Electroacupuncture Promotes Neural Proliferation in Hippocampus of Perimenopausal Depression Rats via Wnt/ß-Catenin Signaling Pathway.

BACKGROUND AND OBJECTIVE: Perimenopausal depression is caused by the impaired function of the ovarium before menopause and with a series of symptoms. Electroacupuncture (EA) therapy has been demonstrated to improve clinically depression. However, the mechanism underlying its therapeutic activity remains unknown. This study aimed to investigat the effects of EA treatment on the hippocampal neural proliferation through Wnt signaling pathway. METHODS: Chronic unpredictable mild stress (CUMS) combined with bilateral ovariectomy (OVX) were used to establish a rat model of perimenopausal depression. The open field test (OFT) and sucrose preference test (SPT) were used to assess depression-like behaviors in rats. ELISAs were used to measure estrogen (E2), luteinizing hormone (LH) and gonadotropin-releasing hormone (GnRH) levels in the serum. RT-PCR and Western blot assay were utilized for measuring the mRNA expressions and protein expressions of GSK-3ß/ß-catenin. RESULTS: Four-week EA treatment at three points including "Shenshu" (BL23), "Baihui" (GV20) and "Sanyinjiao" (SP6) simultaneously ameliorated depression-like behaviors in rats with CUMS and OVX, whereas rescued the decreased serum level of E2 and prevented the increased serum levels of GnRH and LH. EA treatment ameliorated CUMS and OVX-induced alterations of glycogen synthase kinase-3ß (GSK-3ß) and ß-catenin mRNA levels, ß-catenin and phosphorylated ß-catenin (p-ß-catenin) protein levels. CONCLUSIONS: The results showed that EA treatment promoted hippocampal neural proliferation in perimenopausal depression rats via activating the Wnt/ß-catenin signaling pathway, indicating that EA may represent an efficacious therapy for perimenopausal depression.

Velvet antler polypeptide partially rescue facet joint osteoarthritis-like phenotype in adult ß-catenin conditional activation mice.

BACKGROUND: Wnt/ß-catenin signaling pathway is closely related to osteoarthritis. In our preliminary study, ß-catenin conditional activation (cAct) mice that specifically over-express ß-catenin gene in cartilage chondrocyte exhibits osteoarthritis-like phenotype in the lumbar disc and knee joint. Therefore, we used the mice to model FJ-OA and test the potential curative effect of Velvet Antler Polypeptide (VAP) on this mice model. METHODS: We tested the effect of VAP on ß-catenin conditional activation mice, and used Cre negative littermates as controls. Micro-CT, histology and histomorphometry analysis were performed to evaluate the curative effect of VAP on mice facet joint-like phenotype. Expression of ß-catenin and collagen II was detected by immunohistochemistry (IHC) and western-blot., MMP13, ADAMTS4 and ADAMTS5 was detected by immunofluorescence (IF). RT-PCR analysis was preformed to detect mRNA expression of cartilage degrading enzymes, such as MMP13, ADAMTS4 and ADAMTS5. RESULTS: Results of micro-CT (µCT) analysis showed that VAP could partially reverse lumbar disc osteophyte formation observed in ß-catenin(ex3)Col2ER mice. Histology data revealed VAP partially improved facet joint cartilage tissue invades. Histomorphometry analysis showed an increase in total cartilage area after VAP treatment. IHC show that VAP reduced ß-catenin protein levels and moderately up-regulated collagen II protein levels. RT-PCR and IF data showed that VAP down-regulated the expression of extracellular matrix synthesis (ECM) degradation enzymes MMP13, ADAMTS4 and ADAMTS5. CONCLUSION: Taken together, VAP may modulate ECM by inhibits MMP13, ADAMTS4 and ADAMTS5 via Wnt /ß-catenin signaling pathway. Velvet Antler Polypeptide may be a potential medicine for FJ-OA.

[Effect of astragaloside on mRNA expression of PI3K/Akt/mTOR signal transduction in anemia model mice induced by chemotherapy].

To study the influence of astragaloside on mRNA expression of PI3K/Akt/mTOR signal transduction in anemia model mice induced by chemotherapy, 48 male BALB/c mice which were 6-7 week old were picked as the research objects and randomly divided into four groups, blank group, model group, astragaloside group and astragaloside IV group. Each group was 12 mice. Chemotherapy anemia model was established by cyclophosphamide. The mice were drawn blood from eyeball after 14 days treatment. The QPCR was used to test the mRNA concentrations of Akt, PI3K, BCL-xl, bad, FoxO, mTOR, PTEN in mouse spleen. In comparison of blank group, astragaloside group and astragaloside IV group,the erythrocyte counting and values of Hb in model group were significantly lower (P<0.05). The volumes mRNA of Akt,PI3K,BCL-xl,bad,mTOR were lower in blank group, compared with other groups (P<0.05 or P<0.01). The similar trend in astragaloside IV group except PI3K, comparing with blank group (P<0.05 or P<0.01). The contents of these five genes were no significant differentiations between astragaloside group and blank group. The statistics were obvious between astragaloside group and astragaloside IV group (P<0.05 or P<0.01). The concentrations of FoxO, PTEN were higher in model group,compared with blank group and astragaloside group (P<0.05 or P<0.01), but no difference with astragaloside IV group. Comparing with blank group, the volumes of these two genes were increased in astragaloside IV group (P<0.05), FoxO was higher in astragaloside group (P<0.05), but PTEN was not significant. There was no the same as astragaloside group and Astragaloside IV group. Therefore, astragaloside could increase the contents of Akt, PI3K, BCL-xl, bad, mTOR (P<0.01), decrease the concentrations of FoxO, PTEN (P<0.05). The changes in cyclophosphamide-induced anemia were highly significant by astragaloside. It could be related to the mRNA expression of PI3K/Akt/mTOR Signal Transduction.