associated with serotonin system dysfunction.

[Effects of Citalopram on frontal cortical neurons' bax mRNA bcl-2 mRNA expression and cell apoptosis of rat after stress].

OBJECTIVE: To study the effects of Citalopram on the mRNA expression of bax and bel-2 in frontal cortical neurons and on cell apoptosis of rats after stress. METHODS: Twenty-four healthy male SD rats were randomly divided into three groups (n = 8). The control group did no receive any treatment, the stress group was subject to stress and given normal saline and experimental group was given Citalopram irrigation stomach after stress. Rats were forced to swim to establish chronic stress model (15 min/d, 4 weeks), bax, bcl-2 mRNA expression were tested by in situ hybridization technique (ISH), TUNEL assay was used to determine cell apoptosis, Nikon image analysis software were used to measure the number of positive cells in each index. RESULTS: Compared with the control group, the stress group showed a larger number of bax mRNA expressing cells( P < 0.01), a smaller number of bcl-2 mRNA expressing cells (P < 0.01), and the staining intensity of positive cells was significantly reduced( P < 0.01). Compared with the stress group, the experiment group showed more reduced number of bax mRNA positive cells( P < 0.01) and significantly increased bcl-2 mRNA positive cells( P < 0.05), a small amount of positive cells were found, compared with that in the stress group, nuclear condensation in the experimental group was reduced significantly and the staining was obviously weaker( P < 0.01). CONCLUSION: Citalopram significantly antagonizes bax mRNA and potentiatesbcl-2 mRNA protein expression and inhibits apoptosis of rat prefrontal cortical neurons caused by chronic stress, which might be one possible mechanism of Citalopram for prevention and treatment of psychosis caused by chronic stress.

[Gastric expressions of neuron-specific enolase and synaptophysin in human fetuses of 2 to 4 gestational months].

OBJECTIVE: To investigate the distribution patterns of neuron-specific enolase (NSE) and synaptophysin (SYN) during the development of human fetal stomach. METHODS: Sixteen specimens of human fetal (gestational age 2 to 4 months) gastric tissues were examined with immunohistochemistry for detecting the distribution of NSE and SYN expressions in the gastric walls. RESULTS: During the second to fourth gestational months, NSE was strongly expressed in the nerve cells and nerve fibers of the myenteric nerve plexus of human fetal stomach. As the gestational age increased, the numbers of NSE positive cells and fibers increased gradually in the gastric submucosa, but NSE was negative in the gastric mucosa. At the second gestational month, SYN expression was negative in the mucosa but positive in the myenteric nerve plexus; during the third to fourth months, positive SYN expression was found in the mucosa, submucosa and myenteric nerve plexus of the embryonic gastric walls and its expression intensity increased with the gestational age. CONCLUSION: SYN and NSE are both involved in the regulation of the nervous system in the gastric wall but their expressions and distributions follow different patterns during the development of human fetal stomach.

[Effects of citalopram on the expression of PCNA and C-fos and cell apoptosis in rat frontal cortical neurons after stress].

OBJECTIVE: To study the effects of citalopram on the expression of proliferating cell nuclear antigen (PCNA) and proto-oncogene protein (C-fos) and cell apoptosis in frontal cortical neurons of rat after stress. METHODS: Twenty four healthy male SD rats were randomly divided into three groups (n = 8): control group, stress group (treated with saline, ig) , experimental group (treated with Citalopram 4 mg/kg x d for 28 days, ig). Rats were forced to swim to establish chronic stress model. The protein expression levels of PCNA and C-fos were tested by immunohistochemistry assay. TUNEL assay was used to test cell apoptosis. Nikon image analysis software was used to determine the number of positive cells in each index. RESULTS: Compared with the control group, the stress group showed a smaller amount of PCNA-positive cells, a larger number of C-fos positive cells, and the volume of positive cells was significantly reduced. Compared with the stress group, the PCNA positive cells were increased significantly, the C-fos positive cells and TUNEL positive cells were decreased significantly, nuclear condensation phenomenon in frontal cortical neurons and the staining was significantly lighter in experimental group (P < 0.05). CONCLUSION: Citalopram significantly antagonize PCNA, C-fos protein expression and cell apoptosis of rat prefrontal cortical neurons caused by chronic stress, which might be the one of mechanisms of citalopram for prevention and treatment of psychosis caused by chronic stress.

Inhibitory effects of ß-tricalciumphosphate wear particles on osteocytes via apoptotic response and Akt inactivation.

Wear debris-induced osteolysis, a major contributing factor of orthopedic implant aseptic loosening, affects long-term survival of orthopedic prostheses following joint replacement and revision surgery. Pathogenic effects of wear debris on various cell types including macrophages/monocytes, osteoblasts, and osteoclasts have been well studied. However, the interactions between wear debris particles and osteocytes, which make up over 90% of all bone cells, have not been clearly illustrated. Here, we explored the biological effects of endotoxin-free beta-tricalciumphosphate (ß-TCP) wear particles with the average diameter of 1.997 µm (range 1.3-3.2 µm) on osteocytes in vitro. Our results showed that 24 h or 48 h incubation of ß-TCP particles dose-dependently inhibited cell viability of osteocytes MLO-Y4. Alternatively, ß-TCP particles treatment for 24 h significantly increased the osteocytic marker SOST/sclerostin mRNA expression and the release of inflammatory cytokines including TNF-α and IL-1ß into the culture media, but decreased the mRNA expression of another osteocytic marker dentin matrix protein-1 (DMP-1). Furthermore, these osteocytes dysfunctions were accompanied by F-actin disassembly, cell apoptosis, sustained enhancement of intracellular reactive oxygen species (ROS) and mitochondrial injury upon ß-TCP particles stimulation. In addition, ß-TCP particles also caused Akt inactivation at Ser473 resides with a dose- and time-dependent pattern. Taken together, ß-TCP wear particles could cause osteocytes dysfunctions, which may be mediated by apoptotic death and Akt inactivation in MLO-Y4 cells. These findings strongly suggest that osteocytes may play an important role in the ß-TCP wear particles-induced osteolysis, and provide valuable insights for understanding the molecular mechanisms of osteocytes death involved in tissue damage during bone cement and intolerance of cemented prostheses.

Polymorphisms of androgen receptor gene in childhood and adolescent males with first-onset major depressive disorder and association with related symptomatology.

This study was designed to explore the association between CAG repeats in AR gene and major depressive disorder (MDD) in male children and adolescents. The results showed that there were differences between adolescent depressive patients and adolescent controls in CAG repeats' length and alleles' distributions, and the severity of depression and anxiety was negatively correlated with the length of CAG repeats in adolescent patients. This suggested that AR gene might be involved in the depressive upset in adolescents, and the age- and sex-related prevalent differences might also be associated to CAG repeats.

Comparison of the polymorphisms of androgen receptor gene and estrogen alpha and beta gene between adolescent females with first-onset major depressive disorder and controls.

This study was to elucidate the role of genetic variation in androgen receptor (AR) gene, estrogen receptor alpha (ER alpha) and ER beta gene on first-onset major depressive disorder (MDD) in female adolescents. Results showed that AR gene in MDD group have shorter microsatellites' length, and ER beta gene have shorter microsatellites' length and higher rates of S alleles, SS, genotype, and lower rate of LL genotype than control group. The results suggest that shorter length of AR and ER beta gene microsatellites might influence the onset of MDD in female adolescents, a further elucidation of the mechanisms is warranted.