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1.
Journal of Southern Medical University ; (12): 853-857, 2017.
Article Dans Chinois | WPRIM | ID: wpr-360175

Résumé

<p><b>OBJECTIVE</b>To investigate the inhibitory effect of 420 nm intense pulsed light on Trichophyton rubrum growth in vitro and explore the mechanism.</p><p><b>METHODS</b>The fungal conidia were divided into treatment group with intense pulse light irradiation and control group without irradiation. The surface areas of the fungal colonies were photographed before irradiation and on the 2nd and 3rd days after irradiation to observe the changes in fungal growth. The viability of the fungus in suspension was detected at 6 h after irradiation using MTT assay. The intracellular reactive oxygen species (ROS) level in the fungus was determined using DCFH-DA fluorescent probe, and the MDA content was detected using TBA method.</p><p><b>RESULTS</b>Intense pulse light (420 nm) irradiation caused obvious injuries in Trichophyton rubrum with the optimal effective light dose of 12 J/cmin 12 pulses. At 6 h after the irradiation, the fungus in suspension showed a 30% reduction of viability (P<0.05), and the fungal colonies showed obvious growth arrest without further expansion. Compared to the control group, the irradiated fungus showed significant increases in ROS level and MDA content (P<0.05).</p><p><b>CONCLUSION</b>Intense pulse light (420 nm) irradiation can induce oxidative stress in Trichophyton rubrum to lead to fungal injuries and death.</p>

2.
Journal of Southern Medical University ; (12): 391-395, 2016.
Article Dans Chinois | WPRIM | ID: wpr-264034

Résumé

<p><b>OBJECTIVE</b>To investigate the role of NADPH oxidase (Nox) in the oxidative stress injury of human dermal fibroblasts (HFbs).</p><p><b>METHODS</b>An oxidative stress injury model was established in HFbs by exposure to H(2)O(2). Normal HFbs and HFbs exposed to H(2)O(2) with and without pretreatment with NADPH oxidase inhibitor were tested for cell viability using MTT assay, and the intracellular reactive oxygen species (ROS) were determined with a DCFH-DA fluorescent probe. Western blotting was used to measure the protein expressions of membrane-bound subunit gp91phox of NADPH oxidase in the cells.</p><p><b>RESULT</b>H(2)O(2) time- and concentration-dependently induced oxidative stress injury in the fibroblasts, causing a reduction of the cell viability to 40% after a 24-h exposure at 700 µmol/L (P<0.05) and an increase of ROS by 2 folds after a 2-h exposure at 700 µmol/L (P<0.05). Compared with the cells with oxidative stress injury, the cells with NADPH oxidase inhibitor pretreatment showed a 20% higher cell viability (P<0.05) and normal ROS level (P<0.05) following H(2)O(2) exposure. Western blotting demonstrated increased expression of gp91phox in the cells exposed to increasing H(2)O(2) concentrations, but gp91phox expression remained normal in cells pretreated with NADPH oxidase inhibitor.</p><p><b>CONCLUSION</b>H(2)O(2) can induce oxidative stress injury in the fibroblasts by affecting NADPH oxidase, especially its membrane-bound subunit gp91phox.</p>


Sujets)
Humains , Survie cellulaire , Cellules cultivées , Fibroblastes , Biologie cellulaire , Peroxyde d'hydrogène , Glycoprotéines membranaires , Métabolisme , NADPH Oxidase 2 , NADPH oxidase , Métabolisme , Oxydoréduction , Stress oxydatif , Espèces réactives de l'oxygène , Métabolisme
3.
Journal of Huazhong University of Science and Technology (Medical Sciences) ; (6): 634-638, 2016.
Article Dans Anglais | WPRIM | ID: wpr-238444

Résumé

Tumor necrosis factor-alpha (TNF-α) has been found to be centrally involved in the development of ischemia-reperfusion injury (IRI)-induced inflammation and apoptosis. Knockdown of TNF-α gene using small interfering RNA (siRNA) may protect renal IRI. Renal IRI was induced in mice by clamping the left renal pedicle for 25 or 35 min. TNF-α siRNA was administered intravenously to silence the expression of TNF-α. The therapeutic effects of siRNA were evaluated in terms of renal function, histological examination, and overall survival following lethal IRI. A single systemic injection of TNF-α siRNA resulted in significant knockdown of TNF-α expression in ischemia-reperfusion injured kidney. In comparison with control mice, levels of BUN and serum creatinine were significantly reduced in mice treated with siRNA. Pathological examination demonstrated that tissue damage caused by IRI was markedly reduced as a result of TNF-α siRNA treatment. Furthermore, survival experiments showed that nearly 90% of control mice died from lethal IRI, whereas more than 50% of siRNApretreated mice survived until the end of the eight-day observation period. We have demonstrated for the first time that silencing TNF-α by specific siRNA can significantly reduce renal IRI and protect mice against lethal kidney ischemia, highlighting the potential for siRNA-based clinical therapy.


Sujets)
Animaux , Humains , Souris , Apoptose , Modèles animaux de maladie humaine , Thérapie génétique , Inflammation , Génétique , Anatomopathologie , Thérapeutique , Rein , Plaies et blessures , Anatomopathologie , Petit ARN interférent , Génétique , Lésion d'ischémie-reperfusion , Génétique , Anatomopathologie , Thérapeutique , Facteur de nécrose tumorale alpha , Génétique
4.
Asian Pacific Journal of Tropical Medicine ; (12): 313-316, 2014.
Article Dans Anglais | WPRIM | ID: wpr-819675

Résumé

OBJECTIVE@#To investigate the role of T help 17 cells (Th17) and STAT3-VEGF pathway in pathogenesis of psoriasis.@*METHODS@#A total of 50 cases of psoriasis guinea pigs and 20 normal guinea pigs were selected. The ratio of Th17/ IL-17 cell in peripheral blood were detected by flow cytometric analysis; STAT3 and VEGF concentrations were measured by immunohistochemistry and Western blot.@*RESULTS@#The expression of Th17 in peripheral blood were significantly increased in psoriasis [(1.76±0.88)%] compared with controls [(0.48±0.27)%] (P<0.05). Th17 related cytokine STAT3 and VEGF were significantly increased in psoriasis compared with controls (P<0.05), and were positively correlated the expression of Th17.@*CONCLUSIONS@#The expressions of Th17, STAT3 and VEGF are elevated in psoriasis, which suggests Th17 cells have a potential role in the pathogenesis of psoriasis by STAT3-VEGF pathway.


Sujets)
Animaux , Différenciation cellulaire , Physiologie , Modèles animaux de maladie humaine , Cochons d'Inde , Psoriasis , Métabolisme , Anatomopathologie , Facteur de transcription STAT-3 , Sang , Métabolisme , Transduction du signal , Peau , Chimie , Biologie cellulaire , Métabolisme , Cellules Th17 , Biologie cellulaire , Facteur de croissance endothéliale vasculaire de type A , Sang , Métabolisme
5.
Journal of Forensic Medicine ; (6): 51-53, 2003.
Article Dans Chinois | WPRIM | ID: wpr-982966

Résumé

The gene complex of Human Leukocyte Antigen (HLA) is located of chromosome 6p21, which is the most complicated dominant polymorphic genetic system. The HLA system has 108 genotypes. It is the best human genetic marker. It has been applied to forensic paternity test and individual identification. This article discusses the research development of HLA polymorphism and its application in forensic medicine.


Sujets)
Humains , Médecine légale , Fréquence d'allèle , Antigènes HLA/génétique , Antigène HLA-A3/génétique , Polymorphisme génétique
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