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Tang X.,Anhui University of Science and Technology | Tang X.,Hubei University | Zhu H.,Institute of Skin Damage and Repair | Sun L.,Southern Medical University | And 4 more authors.
International Journal of Nanomedicine

Background: Amphotericin B (AMB) is a polyene antibiotic with broad spectrum antifungal activity, but its clinical toxicities and poor solubility limit the wide application of AMB in clinical practice. Recently, new drug-loaded nanoparticles (NPs) – diblock copolymer D-α-tocopheryl polyethylene glycol 1000 succinate-b-poly(ε-caprolactone-ran-glycolide) (PLGA-TPGS) – have received special attention for their reduced toxicity, and increased effectiveness of drug has also been reported. This study aimed to develop AMB-loaded PLGA-TPGS nanoparticles (AMB-NPs) and evaluate their antifungal effects in vitro and in vivo.Methods: AMB-NPs were prepared with a modified nanoprecipitation method and then characterized in terms of physical characteristics, in vitro drug release, stability, drug-encapsulation efficiency, and toxicity. Finally, the antifungal activity of AMB-NPs was investigated in vitro and in vivo.Results: AMB-NPs were stable and spherical, with an average size of around 110 nm; the entrapment efficacy was closed to 85%, and their release exhibited a typically biphasic pattern. The actual minimum inhibitory concentration of AMB-NPs against Candida albicans was significantly lower than that of free AMB, and AMB-NPs were less toxic on blood cells. In vivo experiments indicated that AMB-NPs achieved significantly better and prolonged antifungal effects when compared with free AMB.Conclusion: The AMB-PLGA-TPGS NP system significantly improves the AMB bioavailability by improving its antifungal activities and reducing its toxicity, and thus, these NPs may become a good drug carrier for antifungal treatment. © 2014 Tang et al. Source

Hao Z.-F.,Chongqing Medical University | Hao Z.-F.,Institute of Skin Damage and Repair | Ao J.-H.,Institute of Skin Damage and Repair | Zhang J.,Institute of Skin Damage and Repair | And 2 more authors.
Asian Pacific Journal of Cancer Prevention

Aim: ATF3, a member of the ATF/CREB family of transcription factors, has been found to be selectively induced by calcineurin/NFAT inhibition and to enhance keratinocyte tumor formation, although the precise role of ATF3 in human skin cancer and possible mechanisms remain unknown. Methods: In this study, clinical analysis of 30 skin cancer patients and 30 normal donors revealed that ATF3 was accumulated in skin cancer tissues. Functional assays demonstrated that ATF3 significantly promoted skin cancer cell proliferation. Results: Mechanically, ATF3 activated Stat3 phosphorylation in skin cancer cell through regulation of p53 expression. Moreover, the promotion effect of ATF3 on skin cancer cell proliferation was dependent on the p53-Stat3 signaling cascade. Conclusion: Together, the results indicate that ATF3 might promote skin cancer cell proliferation and enhance skin keratinocyte tumor development through inhibiting p53 expression and then activating Stat3 phosphorylation. Source

Hao Z.-F.,Institute of Skin Damage and Repair | Hao Z.-F.,Chongqing Medical University | Su Y.-M.,Institute of Skin Damage and Repair | Wang C.-M.,Institute of Skin Damage and Repair | Yang R.-Y.,Institute of Skin Damage and Repair
Tumor Biology

Inhibition of histone deacetylase (HDAC) activity by HDAC inhibitors (HDACis) results in cancer cell growth inhibition, and HDACis have been revealed as potential anti-skin cancer agents. p21 is a cyclin-dependent kinase inhibitor and an essential regulator of growth inhibition. Recently, we reported that activating transcription factor 3 (ATF3) could significantly promote skin cancer cell growth. This study explored the relationship between ATF3 and HDACi-induced growth inhibition of epidermoid carcinoma cells. We found that trichostatin A (TSA) treatment inhibited cell growth in A431 epidermoid carcinoma cells in a dose-dependent manner. Simultaneously, p21 and ATF3 expression levels were upregulated and downregulated upon TSA stimulation, respectively. ATF3 overexpression promoted cell growth and downregulated p21 expression. In contrast, ATF3 depletion resulted in cell growth reduction and p21 transcriptional upregulation. More importantly, ATF3 overexpression partially antagonized TSA-induced growth inhibition and p21 activation. Collectively, these data demonstrate that ATF3 acts as an essential negative regulator of TSA-induced cell growth inhibition through interfering with TSA-induced p21 activation. © 2014, International Society of Oncology and BioMarkers (ISOBM). Source

Zhou Z.-Q.,Chinese PLA General Hospital | Zhou Z.-Q.,Institute of Skin Damage and Repair | Sui Z.-F.,Institute of Skin Damage and Repair | Tian Y.-L.,Institute of Skin Damage and Repair | And 4 more authors.
International Journal of Clinical and Experimental Medicine

Background: To investigate effects of leptin on ultraviolet-induced skin photoaging in human skin fibro­blasts (HSFs) and mice and the underlying mechanism. Methods: HSFs in 3-5 subcultures and 50 CD-1 (ICR) mice were randomly divided into blank group, model group and leptin-treated groups. Changes of HSFs and HE stained mouse skin tissue structure exposed to UVA/B irradiation were observed. Senescence-associated β-galactosidase staining of HSFs was determined. Activity of CAT, SOD and GSH-Px and concentrations of MDA, Hyp and LDH were determined by biochemical analysis. Expressions of p67phox, PKCε and p66Shc were detected by Western blot­ting. Results: UV-induced photoaging models were successfully established. In HSFs, compared with blank group, significantly decreased SA β-gal staining rate and concentrations of CAT, SOD, GSH-Px and Hyp but significantly in­creased concentrations of MDA, LDH and ROS were found in model group; compared with model group, significantly increased concentrations of CAT, SOD, GSH-Px and Hyp and significantly decreased MDA, LDH and ROS were found in leptin-treated groups. Similar trends were observed regarding the concentrations of CAT, SOD, GSH-Px, Hyp, MDA, LDH and ROS in mouse skin tissues. In both HSFs and mouse skin tissues, the expressions of NADPH, p67phox, PKCε and p66Shc were significantly up-regulated in model group compared with blank group; while the expressions of p67phox, PKCε and p66Shc were significantly down-regulated in leptin-treated groups in comparison with model group. Conclusion: Leptin may prevent skin photoaging by scavenging free radicals, improving antioxidant capacity and enzyme activity, alleviating oxidative damage and promoting collagen synthesis in HSFs and mouse skin tis­sues. © 2016, E-Century Publishing Corporation. All rights reserved. Source

Ao J.-H.,Institute of Skin Damage and Repair | Hao Z.-F.,Institute of Skin Damage and Repair | Zhu H.,Institute of Skin Damage and Repair | Wen L.,Chinese Peoples Liberation Army | Yang R.-Y.,Institute of Skin Damage and Repair

Invasive fungal infections due to Aspergillus species have become a major cause of morbidity and mortality among immunocompromised patients. In order to determine the possible relationship between environmental contamination by Aspergillus and the occurrence of invasive aspergillosis, a 1-year prospective study was carried out in a tertiary hospital in China. Air, surface, and tap water sampling was performed twice monthly at the bone marrow transplant (BMT) department, intensive care unit (ICU), neurosurgery intensive care unit (NICU), and outdoors. Nose, pharynx, and sputum samples were collected from high-risk patients. Isolates of Aspergillus from the environment and patients were genotyped by random amplification of polymorphic DNA (RAPD) assay to investigate the origin of infection. Mean total Aspergillus count was 7.73, 8.94, 13.19, and 17.32 cfu/m3 in the BMT department, ICU, NICU, and outdoors, respectively. RAPD analysis by R108 primer demonstrated that strains isolated from patients in NICU were identical to the environmental strain. Strains isolated from patients in ICU differed from the environmental strain. Aspergillus contamination was found in the BTM department, NICU, and ICU. Clinical and environmental strains from NICU had identical genotypes. These findings suggest that Aspergillus is found in the hospital environment including the air, surface, and tap water. The genotypes of Aspergillus were identical from patients and the environment, suggesting that clinical infection may originate from the hospital environment. © 2014 Springer Science+Business Media Dordrecht. Source

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