Objective To investigate the clinical efifcacy of estradiol on perimenopausal syndrome,and evaluate its safety. Methods 64 cases with perimenopausal syndrome collected in our hospital from January 2010 to January 2011 were used as observation group, and treated with Estradiol valerate. Another 64 cases during the same period were used as control group, and treated with conventional therapy. After treatment, the symptom improvement of both groups were evaluated by the scoring criteria of HAMD and Kupperman, and the related hormone levels were detected and recorded. Adverse reactions after treatment were also observed. Results Clinical results showed that the HAMD and Kupperman score of both groups in end of treatment were better than before treatment, and the improvement degree in observation group were better than control in. The differences were signiifcant (P<0.05). Test results showed that the improvement of various hormonal indicators in observation group were also better than that in control group, the diffierences were significant (P<0.05). 8 cases of adverse reactions were observed in observation group after treatment, 12 cases in control group. Adverse reactions included breast tenderness, vaginal bleeding and gastrointestinal discomfort. The side effects between both groups had no signiifcant difference. Conclusion The efifcacy of Estradiol on perimenopausal syndrome was obvious, it can improve the menopausal symptoms, with less adverse reactions, and improve the life quality of perimenopausal women.

Objective: To investigate anemia rate and to analyze related factors in maternal women in Taicang of Jiangsu province. Methods: There were 13 278 pregnant women who had prenatal care and gave birth in 25 hospitals during 2014-2016 in Taicang of Jiangsu Province. We excluded 1 179 women who registered after 12 weeks of gestation, 144 women who did not test hemoglobin during gestation, and 25 women whose gestational weeks were incorrect. Finally, data from 11 930 pregnant women were analyzed. From the electronical medical record system of maternal and child health care, we obtained basic information of these pregnant women, their hemoglobin levels and related data during gestation and postpartum. Anemia rate was descripted, and factors associated with anemia were identified using multiple unconditional logistic regression. Results: Age of the 11 930 pregnant women was (27.0±4.5) years old, and the P₅₀ (P₂₅-P₇₅) of BMI at the first trimester was 21.4 (19.6-23.7) kg/m². The anemia rate during gestation was 37.2% (4 434/11 930). The anemia rate was 5.5% (276/5 035), 24.4% (1 802/7 377), and 47.8% (3 328/6 966) at the first, second and third trimesters, respectively. Anemia rate at 42 days postpartum was 19.9% (680/3 418). Multiple unconditional logistic regression indicated that anemia during gestation was related with maternal age <21 years old at prenatal registration (OR (95%CI): 1.28 (1.07-1.53)), body mass index(BMI) <18.5 kg/m² at the first trimester (OR (95%CI): 1.14 (1.00-1.29)), non-local residence (OR (95%CI): 1.35 (1.20-1.52)), education of middle school and lower (OR (95%CI): middle school: 1.24 (1.05-1.47), primary school: 1.36 (1.01-1.82)), occupation of housewife or farmer (OR (95%CI): housewife: 1.21 (1.06-1.38), farmer: 1.21 (1.03-1.44)). Anemia at 42 days postpartum was associated with multipara (OR(95%CI): 1.59 (1.12-2.27)), anemia at the first trimester (OR(95%CI): 3.26 (1.92-5.55)), no folic acid supplementation at the first trimester (OR(95%CI): 1.34 (1.00-1.80)), and hemorrhage≥500 ml during 24 h postpartum (OR(95%CI): 2.26 (1.02-4.97)). Conclusion Anemia rate was low for maternal women in Taicang of Jiangsu Province. The factors associated with gestational anemia included pregnant women's age, BMI, local or non-local residence, occupation, and education. The factors associated with postpartum anemia included multipara, anemia at the first trimester, no folic acid supplementation at the first trimester, and hemorrhage 24 h postpartum.

ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids （MA） in ameliorating depression by network pharmacology， molecular docking， and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. Protein-protein interaction （PPI） network was constructed by protein interaction analysis （STRING） database. Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses were performed through Bioinformatics （DAVID） database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone （CORT） once a day for 35 consecutive days. Sixty mice were randomly allocated into control （0.9% normal saline）， model （CORT， 20 mg·kg^-1）， positive control （fluoxetine hydrochloride， 3.6 mg·kg^-1）， and MA （10， 5， and 2.5 mg·kg^-1） groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling （TUNEL） was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor （BDNF）， dopamine （DA）， 5-hydroxytryptamine （5-HT）， and norepinephrine （NE） in mice. The mRNA levels of cyclic adenosine monophosphate （cAMP） pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 （Cx43）. ResultsA total of 434 component targets and 545 depression targets were obtained， including 84 common targets， among which 10 core targets were screened out. GO analysis predicted 34 biological processes， 15 cell components， and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group， CORT prolonged the immobility time of mice in forced swimming and tail suspension tests （P<0.01）， lowered the serum levels of NE， BDNF， and 5-HT （P<0.05）， up-regulated the mRNA levels of nuclear factor-κB （NF-κB） and interleukin-6 （IL-6） in the brain tissue （P<0.05）， and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein （CREB） and BDNF （P<0.05） and the protein levels of protein kinase （PRKACA）， phosphorylation （p）-CREB/CREB， BDNF， and Cx43 （P<0.05） in the brain tissue. Compared with the model group， high-dose MA reduced the immobility time of mice in forced swimming （P<0.05） and tail suspension （P<0.01） tests， raised the serum levels of NE， BDNF， and 5-HT （P<0.01）， down-regulated the mRNA level of NF-κB （P<0.01）， and up-regulated the mRNA level of BDNF （P<0.01） and protein levels of PRKACA， p-CREB/CREB， BDNF， and Cx43 （P<0.05）. ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway， improving synaptic plasticity and gap junction function， and reducing neuroinflammation.

ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids （MA） in ameliorating depression by network pharmacology， molecular docking， and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. The depression targets were collected through TCMIP， Genecards， HPO， DrugBank and OMIM database. Protein-protein interaction （PPI） network was constructed by protein interaction analysis （STRING） database. Gene ontology （GO） and Kyoto Encyclopedia of Genes and Genomes （KEGG） analyses were performed through Bioinformatics （DAVID） database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone （CORT） once a day for 35 consecutive days. Sixty mice were randomly allocated into control （0.9% normal saline）， model （CORT， 20 mg·kg^-1）， positive control （fluoxetine hydrochloride， 3.6 mg·kg^-1）， and MA （10， 5， and 2.5 mg·kg^-1） groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling （TUNEL） was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor （BDNF）， dopamine （DA）， 5-hydroxytryptamine （5-HT）， and norepinephrine （NE） in mice. The mRNA levels of cyclic adenosine monophosphate （cAMP） pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 （Cx43）. ResultsA total of 434 component targets and 545 depression targets were obtained， including 84 common targets， among which 10 core targets were screened out. GO analysis predicted 34 biological processes， 15 cell components， and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group， CORT prolonged the immobility time of mice in forced swimming and tail suspension tests （P<0.01）， lowered the serum levels of NE， BDNF， and 5-HT （P<0.05）， up-regulated the mRNA levels of nuclear factor-κB （NF-κB） and interleukin-6 （IL-6） in the brain tissue （P<0.05）， and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein （CREB） and BDNF （P<0.05） and the protein levels of protein kinase （PRKACA）， phosphorylation （p）-CREB/CREB， BDNF， and Cx43 （P<0.05） in the brain tissue. Compared with the model group， high-dose MA reduced the immobility time of mice in forced swimming （P<0.05） and tail suspension （P<0.01） tests， raised the serum levels of NE， BDNF， and 5-HT （P<0.01）， down-regulated the mRNA level of NF-κB （P<0.01）， and up-regulated the mRNA level of BDNF （P<0.01） and protein levels of PRKACA， p-CREB/CREB， BDNF， and Cx43 （P<0.05）. ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway， improving synaptic plasticity and gap junction function， and reducing neuroinflammation.