Enhancing Sperm Motility Parameters in Patients with Asthenospermia: A Combined Approach of Acupuncture at Fusiguan Point and Tamoxifen Citrate Tablets.

OBJECTIVE: To explore the effect of acupuncture at Fuguan point combined with tamoxifen citrate tablet on sperm motility parameters. METHODS: A total of 115 individuals with asthenospermia were categorized based on different treatment regimens: 53 patients in the control group (receiving tamoxifen citrate tablets) and 62 patients in the observation group (undergoing acupoint acupuncture in conjunction with tamoxifen citrate tablets). Both groups underwent a 3-month treatment period. The computer-assisted sperm analysis system was employed to measure various motility parameters of human sperm, including sperm motility rate, average path velocity (VAP), lateral swing amplitude (ALH), percentage of class a sperm, and percentage of class a + b sperm. RESULTS: Prior to treatment, no statistically significant differences were observed between the two groups in terms of sperm motility rate, VAP, ALH, percentage of class a sperm, and percentage of class a + b sperm (p > 0.05). Following treatment, both groups exhibited significant enhancements in sperm motility rate, VAP, ALH, percentage of class a sperm, and percentage of class a + b sperm compared to pretreatment levels (p < 0.05). Furthermore, all measured indicators in the observation group demonstrated significantly superior improvements than those of the control group, with the differences proving statistically significant (p < 0.05). CONCLUSIONS: The combination of acupuncture at Fusiguan point and tamoxifen citrate tablets exerts a notably positive effect on sperm motility in individuals diagnosed with asthenospermia.

Estrogen receptor ß suppresses inflammation and the progression of prostate cancer.

Previous studies demonstrated that estrogen receptor ß (ERß) signaling alleviates systemic inflammation in animal models, and suggested that ERß­selective agonists may deactivate microglia and suppress T cell activity via downregulation of nuclear factor κ­light­chain­enhancer of activated B cells (NF­κB). In the present study, the role of ERß in lipopolysaccharide (LPS)­induced inflammation and association with NF­κB activity were investigated in PC­3 and DU145 prostate cancer cell lines. Cells were treated with LPS to induce inflammation, and ELISA was performed to determine the expression levels of inflammatory cytokines, including tumor necrosis factor­α (TNF­α), monocyte chemoattractant protein 1 (MCP­1), interleukin (IL)­1ß and IL­6. MTT and Transwell assays, and Annexin V/propidium iodide staining were conducted to measure cell viability, apoptosis and migration, respectively. Protein expression was determined via western blot analysis. LPS­induced inflammation resulted in elevated expression levels of TNF­α, IL­1ß, MCP­1 and IL­6 compared with controls. ERß overexpression significantly inhibited the LPS­induced production of TNF­α, IL­1ß, MCP­1 and IL­6. In addition, the results indicated that ERß suppressed viability and migration, and induced apoptosis in prostate cancer cells, which was further demonstrated by altered expression of proliferating cell nuclear antigen, B­cell lymphoma 2­associated X protein, caspase­3, E­cadherin and matrix metalloproteinase­2. These effects were reversed by treatment with the ERß antagonist PHTPP or ERß­specific short interfering RNA. ERß overexpression reduced the expression levels of p65 and phosphorylated NF­κB inhibitor α (IκBα), but not total IκBα expression in LPS­treated cells. In conclusion, ERß suppressed the viability and migration of the PC­3 and DU145 prostate cancer cell lines and induced apoptosis. Furthermore, it reduced inflammation and suppressed the activation of the NF­κB pathway, suggesting that ERß may serve roles as an anti­inflammatory and anticancer agent in prostate cancer.

Effects of Panax notoginseng ginsenoside Rb1 on abnormal hippocampal microenvironment in rats.

Cerebral ischemia damages central neurons, and abnormal microenvironment in ischemic condition is the key factor to the damages. The increase of local concentration of glutamic acid, the overload of Ca2+, and the mitochondrial stress caused by release of cytochrome C are important factors of abnormal microenvironment in cerebral ischemia. In this study ginsenoside Rb1, a compound from Panax Notoginseng, was used to intervene abnormal environment of neurons in the hippocampal CA1 region in two animal models (microperfusion model and photothrombosis model). RESULTS: Compared with the vehicle in the sham group, ginsenoside had following effects. a) ginsenoside Rb1 increased the regional cerebral blood flow (rCBF) and the stability of neuronal ultrastructure in in the hippocampal CA1 region and improved the adaptability of neurons in two models. b) ginsenoside Rb1 improved the expression level of glial glutamate transporter1 (GLT-1) and reversed the uptake of glutamate (Glu) after ischemia, and as a result thereby decreased the excitability of Glu and the expression level of GLT-1 was proportional to the dose of ginsenoside Rb1 and similar to that of Nimodipine. c) ginsenoside Rb1 inhibited the expression level of NMDAR and the overload of Ca2+, thereby reducing neuronal damages. Meanwhile, the expression level of NMDAR was inversely proportional to the dose of ginsenoside Rb1, which was similar to that of Nimodipine. d) ginsenoside Rb1 decreased the release of cytochrome C (Cyt-C) and reduced the damages caused by neuronal mitochondrial stress. Meanwhile, the release of Cyt-C was inversely proportional to the dose of ginsenoside Rb1, which was similar to that of Nimodipine. Ginsenoside Rb1 may be as an effective drug for neuroprotection and improve cerebral blood flow after acute ischemia and prevent the secondary brain damage induced by stroke.

Exploring the mechanism of non-small-cell lung cancer cell lines resistant to epidermal growth factor receptor tyrosine kinase inhibitor.

PURPOSE: Here we aimed to explore the possible mechanism and potential regulatory relationships in which the non.small.cell lung cancer. (NSCLC)-resisted epidermal growth factor receptor. (EGFR) tyrosine kinase inhibitor erlotinib. MATERIALS AND METHODS: GSE38310, the gene expression profiles of NSCLC cell lines treated with dimethylsulfoxide or erlotinib, including HCC827, ER3, and T15-2, were downloaded from Gene Expression Omnibus database and preprocessed by normalization. Basing on the regulatory relationships of transcriptional factors obtained from University of California Santa Cruz. (UCSC) database, the differentially expressed genes. (DEGs) were screened using limma package in R with. |logFC| >1 and P < 0.05, and regulatory networks of these DEGs were built with supervised inference of regulatory networks (SIRENE). Subsequently, differentially regulatory networks were compared basing on Limit Fold Change. (LFC) method. RESULTS: Totally 24,380 genes were obtained, 1,531 DEGs were identified in HCC827 cell lines, 37 DEGs in ER3 cell lines, 156 DEGs in T15-2 cell lines. After removing the redundancy genes, 1,575 differentially expressed genes were got at last. Basing on three regulatory networks of HCC827 cell lines, ER3 cell lines and T15-2 cell lies, sex-determining region Y (SRY).related high mobility group-box gene 9. (SOX9) and Suppressor of cytokine signaling 3 (STAT3) were identified by comparing with HCC827 and ER3 networks. And suppressor of cytokine signaling 5 B (STAT5B), early growth response-1 (EGR1) and STAT6 were obtained in comparison of HCC827 and T15-2 networks. CONCLUSIONS: The regulatory edges with remarkable changes between HCC827 and ER3, HCC827 and T15.2 included some transcription factors and genes. (e. g., STAT3 and SOX9). STAT3, SOX9, STAT5B, EGR1, and STAT6 might affect the resistance of NSCLC to erlotinib.