RESUMEN
The purpose of this study was to investigate the anti-hyperlipidemic effect of soy bean extract solution fermented by Bacillus subtilis MORI (BTD-1E) in obese db/db mice. Eight-week-old male db/db mice were administered 33.3 mg/kg BTD-1E solution orally once a day for four weeks. The BTD-1E group showed significantly lower body weight compared with the db control group (P<0.05). The BTD-1E group showed significantly lower serum total cholesterol and LDL cholesterol levels compared with the db control group, respectively (P<0.05, P<0.01). The BTD-1E group showed significantly decreased liver weight relative to final body weight compared with the db control group (P<0.01). After four weeks of BTD-1E administration, lipid droplets in the liver were apparently decreased in the BTD-1E group compared to the db control group. In summary, our results suggest that BTD-1E has an anti-hyperlipidemic effect in the obese mouse model.
RESUMEN
Loss-of function mutations in the transmembrane inner ear expressed (Tmie/TMIE) gene have been shown to cause deafness in mice and humans (DFNB6). Previous studies report that the circling mouse can be an animal model for DFNB6. However, the expression pattern of Tmie protein in postnatal developmental stages has not been clearly revealed. In this study we tried to investigate the expression of Tmie protein in the liver, spleen, kidney, and lung, as well as in the cochlea. We examined various tissue samples from five different age groups of C57BL/6J animals. Using western blotting analysis, the expression of Tmie protein in these organs has been identified. The results show that Tmie protein expression in the cochlea has been increased in postnatal developmental stages, indicating that Tmie plays an important role in not only the development and also in the function of the cochlea. The expression pattern of Tmie in adult mouse organs such as the liver, spleen, kidney, and spleen significantly vary in adult rats. The order of Tmie expression level in mice (63 days after birth) was spleen, liver, lung, cochlea, and kidney, whereas in the adult rat it was liver, cochlea, lung, spleen, and kidney.
RESUMEN
The faded mouse is a coat color mutant that shows faded coat color and age-related loss of pigmentation. This mutation is transmitted by an autosomal recessive gene with 100% penetrance. In the present study, we carried out linkage analysis of the faded (fe) gene using intra-specific backcross panels. Affected faded mice were carefully confirmed by their faded coat color at about 4 weeks of age. In the intra-specific backcross between faded and CBA mice (n=198), the fe gene was mapped to a region 2.1 cM distal to D10mit191. Therefore, the gene order was defined as follows: centromere-D10mit51 (12.4±2.4 cM)-D10mit191 (2.1±1.0 cM)-fe-D10mit44 (13.3±2.4 cM)-D10mit42 (14.4±2.5 cM). This linkage map of the fe locus will provide a good entry point to isolate the fe gene. Since the faded mouse has pigmentary abnormalities, this mutant may be a useful model for studies of pigmentary abnormalities in humans.
RESUMEN
High glucose levels induce cell death in many cell types, including pancreatic ß-cells. Although protective agents against glucotoxicity have been searched for extensively, so far none have been found. In this report, we tested silk fibroin (SF) as a candidate material for antiglucotoxicity in the pancreatic ß-cell (HIT-T15 cell) line. Approximately 50% of cells were killed after treatment with 80 mg/mL glucose. This reduction of cell number was recovered by the addition of SF at 50 mg/mL. SF treatment also decreased cellular reactive oxygen species (ROS) and increased proliferating cellular nuclear antigen (PCNA) immunoreactivity. In addition, TUNEL assays demonstrated that SF protects against glucose-induced apoptosis of HIT-T15 cells, suggesting that SF might protect cells from cell death by lowering cellular ROS levels. SF also induced expression of the insulin-like growth factor-1 (IGF-1) gene, and IGF-1 expression may be the cause of SF-induced protection against glucose toxicity. Taken together, these results suggest that SF could serve as a potential therapeutic agent to treat the hyperglycemia-induced death of pancreatic ß-cells.
Asunto(s)
Apoptosis/efectos de los fármacos , Fibroínas/farmacología , Glucosa/toxicidad , Sustancias Protectoras/farmacología , Animales , Línea Celular , Proliferación Celular/efectos de los fármacos , Supervivencia Celular/efectos de los fármacos , Cricetinae , Citoprotección , Expresión Génica/efectos de los fármacos , Glucosa/fisiología , Factor I del Crecimiento Similar a la Insulina/genética , Factor I del Crecimiento Similar a la Insulina/metabolismo , Especies Reactivas de Oxígeno/metabolismoRESUMEN
Ginkgo biloba leaf extract (Gb) has been known to improve blood flow and preclude the tissue from free radical damage. Effects of Gb were examined by using Ki67, a specific proliferative marker for cellular proliferation, and doublecortin (DCX), a marker for immature neurons, indicating degree of neuroblast differentiation in the hippocampal dentate gyrus (DG) of adult C57BL/6 mice. The mice were fed with Gb at 40 and 100 mg/kg once daily for 28 days. The increase of Ki67- and DCX-immunoreactive cells in the DG was increased in a dose-dependent manner. Especially, the group having 100 mg/kg Gb showed a significant increase of DCX-immunoreactive neuroblasts with well-developed tertiary dendrites. Expression of DCX protein in the Gb groups was also significantly increased upon compared with the vehicle group. The results suggested that repeated intake of Gb would enhance cell proliferation and neuroblast differentiation in the mouse DG.
Asunto(s)
Giro Dentado/citología , Giro Dentado/efectos de los fármacos , Ginkgo biloba/química , Neurogénesis/efectos de los fármacos , Extractos Vegetales/farmacología , Animales , Anticuerpos , Proteínas de Dominio Doblecortina , Proteína Doblecortina , Regulación de la Expresión Génica , Antígeno Ki-67/genética , Antígeno Ki-67/metabolismo , Ratones , Ratones Endogámicos C57BL , Proteínas Asociadas a Microtúbulos/genética , Proteínas Asociadas a Microtúbulos/inmunología , Proteínas Asociadas a Microtúbulos/metabolismo , Neuropéptidos/genética , Neuropéptidos/inmunología , Neuropéptidos/metabolismo , Extractos Vegetales/química , Hojas de la Planta/químicaRESUMEN
A novel autosomal recessive mutant was produced using N-ethyl-N-nitrosourea mutagenesis. The characteristics of the mutant mice included progressive irreversible hair loss within a month of birth, wrinkled skin, and long curved nails. Linkage analysis revealed that the causative gene is linked to D14Mit193 on chromosome 14. Sequence analysis of the complete cDNA of the candidate gene, hairless (Hr), identified a homozygous G-to-T transition at nucleotide 3572, leading to the substitution of glycine by tryptophan, designated Gly960Trp. This missense mutation occurs in the vicinity of repression domain 3 of the hairless protein (HR). This allele was named Hr(m1Enu). The relative amounts of Hr mRNA and HR protein determined by real-time PCR and Western blot analyses, respectively, were slightly elevated in the mutant mice. Quantitative real-time PCR analysis revealed the increased expression of Kc1 and Vdr in the mutant mice, whereas the expression of Nrs1 and Krtap16-6 was decreased. These results suggest that the Gly960Trp substitution in HR protein in Hr(m1Enu) mice may alter the function of HR as a transcriptional corepressor.