-
International journal of dermatology 09/2011; · 1.18 Impact Factor
-
Do Kyung Lee,
Shin Young Park,
Hyang Mi An,
Jung Rae Kim,
Mi Jin Kim,
Si Won Lee,
Min Kyeong Cha, Sun Ae Kim,
Myung Jun Chung,
Kang Oh Lee,
Nam Joo Ha
[show abstract]
[hide abstract]
ABSTRACT: Dental caries is the main common infectious disease in the human oral cavity. Streptococcus mutans and Streptococcus sobrinus were reported to be the most important etiological factors in human dental caries. Thus, we examined the inhibitory effects of Bifidobacterium spp. cells and culture supernatants against S. mutans and S. sobrinus, including Streptococcus gordonii, and Aggregatibacter actinomycetemcomitans, which is associated with periodontal disease.
Mutans streptococci or A. actinomycetemcomitans and lactic acid bacteria (LAB) were mixed in 1:1 ratio and then incubated for 90 min at 37°C. After the incubation, the viability of mutans streptococci or A. actinomycetemcomitans was determined by plate count technique. We also investigated the morphological changes of S. mutans treated with LAB using scanning electron microscopy (SEM).
In vitro viability of S. mutans, S. sobrinus, S. gordonii, and A. actinomycetemcomitans was affected by human intestinal LAB identified as Bifidobacterium adolescentis SPM1005 and Bifidobacterium longum SPM1207. Especially, B. adolescentis SPM1005 cells at 1.0 × 10(8) CFU had a strong growth-inhibiting effect against S. mutans and induced a 64% loss of its viability (p<0.05). In addition, swollen and disrupted S. mutans were observed after incubation with B. adolescentis SPM1005. However, the culture supernatant of this strain did not show such inhibitory activity.
B. adolescentis SPM1005 cells decreased the growth of S. mutans, which is a risk factor for dental caries. Therefore, we suggest that this Bifidobacterium strain may be a useful probiotic microorganism for prevention of dental caries that does not have adverse effects.
Archives of oral biology 03/2011; 56(10):1047-54. · 1.65 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Tobacco smoking is one of the many factors that contribute to premature skin aging, but the exact mechanism by which smoking induces facial wrinkling is still poorly understood. To investigate the regulatory potential of early growth response-1 (Egr-1) on the premature skin aging by smoking, this study examined the hypothesis that cigarette smoke-induced Egr-1 represses T beta R-II expression in human skin dermal fibroblasts (HSDFs). The protein and mRNA expressions of Egr-1 and T beta R-II were detected using Western blot and real-time RTPCR in HSDFs after exposure to cigarette smoke extract (CSE). Egr-1 and T beta R-II promoter activities were analyzed in CSE-exposed fibroblasts using luciferase assay. T beta R-II promoter activity was also evaluated in HSDFs to be transfected with Egr-1 overexpression vector. To investigative Egr-1-specific effects, we utilized Egr-1 small interfering RNA (siRNA) to inhibit Egr-1 expression. The expressions of Egr-1 protein and mRNA were increased in a time and dose-dependent manner. CSE also induced Egr-1 at the transcription level. Egr-1 was induced though phosphorylation of Erk1/2 after CSE exposure in HSDFs. We also observed the immunostained Egr-1 proteins were mainly localized from the cytoplasm to the nucleus after CSE treatment by immunocytochemical analyzes. Furthermore, T beta R-II protein and mRNA levels were decreased in a dose-dependent manner by CSE and T beta R-II promoter activity was significantly repressed by CSE. HSDFs transfected with Egr-1 overexpression vector showed significantly reduced T beta R-II promoter activity. In addition, T beta R-II mRNA levels were upregulated in HSDFs transfected with Egr-1 siRNA, suggesting that T beta R-II expressional downregulation by CSE is induced via an Egr-1-dependent mechanism. This study suggests that the downregulation of T beta R-II expression by cigarette smoke-induced Egr-1 may contribute to smoking-induced premature skin aging.
Toxicology 09/2010; 275(1-3):29-35. · 3.68 Impact Factor
-
Hea Soon Shin,
Shin Young Park,
Do Kyung Lee, Sun Ae Kim,
Hyang Mi An,
Jung Rae Kim,
Mi Jin Kim,
Min Gyeong Cha,
Si Won Lee,
Kyung Joo Kim,
Kang Oh Lee,
Nam Joo Ha
[show abstract]
[hide abstract]
ABSTRACT: We have previously reported that live Bifidobacterium longum SPM1207, a strain isolated from healthy adult Koreans, significantly reduced serum cholesterol in broth and rat. We here examined the effect of oral administration of sonication-killed B. longum SPM1207 on serum cholesterol in rats in order to investigate whether this killed strain could be utilized as a potent probiotics for human and animals. Dietary treatments consisted of 3 treatment groups of 24 rats each randomly assigned to either normal diet, high cholesterol diet and saline (HCS), or high cholesterol diet and sonication-killed B. longum SPM1207 (HCKB) for 3 weeks. Although HDL-cholesterol levels in the serum were not significantly (p > 0.05) different between HCKB rats and HCS rats, total and LDL-cholesterol levels in the serum were significantly (p < 0.05) less increased in HCKB (total: 177.71 mg/dL, LDL-: 60.50 mg/dL) rats when compared to HCS (total: 237.17 mg/dL, LDL-: 71.50 mg/dL) rats. AI was significantly (p < 0.05) lower in HCKB (4.95 mg/dL) rats when compared to HCS (9.22 mg/dL) rats. Body weight increase and relative liver weight were significantly (p < 0.05) lower in HCKB rats when compared to HCS rats. Over the time, high cholesterol diet caused dry feces accompanied by decreased fecal water content (66.00 to 61.94%) but sonication-killed B. longum SPM1207 administration increased fecal water content (71.58 to 74.25%). The results in the current study provide evidence that the sonication-killed cells of B. logum SPM1207 isolated from healthy adult Koreans have a greater potential to be used as a cholesterol-lowering agent. Furthermore, the current study suggest that this killed specific strain may play role in part in blocking the body weight increase and relieving or eliminating constipation.
Archives of Pharmacal Research 09/2010; 33(9):1425-31. · 1.59 Impact Factor
-
[show abstract]
[hide abstract]
ABSTRACT: Cholesterol is a major component of biological membranes and is known to affect vesicle fusion. However, the mechanism by which cholesterol modulates SNARE-dependent intracellular fusion is not well understood. Using the fluorescence assay and dye-labeled SNAREs and the fluorescent lipids, we dissected cholesterol effects on individual fusion steps including SNARE complex formation, hemifusion, pore formation, and pore dilation. At physiological high concentrations, cholesterol stimulated hemifusion as much as 30-fold, but its stimulatory effect diminished to 10-fold and three-fold for subsequent pore formation and pore expansion at 40 mol %, respectively. The results show that cholesterol serves as a strong stimulator for hemifusion but acts as mild stimulators for pore opening and expansion. Strong stimulation of hemifusion and mild stimulation of pore formation are consistent with the fusion model based on the intrinsic negative curvature of cholesterol. However, even a milder effect of cholesterol on pore expansion is contradictory to such a simple curvature-based prediction. Thus, we speculate that cholesterol also affects the conformation of the transmembrane domains of SNAREs, which modulates the fusion kinetics.
Biophysical Journal 04/2009; 96(5):1839-46. · 3.65 Impact Factor
