Vitamin D Status and Vitamin D Receptor Gene Polymorphisms Are Associated with Pelvic Floor Disorders in Women

OBJECTIVES: To investigate if vitamin D receptor (VDR) gene polymorphisms and circulating vitamin D levels are associated with pelvic floor disorders (PFDs). METHODS: In this case-control study, 25-hydroxy-vitamin D (25[OH]D) serum levels were analyzed in 47 females with PFDs and 87 healthy females (controls), respectively. The VDR gene polymorphisms were determined by using polymerase chain reaction and performing digestions with 4 restriction enzymes i.e., ApaI, TaqI, FokI, and BsmI. Vitamin D levels of patients were divided into 0.05). However, there was a significant difference in the distribution of vitamin D levels between study group and controls using Pearson's χ2 test (30 ng/mL: 87.2%, 12.8%, and 0% in the study group and 75.9%, 16.1%, and 8.0% in controls, respectively, P < 0.05). Taken together, our observations suggest that vitamin D levels could be associated with PFDs and that 2 polymorphisms (i.e., ApaI and BsmI) in the VDR gene may contribute to an increased prevalence of PFDs in women with insufficient levels of vitamin D. CONCLUSIONS: Examining vitamin D levels and performing a VDR genotype analysis may be helpful for assessing PFD risk.

Extract Promotes Neurogenesis in the Hippocampal Dentate Gyrus of the Adult Mouse through Increasing Expressions of Brain-Derived Neurotrophic Factor and Tropomyosin-Related Kinase B / 中华医学杂志(英文版)

<p><b>Background</b>Glehnia littoralis has been used for traditional Asian medicine, which has diverse therapeutic activities. However, studies regarding neurogenic effects of G. littoralis have not yet been considered. Therefore, in this study, we examined effects of G. littoralis extract on cell proliferation, neuroblast differentiation, and the maturation of newborn neurons in the hippocampus of adult mice.</p><p><b>Methods</b>A total of 39 male ICR mice (12 weeks old) were randomly assigned to vehicle-treated and 100 and 200 mg/kg G. littoralis extract-treated groups (n = 13 in each group). Vehicle and G. littoralis extract were orally administrated for 28 days. To examine neurogenic effects of G. littoralis extract, we performed immunohistochemistry for 5-bromo-2-deoxyuridine (BrdU, an indicator for cell proliferation) and doublecortin (DCX, an immature neuronal marker) and double immunofluorescence staining for BrdU and neuronal nuclear antigen (NeuN, a mature neuronal marker). In addition, we examined expressional changes of brain-derived neurotrophic factor (BDNF) and its major receptor tropomyosin-related kinase B (TrkB) using Western blotting analysis.</p><p><b>Results</b>Treatment with 200 mg/kg, not 100 mg/kg, significantly increased number of BrdU-immunoreactive () and DCX cells (48.0 ± 3.1 and 72.0 ± 3.8 cells/section, respectively) in the subgranular zone (SGZ) of the dentate gyrus (DG) and BrdU/NeuN cells (17.0 ± 1.5 cells/section) in the granule cell layer as well as in the SGZ. In addition, protein levels of BDNF and TrkB (about 232% and 244% of the vehicle-treated group, respectively) were significantly increased in the DG of the mice treated with 200 mg/kg of G. littoralis extract.</p><p><b>Conclusion</b>G. littoralis extract promots cell proliferation, neuroblast differentiation, and neuronal maturation in the hippocampal DG, and neurogenic effects might be closely related to increases of BDNF and TrkB proteins by G. littoralis extract treatment.</p>

Improvement of andropause symptoms by dandelion and rooibos extract complex CRS-10 in aging male

Many aging male suffer various andropause symptoms including loss of physical and mental activities. This study evaluated the putative alleviative effects of CRS-10 dandelion and rooibos extract complex (CRS-10) on the symptoms of andropause. The survival rate of TM3 Leydig cells (TM3 cells) treated with CRS-10 was measured based on typical physiological stress. After daily intake of CRS-10 for 4 weeks, the level of testosterone, physical activity and both the number and activity of sperm in older rats (18 weeks) were measured. Furthermore, thirty males were surveyed with AMS (Aging Males' Symptoms) questionnaire after intake of 400 mg of CRS-10. Overall, CRS-10 protected TM3 cells from serum restriction and oxidative stress via activation of ERK and Akt pathways. The level of testosterone and activation of spermatogenesis in rats were significantly enhanced. In addition, physical locomotion was markedly improved. Daily intake of 400 mg of CRS-10 improved the quality of life among agingmale respondents, according to a clinical survey using the AMS. The results indicate the potential of CRS-10 as a safe and efficacious natural substance for reducing or alleviating andropause symptoms.

Study on the Mitochondrial Dysfunction by p53 Regulation in Ceramide-induced Neuronal Cell Death / 체질인류학회지

Ceramide induces cell death in a dose- and time-dependent manner in neuroblastoma SK-N-SH cells. To investigate the mechanism of SK-N-SH cell death by C2-ceramide, morphological features and Hoechst 33258 staining were analyzed. In these morphlogic study the cell death by ceramide showed typical apoptotic features, nuclear condensation, fragmentation, and membrane blebbing. Ceramide-induced apoptosis was accompanied by nuclear accumulation of p53. Inhibition of p53 expression with p53 antisense oligonucleotides inhibited apoptosis evoked by ceramide. Also, ceramide induced mitochondrial event, collapse of mitochondrial membrane potential (delta psi m) and interestingly, inhibition of p53 attenuated collapse of mitochondrial membrane potential, suggests that ceramide induces mitochondrial dysfunction through upregulation of p53 expression. These results suggest that ceramide-induced apoptosis is dependent upon increase in cellular p53 levels which play a critical role in the regulation of apoptotic cell death and p53 modulates mitochondrial function such as mitochondrial membrane potential level.

Protective Effect of Green Tea Extract on Neuronal Cell Death in Alzheimer Model using beta-amyloid Peptide / 대한해부학회지

In the present study, we determined whether green tea extract, EGCG protected against beta-amyloid induced neurotoxicity and learning impairment in vitro and in vivo models. Incubation of SK-N-SH cells with Abeta induced activation of caspase-3, mitochondrial dysfunction such as collapse of mitochondrial membrane potential (MMP) and release of cytosolic cytochrome c. Interestingly, pre-treatment of EGCG reduced significantly activation of caspase-3 and increase of mitochondrial damage such as the breakdown of MMP and release of cytochrome c, eventually attenuated the cell death induced by Abeta. These results show that EGCG inhibited caspase activity and blocked mitochondrial damage. For in vivo experiment, ICR mice received vehicle or vehicle plus EGCG (10 mg/kg) i.p. for 3 days. Before 2 days of treatment, 5 microliter of PBS containing 8 nmol of Abeta1-42 were injected into the lateral ventricle. On the 14th day of treatment, animals were applied to passive avoidance test, and after behavial test, animals were sacrificed. Then, morphological techniques were used to determine the extent of neuronal degeneration in the hippocampus. Abeta, but not PBS, injections into hippocampus led to neuronal loss and evidence of widespread apoptosis. EGCG treated animals had significant reductions in the amount of neuronal degeneration, and TUNEL positive cells compared with Abeta alone treated animals. These data suggest that EGCG at therapeutically relevant concentrations, might protect against neuronal degeneration induced by Abeta.

Down-regulated Reactive Oxygen Species by Heat Shock Protein 90 in 3-Hydroxykynurenine-induced SKN-SH Cell Death / 체질인류학회지

In this present study, we show that 3HK-induced reactive oxygen species (ROS) accumulation and caspase activation lead to apoptotic cell death. Pretreatment with N-acetylcysteine (NAC), an effective antioxidant, significantly attenuated 3HK-induced apoptosis by way of a reduction of ROS accumulation and caspase activity. SKN-SN cells were protected from 3HK-induced cytotoxicity by heat shock protein (HSP). HSP90 effectively attenuated 3HK-mediated ROS accumulation and apoptosis. In addition, the protective effect of HSP90 was abolished by pretreatment with HSP90 anti-sense oligonucleotide, but not when pretreated with anti-senses for other HSPs. These results suggest that HSP90 protects SKN-SH cells from 3HK-induced cytotoxicity by reducing ROS levels and caspase activity.

The Activation of ERK1/2 Via Tyrosine Kinase Pathway Attenuates TRAIL-induced Apoptosis in HeLa cell / 체질인류학회지

Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) serves as an extracellular signal triggering apoptosis in tumor cells. To characterize the molecular events involved in TRAIL-induced apoptotic signaling, we investigated the role of extracellular signal-regulated kinase 1/2(ERK1/2) in the apoptosis using HeLa cells. Here we show that TRAIL pronounced ERK1/2 activation through a tyrosine kinase-dependent mechanism, subsequently elevated anti-apoptotic Bcl-2 protein levels. Pretreatment with Genistein, an inhibitor of tyrosine kinase, significantly attenuated ERK1/2 activation and enhanced cell death. Moreover, inhibition of ERK1/2 with PD98059 promoted apoptotic cell death through the down-regulation of ERK1/2 activity and Bcl-2 protein levels. Taken together, our results suggest that the activation of ERK1/2 via tyrosine kinase pathway plays a protective role as the mechanism of cellular defense through the up-regulation of Bcl-2 protein levels in TRAIL-induced apoptosis.