Bioactive flavonoids have been shown to improve the biological activity of stem cells derived from different sources in tissue regeneration. The goal of this study was to see how naringin, a natural flavonoid discovered in citrus fruits, affected the biological properties of human dental pulp stem cells (HDPSCs). In this study, we found that naringin increases the migratory ability of HDPSCs. Naringin increased matrix metalloproteinase-2 (MMP-2) and C-X-C chemokine receptor type 4 (CXCR4) mRNA and protein expression in HDPSCs. ARP100, a selective MMP-2 inhibitor, and AMD3100, a CXCR4 antagonist, both inhibited the naringin-induced migration of HDPSCs. Furthermore, naringin increased osteogenic differentiation of HDPSCs and the expression of the osteogenic-related marker, alkaline phosphatase in HDPSCs. Taken together, our findings suggest that naringin may be beneficial on dental tissue or bone regeneration by increasing the biological activities of HDPSCs.

Vinpocetine induces anti-inflammatory effects in various inflammatory diseases via the inhibition of phosphodiesterase type-1-independent nuclear factor-κB signaling pathway and the release of inflammatory cytokines. In this study, we investigated the effect of vinpocetine on the proliferation of colon cancer cells and its underlying molecular mechanisms. Our data showed that vinpocetine inhibits the viability and proliferation of colon cancer cells. Vinpocetine treatment induced cell death in HCT116 cells, which the percentages of sub-G1 phase were significantly increased, and the apoptosis-related genes were regulated after HCT116 cells were treated with vinpocetine. In sum, our findings indicated that vinpocetine could be a therapeutically useful candidate in the treatment of colon cancer.

Periodontal diseases have been associated with the development of cardiovascular diseases. Accumulating evidences have indicated that Porphyromonas gingivalis , a major periodontopathic pathogen, plays a critical role in the pathogenesis of atherosclerosis. In the present study, we demonstrated that P. gingivalis lipopolysaccharide (LPS) increases the mRNA and protein expression of matrix metalloproteinase-9 (MMP-9) in rat vascular smooth muscle cells. We showed that the MMP-9 expression induced by P. gingivalis LPS is mediated by the activation of signal transducer and activator of transcription 3 (STAT3) in vascular smooth muscle cells. Furthermore, the inhibition of STAT3 activity reduced P. gingivalis LPS-induced migration of vascular smooth muscle cells. Overall, our findings indicate that P. gingivalis LPS stimulates the migration of vascular smooth muscle cells via STAT3-mediated MMP-9 expression.

The objective of this study was to evaluate the effect of treating dairy cattle with exogenous human chorionic gonadotrophin (hCG), five (5) days post artificial insemination (AI) on serum progesterone (P4) concentration and pregnancy rate. In this experiment, five days after AI, cows were assigned randomly to two groups namely: a) treated group (67) which were administrered with 1500 IU hCG (Chorulon) and b) control group (61), which received no treatment. On day 5, 10, 15 and 20 after the artificial insemination, blood samples from a total of 8 cows (4 from each group) were collected and were analyzed for serum P4 concentration. Cows were detected for estrus according to standing heat by visual observation. Cows that were detected still in estrus after days 18-24 were re-inseminated and recorded as not pregnant (open). Pregnancy diagnosis was conducted by ultrasonographic examination and transrectal palpation of the uterus on approximately 60 days in cows that observed to be not in estrus. The conception rate in hCG treated and control groups were 52.5 and 36.1%, respectively. The results proved that there were no significant differences in conception rate between two groups (p=0.0568). However, pregnancy rates were reduced by hCG treatment. Average serum P4 concentrations did not differ between Hcg-treated and control groups on day 5 (0.377 versus 0.375 ng/ml). On day 20 serum P4 concentrations were greater in the treated group compared with the control group (3.085 versus 2.010 ng/ml). The treatment with hCG seemed to increase P4 level compared with the control. In conclusion, the results of this study showed that 1500 IU of hCG administered on 5 day post AI increased conception rate in dairy cows. This was supported by the results on serum P4 concentration which was greater in hCG treated group.

Although anti-aging activities of melatonin, a hormone secreted by the pineal gland, have been reported in senescence-accelerated mouse models and several types of cells, its impact and mechanism on the senescence of human dental pulp cells (HDPCs) remains unknown. In this study, we examined the impact of melatonin on cellular premature senescence of HDPCs. Here, we found that melatonin markedly inhibited senescent characteristics of HDPCs after exposure to hydrogen peroxide (H2O2), including the increase in senescence-associated β-galactosidase (SA-β-gal)-positive HDPCs and the upregulation of p21 protein, an indicator for senescence. In addition, as melatonin attenuated H2O2-stimulated phosphorylation of c-Jun N-terminal kinase (JNK), while selective inhibition of JNK activity with SP600125 significantly attenuated H2O2-induced increase in SA-beta-gal activity. Results reveal that melatonin antagonizes premature senescence of HDPCs via JNK pathway. Thus, melatonin may have therapeutic potential to prevent stress-induced premature senescence, possibly correlated with development of dental pulp diseases, and to maintain oral health across the life span.

Porphyromonas gingivalis, a foremost periodontal pathogen, has been known to cause periodontal diseases. Epidemiologic evidences have indicated the involvement of P. gingivalis in the development of cardiovascular diseases. In this study, we show that the P. gingivalis lipopolysaccharide increases the mRNA expression and protein secretion of interleukin-6 in vascular smooth muscle cells. We demonstrate that P. gingivalis LPS activates the extracellular signalregulated kinase 1/2 (ERK1/2), p38 mitogen-activated protein kinase (MAPK), and Akt, which mediate the IL-6 expression in vascular smooth muscle cells. Also, P. gingivalis LPS stimulates the vascular smooth muscle cell migration, which is a critical step for the progression of atherosclerosis. Moreover, neutralization of the IL-6 function inhibits the migration of vascular smooth muscle cells induced by P. gingivalis LPS. Taken together, these results indicate that P. gingivalis LPS promotes the expression of IL-6, which in turn increases the migration of vascular smooth muscle cells.

Dental pulp is a highly vascularized tissue with high regenerative potential. Revascularization of severed vasculature in the tooth is required for pulp healing during avulsed tooth treatment. In this study, the relative expression of angiogenesis-related proteins was determined in human dental pulp cells using a human angiogenesis proteome profiler array. The proteome profiler array detected differentially expressed angiogenesis-related factors under conditions of hypoxia, which enhances the angiogenic potential of dental pulp cells. We confirmed that hypoxia regulates the mRNA expression of angiogenesis-related factors, including CXCL16 in dental pulp cells. Furthermore, conditioned media of hypoxic pulp cells induced tube-like structures of vascular endothelial cells, which were reduced by the neutralization of CXCL16 function. In conclusion, our data show that angiogenesisrelated factors are differentially expressed by hypoxia in dental pulp cells and suggest that CXCL16 may involve in the revascularization of hypoxic dental pulp.

Neuromedin B (NMB) acts as a growth factor or a morphogen and plays a role in cancer progression. Indeed, the NMB receptor (NMB-R) is overexpressed in different types of tumors. In our current study, we investigated the involvement of NMB-R in the proliferation of oral cancer cells. Human oral squamous cell carcinoma (SCC) and human oral cancer cells, SCC-25 cells were found to be NMB-R-positive. The NMB-R antagonist PD168368 inhibited the proliferation of SCC-25 cells and reduced their colony formation capacity. We also found that PD168368 induced the cell cycle arrest and apoptosis of SCC-25 cells in a dose-/time-dependent manner. Overall, this antitumor activity of PD168368 in human oral cancer cells suggests that NMB-R is a potential target for the future prevention and treatment of human cancers.

목적: 역기하렌즈 착용 후 안광학 성분들의 변화에 대한 관련성을 알아보고자 한다. 방법: 7세에서 15세 사이의 -1.00D에서 -6.50D 이하, 총 27명(54안)을 대상으로 역기하렌즈 착용 전, 3~6개월, 7~12개월, 13~24개월, 25~36개월 후의 나안시력, 동공직경, 각막두께, 전방깊이, 각막곡률반경, 굴절교정 값의 변화에 대한 통계적 유의성을 검증하고자 하였다. 결과: 역기하렌즈를 착용하기 전의 나안시력은 0.33±0.19, 3~6개월 후에는 0.97±0.14로 0.63±0.22향상되었고, 7~12개월 후에는 0.95±0.17로 0.61±0.23만큼 향상되었으며, 13~24개월 후에는 0.91±0.22로 0.57±0.27만큼 향상되었고, 25~36개월 후에는 시력 0.86±0.27로 0.52±0.32만큼 향상되어 통계적으로 유의한 변화를 보였다(P＜0.05). 굴절교정 값의 변화는 12개월까지는 변화가 없었고, ㅓ 13~24개월은-0.19±0..50D로, 25~36개월은 -0.30±0.62D로 증가해 통계적으로 유의(PV0.05)한 변화를 보였다. 각막곡률반경은 3~6개월은 1.45±0.97mm로, 7~12개월은 1.40±1.12mm로, 13~24개월은 1.26±1.34mm, 25~36개월은 1.08±1.54 mm로 감소하여 통계적으로 유의한 변화를 보였다(P＜0.05). 각막두께는 3~6개월은 2.21±10.70 Чm로, 7~12개월은 1.21±12.42 Чm로 감소했지만 유의하지 않았고. 13~24개월은0.79± 1..17± m로, 25~36개월은 1.93± 13.97 μm증가했지만 유의하지 않았다. 동공크기는 3~6개월은0.18±0.64mm로, 7~12개월은 0.20±0.64 mm, 13~24개월은 0.14±0.53 mm로, 25~36개월은 0.25±0.56mm 감소해 유의한 변화를 보였다(P；＜0.05). 전방깊이는 3~6개월은 0.66±0.08 mm, 7~12개월은0.03±0.99mm 로 유의하게 감소했으며(P＜0.05), 13~24개월은 0.03±0.13mm 감소했지만 통계적으로는유의(P=0.14)하지 않았고, 25~36개월은 0.05±0.14 mm 감소해 통계적으로 유의(P＜0.05)한 변화를 보였다. 결론: 역기하렌즈를 착용하고 36개월 동안 나안시력이 향상되고, 굴절교정 값의 변화는 크지 않았으며, 각막곡률과 동공크기 및 전방깊이 등의 유의한 변화가 관찰되었다.

Porphyromonas gingivalis, one of the major periodontal pathogens, is implicated in the initiation and progression of periodontal disease. The initial stages of periodontal inflammation are accompanied by vascular hyperpermeability. In our present study, we report that the P. gingivalis lipopolysaccharide (LPS) increases the mRNA expression of interleukin-8 (IL-8), a major inducer of vascular permeability, in vascular endothelial cells. P. gingivalis LPS also stimulated the induction of IL-8 secretion in endothelial cells. The P. gingivalis LPS-induced expression of IL-8 was primarily modulated by nuclear factor-κB (NF-κB). P. gingivalis LPS significantly enhanced the vascular permeability both in vitro and in vivo, and a blockade of the IL-8 receptor decreased the P. gingivalis LPS-induced vascular permeability. Taken together, these results suggest that P. gingivalis LPS increases vascular permeability through the NF-κB-dependent production of IL-8 in vascular endothelial cells.

Porphyromonas gingivalis, a major periodontal pathogen, has been implicated in the initiation and progression of periodontal disease. Endothelial dysfunction (Editor note: Aberrant and dysfunction are somewhat redundant. The authors may want to choose one or the other.) contributes to chronic periodontal inflammation. Using cDNA-representational difference analysis, we found that P.gingivalis lipopolysaccharide differentially induces a number of genes in human microvascular endothelial cells. Among these upregulated genes, we focused on intercellular adhesion molecule-1 (VCAM-1), which is crucial for leukocyte recruitment during vascular inflammation. P. gingivalis LPS significantly increased the expression of vascular cell adhesion molecule-1 (VCAM-1) as well as ICAM-1. Promoter assays revealed that the transcription of these cell adhesion molecules was mainly regulated by nuclear factor-xB (NF-xB) in endothelial cells. Furthermore, P. gingivalis LPS significantly increased leukocyte adhesiveness to microvascular endothelial cells and to aortic endothelium. Taken together, our results demonstrate that P. gingivalis LPS activates microvascular endothelial cells through NF-xB-dependent expression of cell adhesion molecules.