Sulforaphane Increases Cyclin-Dependent Kinase Inhibitor, p21 Protein in Human Oral Carcinoma Cells and Nude Mouse Animal Model to Induce G2/M Cell Cycle Arrest

Previously, our group reported that sulforaphane (SFN), a naturally occurring chemopreventive agent from cruciferous vegetables, effectively inhibits the proliferation of KB and YD-10B human oral squamous carcinoma cells by causing apoptosis. In this study, treatment of 20 and 40 µM of SFN for 12 h caused a cell cycle arrest in the G2/M phase. Cell cycle arrest induced by SFN was associated with a significant increase in the p21 protein level and a decrease in cyclin B expression, but there was no change in the cyclin A protein level. In addition, SFN increased the p21 promoter activity significantly. Furthermore, SFN induced p21 protein expression in a nude mouse xenograft model suggesting that SFN is a potent inducer of the p21 protein in human oral squamous carcinoma cells. These findings show that SFN is a promising candidate for molecular-targeting chemotherapy against human oral squamous cell carcinoma

Psychophysiological Alteration After Virtual Reality Experiences Using Smartphone-Assisted Head Mount Displays: An EEG-Based Source Localization Study

Brain functional changes could be observed in people after an experience of virtual reality (VR). The present study investigated cyber sickness and changes of brain regional activity using electroencephalogram (EEG)-based source localization, before and after a VR experience involving a smartphone-assisted head mount display. Thirty participants (mean age = 25 years old) were recruited. All were physically healthy and had no ophthalmological diseases. Their corrected vision was better than 20/20. Resting state EEG and the simulator sickness questionnaire (SSQ) were measured before and after the VR experience. Source activity of each frequency band was calculated using the sLORETA program. After the VR experience, the SSQ total score and sub scores (nausea, oculomotor symptoms, and disorientation) were significantly increased, and brain source activations were significantly increased: alpha1 activity in the cuneus and alpha2 activity in the cuneus and posterior cingulate gyrus (PCG). The change of SSQ score (after–before) showed significant negative correlation with the change of PCG activation (after–before) in the alpha2 band. The study demonstrated increased cyber sickness and increased alpha band power in the cuneus and PCG after the VR experience. Reduced PCG activation in alpha band may be associated with the symptom severity of cyber sickness

Protective effect of ginsenoside Re on acute gastric mucosal lesion induced by compound 48/80

The protective effect of ginsenoside Re, isolated from ginseng berry, against acute gastric mucosal lesions was examined in rats with a single intraperitoneal injection of compound 48/80 (C48/80). Ginsenoside Re (20 mg/kg or 100 mg/kg) was orally administered 0.5 h prior to C48/80 treatment. Ginsenoside Re dose-dependently prevented gastric mucosal lesion development 3 h after C48/80 treatment. Increases in the activities of myeloperoxidase (MPO; an index of neutrophil infiltration) and xanthine oxidase (XO) and the content of thiobarbituric acid reactive substances (TBARS; an index of lipid peroxidation) and decreases in the contents of hexosamine (a marker of gastric mucus) and adherent mucus, which occurred in gastric mucosal tissues after C48/80 treatment, were significantly attenuated by ginsenoside Re. The elevation of Bax expression and the decrease in Bcl2 expression after C48/80 treatment were also attenuated by ginsenoside Re. Ginsenoside Re significantly attenuated all these changes 3 h after C48/80 treatment. These results indicate that orally administered ginsenoside Re protects against C48/80-induced acute gastric mucosal lesions in rats, possibly through its stimulatory action on gastric mucus synthesis and secretion, its inhibitory action on neutrophil infiltration, and enhanced lipid peroxidation in the gastric mucosal tissue

Beneficial Effects of SREBP Decoy Oligodeoxynucleotide in an Animal Model of Hyperlipidemia

Hyperlipidemia is a chronic disorder that plays an important role in the development of cardiovascular diseases, type II diabetes, atherosclerosis, hypertension, and non-alcoholic fatty liver disease. Hyperlipidemias have created a worldwide health crisis and impose a substantial burden not only on personal health but also on societies and economies. Transcription factors in the sterol regulatory element binding protein (SREBP) family are key regulators of the lipogenic genes in the liver. SREBPs regulate lipid homeostasis by controlling the expression of a range of enzymes required for the synthesis of endogenous cholesterol, fatty acids, triacylglycerol, and phospholipids. Thereby, SREBPs have been considered as targets for the treatment of metabolic diseases. The aim of this study was to investigate the beneficial functions and the possible underlying molecular mechanisms of SREBP decoy ODN, which is a novel inhibitor of SREBPs, in high-fat diet (HFD)-fed hyperlipidemic mice. Our studies using HFD-induced hyperlipidemia animal model revealed that SREBB decoy ODN inhibited the increased expression of fatty acid synthetic pathway, such as SREBP-1c, FAS, SCD-1, ACC1, and HMGCR. In addition, SREBP decoy ODN decreased pro-inflammatory cytokines, including TNF-α, IL-1β, IL-8, and IL-6 expression. These results suggest that SREBP decoy ODN exerts its anti-hyperlipidemia effects in HFD-induced hyperlipidemia mice by regulating their lipid metabolism and inhibiting lipogenesis through inactivation of the SREPB pathway

Protective Effects of Fermented Oyster Extract against RANKL-Induced Osteoclastogenesis through Scavenging ROS Generation in RAW 264.7 Cells

Excessive bone resorption by osteoclasts causes bone loss-related diseases and reactive oxygen species (ROS) act as second messengers in intercellular signaling pathways during osteoclast differentiation. In this study, we explored the protective effects of fermented oyster extract (FO) against receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL)-induced osteoclast differentiation in murine monocyte/macrophage RAW 264.7 cells. Our results showed that FO markedly inhibited RANKL-induced activation of tartrate-resistant acid phosphatase and formation of F-actin ring structure. Mechanistically, FO has been shown to down-regulate RANKL-induced expression of osteoclast-specific markers by blocking the nuclear translocation of NF-κB and the transcriptional activation of nuclear factor of activated T cells c1 (NFATc1) and c-Fos. Furthermore, FO markedly diminished ROS production by RANKL stimulation, which was associated with blocking the expression of nicotinamide adenine dinucleotide phosphate oxidase 1 (NOX1) and its regulatory subunit Rac-1. However, a small interfering RNA (siRNA) targeting NOX1 suppressed RANKL-induced expression of osteoclast-specific markers and production of ROS and attenuated osteoclast differentiation as in the FO treatment group. Collectively, our findings suggest that FO has anti-osteoclastogenic potential by inactivating the NF-κB-mediated NFATc1 and c-Fos signaling pathways and inhibiting ROS generation, followed by suppression of osteoclast-specific genes. Although further studies are needed to demonstrate efficacy in in vivo animal models, FO may be used as an effective alternative agent for the prevention and treatment of osteoclastogenic bone diseases

The Association between Herpes Zoster and Increased Cancer Risk: A Nationwide Population-Based Matched Control Study

Background: Herpes zoster (HZ) is strongly associated with decreased immune function, a factor of cancer development. Previous studies suggested inconsistent results regarding the association between HZ and increased cancer risk. We aimed to analyze the association between HZ and specific cancer risk. Methods: Of 134,454 patients diagnosed with HZ between 2002 and 2015, 81,993 HZ patients were matched 1:1 with non-HZ individuals by age, sex, and Charlson comorbidity index. Both groups were examined at 1, 3, and 5 years for cancer diagnosis. A Cox proportional hazard regression model was used to estimate cancer risk in both groups. The postherpetic neuralgia (PHN) and non-HZ groups were compared for specific cancer risk. Results: The HZ group showed a slightly decreased overall cancer risk compared with the non-HZ group (hazard ratio [HR] 0.94, 95% confidence interval [CI] 0.90–0.97, p = 0.002). The HRs for specific cancer risk were 0.41 (95% CI, 0.33–0.50, p < 0.001); 0.86 (95% CI, 0.81–0.91, p < 0.001); 0.87 (95% CI, 0.78–0.97, p = 0.014); 0.80 (95% CI 0.73–0.87, p < 0.001); 1.20 (95% CI, 1.07–1.34, p = 0.001); and 1.66 (95% CI, 1.35–2.03, p < 0.001) for cancers of the lips, mouth, and pharynx; digestive system; respiratory system; unknown secondary and unspecified sites; thyroid and endocrine glands; and lymphoid and hematopoietic systems, respectively. The HZ with PHN group showed higher HR for specific cancer risk, such as lymphoid and hematopoietic systems (95% CI, 1.27–2.39, p < 0.001). Conclusion: HZ was associated with increased or decreased incidence of specific cancers. PHN further increased the risk of developing certain cancers in HZ patients