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        A Novel Approach for Sericin-Conjugated Silver Nanoparticle Synthesis and Their Potential as Microbicide Candidates

        ( Xiaowen Lv ),( Huanru Wang ),( Airong Su ),( Ying Chu ) 한국미생물생명공학회(구 한국산업미생물학회) 2018 Journal of microbiology and biotechnology Vol.28 No.8

        Silver nanoparticles have been widely applied for biomedical areas owing to their potent antiviral and antibacterial activities. Synthesis of silver nanoparticles using biomacromolecules is more efficient, environment-friendly, and cost-saving compared with the traditional approach. In this paper, a novel approach was developed to establish a reaction system with Ag<sup>+</sup>-BH4--sericin to synthesize silver nanoparticles conjugated to sericin (AgNPs-Sericin). Sericin could be as a good dispersant and stabilizing agent, which is able to modify nanoscaled AgNPs, the average diameter of which was only 3.78 ± 1.14nm prepared in a 0.3 mg/ml sericin solution. The characterizations of the AgNPs-Sericin were determined by FTIR, thermogravimetry, and XRD analyses. The results showed that the synthesized AgNPs conjugated with sericin as organic phase. Via SAED and XRD analysis, we showed that these AgNPs formed polycrystalline powder with a face-centered cubic structure of bulk metals. Moreover, we investigated the antiviral and antibacterial activities of AgNPs-Sericin, and the results showed that AgNPs-Sericin exhibited potent anti-HIV-1 activity against CCR5-tropic and CXCR4-tropic strains, but no significant cytotoxicity was found toward human genital epithelial cells compared with free silver ions, which are accepted as a commonly used potent antimicrobial agent. Moreover, its antibacterial activity was determined via flow cytometry. The results showed that AgNPs-Sericin could suppress gram-negative (E. coli) and grampositive (S. aureus) bacteria, but more was potent for the gram-negative one. We concluded that our AgNPs-Sericin could be a potential candidate as a microbicide or antimicrobial agent to prevent sexually transmitted infections.

      • KCI등재

        PSMD12 promotes non-small cell lung cancer progression through activating the Nrf2/TrxR1 pathway

        Lv Junqi,Ma Shengmao,Wang Xiaowen,Dang Jifang,Ma Fuchun 한국유전학회 2024 Genes & Genomics Vol.46 No.3

        Background Non-small cell lung cancer (NSCLC) contributes to the vast majority of cancer-related deaths. Proteasome 26S subunit, non-ATPase 12 (PSMD12), a subunit of 26S proteasome complex, is known to play the tumor-promoting role in several types of cancer but its function in NSCLC remains elusive. Objective To explore the role and underlying mechanisms of PSMD12 in NSCLC. Methods The PSMD12 expression in human normal lung epithelial cell line (BEAS-2B) and four NSCLC cell lines (A549, NCI-H1299, NCI-H1975, Calu-1) were determined by qRT-PCR and western blot. Malignant phenotypes of NSCLC cells were detected by CCK-8, EdU staining, immunofluorescence staining for E-cadherin, flow cytometry, and Transwell assays to assess cell viability, proliferation, epithelial-mesenchymal transition (EMT), apoptosis, migration and invasion. Dual luciferase assay was used to verify the regulatory role of transcription factor on the promoter. Results We identified the upregulation of PSMD12 in NSCLC tissues based on the GEO datasets, which further verified in NSCLC and BEAS-2B cell lines. PSMD12 knockdown significantly suppressed malignant behaviors of NSCLC cells, including cell growth, invasion, and migration, while PSMD12 overexpression presented the opposite effects. Interestingly, we found that PSMD12 upregulated the tumor-promoting factor TrxR1 mRNA expression. For its potential mechanisms, we demonstrated that PSMD12 elevated transcription factor Nrf2 protein level and promoted Nrf2 nuclear translocation. And Nrf2 further increased TrxR1 promoter activity and enhanced TrxR1 transcription. Meanwhile, we proved that TrxR1 overexpression erased the inhibitory effect of PSMD12 knockdown. Conclusion PSMD12 promotes NSCLC progression by activating the Nrf2/TrxR1 pathway, providing a novel prognostic and therapeutic target for NSCLC treatment.

      • KCI등재

        CYP19 gene variant confers susceptibility to endometriosis-associated infertility in Chinese women

        Ledan Wang,Xiaosheng Lu,Danhan Wang,,Wenju Li,Xiaowen Xu,Qiusui Huang,Xueying Han,Jieqiang Lv,Wanglei Qu 생화학분자생물학회 2014 Experimental and molecular medicine Vol.46 No.-

        An aromatase encoded by the CYP19 gene catalyzes the final step in the biosynthesis of estrogens, which is related to endometriosis development. To assess the association of CYP19 gene polymorphisms with the risks of endometriosis, chocolate cysts and endometriosis-related infertility, a case–control study was conducted in Chinese Han women by recruiting 225 healthy control females, 146 patients with endometriosis, 94 endometriosis women with chocolate cyst and 65 women with infertility resulting from endometriosis, as diagnosed by both pathological and laparoscopic findings. Individual genotypes atrs2236722:T4C, rs700518:A4G, rs10046:T4C and [TTTA]n polymorphisms were identified. Allelic and genotypic frequencies were compared between the control group and case groups by chi-square analysis. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were determined by logistic regression analysis to predict the association of CYP19 gene polymorphisms with the risk of endometriosis, the related chocolate cysts and infertility. The genotype distributions of the tested CYP19 gene polymorphisms were not significantly different between the healthy control group and the endometriosis/endometriosis with the chocolate cyst group. However, the CYP19 rs700518AA genotype was significantly associated with an increased risk of endometriosis-related infertility (55.4% in the infertility group vs 25.3% in the control group, Po0.001;OR (95% CI): 3.66 (2.06–6.50)) under the recessive form of the A allele. Therefore, we concluded that in Chinese Han females CYP19 gene polymorphisms are not associated with susceptibility to endometriosis or chocolate cysts, whereas CYP19 rs700518AA genotype confers genetic susceptibility to endometriosis-related infertility.

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