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- 저자 : ( Lifang Feng ) (검색결과 4 건)
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Inactivation of Vibrio parahaemolyticus by Aqueous Ozone
( Lifang Feng ),( Kuo Zhang ),( Mengsha Gao ),( Chunwei Shi ),( Caiyun Ge ),( Daofeng Qu ),( Junli Zhu ),( Yugang Shi ),( Jianzhong Han ) 한국미생물생명공학회(구 한국산업미생물학회) 2018 Journal of microbiology and biotechnology Vol.28 No.8
Vibrio parahaemolyticus contamination causes serious foodborne illness and has become a global health problem. As a disinfectant, aqueous ozone can effectively kill a number of bacteria, viruses, parasites, and other microorganisms. In this study, three factors, namely, the aqueous ozone concentration, the exposure time, and the bacterial density, were analyzed by response surface methodology, and the aqueous ozone concentration was the most influential factor in the sterilization ratio. Under low aqueous ozone concentrations (less than 0.125 mg/l), the bacterial cell membranes remained intact, and the ozone was detoxified by intracellular antioxidant enzymes (e.g., superoxide dismutase and catalase). Under high aqueous ozone concentrations (more than 1 mg/l), cell membranes were damaged by the degree of peripheral electronegativity at the cell surface and the concentration of lactate dehydrogenase released into the extracellular space, and the ultrastructures of the cells were confirmed by transmission electron microscopy. Aqueous ozone penetrated the cells through leaking membranes, inactivated the enzymes, inhibited almost all the genes, and degraded the genetic materials of gDNA and total RNA, which eventually led to cell death.
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Junli Zhu,Xuzheng Huang,Fang Zhang,Lifang Feng,Jianrong Li 한국미생물학회 2015 The journal of microbiology Vol.53 No.12
We investigated the quorum sensing (QS) system of Shewanella baltica and the anti-QS related activities of green tea polyphenols (TP) against spoilage bacteria in refrigerated large yellow croaker. Autoinducer-2 (AI-2) and the diketopiperazines (DKPs) cyclo-(L-Pro-L-Leu) and cyclo-(L-Pro-L-Phe) were detected in the culture extract of S. baltica XH2, however, no N-acylhomoserine lactones (AHLs) activity was observed. Green TP at sub-inhibitory concentrations interfered with AI-2 and DKPs activities of S. baltica without inhibiting cell growth and promoted degradation of AI-2. The green TP treatment inhibited biofilm development, exopolysaccharide production and swimming motility of S. baltica in a concentration- dependent manner. In addition, green TP decreased extracellular protease activities and trimethylamine production in S. baltica. A transcriptional analysis showed that green TP repressed the luxS and torA genes in S. baltica, which agreed with the observed reductions in QS activity and the spoilage phenotype. Epigallocatechin gallate (EGCG)-enriched in green TP significantly inhibited AI-2 activity of S.baltica. These findings strongly suggest that green TP could be developed as a new QS inhibitor for seafood preservation to enhance shelf life.
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Regulatory Role of SFN Gene in Hepatocellular Carcinoma and Its Mechanism
Ying Hui,Hao Zeng,Yi Feng,Wenzhou Qin,Peisheng Chen,Lifang Huang,Wenfu Zhong,Liwen Lin,Hui Lv,Xue Qin 한국생물공학회 2021 Biotechnology and Bioprocess Engineering Vol.26 No.3
Purpose: This study aims to explore the differential expression of SFN gene and its regulatory role in different hepatocarcinoma cells, and the impact on hepatocarcinoma. Materials and Methods: High and low SFN expression cells were screened by qRT-PCR and western blotting methods. SFN over expression and interference vectors were constructed. Cell viability was detected by CCK8 kit, cell cycle and apoptosis were detected by flow cytometry. Cell invasion and migration were detected. CCNB1 and CDK1 expression levels were detected by qRT-PCR and Western blotting methods. Results: The high SFN expression BEL7402 cells and the low SFN expression Hep3B cells were screened from Hep3B, HepG2, and BEL7402 cells. The activity of Hep3B cells overexpression vector SFNpcDNA3.1(+) decreased and apoptosis increased, the ratio of G0/G1 decreased and the ratio of S phase increased. The activity of BEL7402 cells transfected with SFN siRNA decreased and apoptosis increased, the ratio of G0/G1 decreased and the ratio of G2/M increased. Interference and overexpression vectors have little effect on the invasion and migration of the two cells. The expression of CDK1 in Hep3B cells decreased significantly, the expression of CDK1 and CCNB1 in BEL7402 cells increased significantly. Conclusions: The differentially expressed SFN gene can regulate the growth of the two hepatocarcinoma cells, high expression of SFN gene can inhibit their growth. The mechanism may be achieved by regulating CCNB1 and CDK1 expression.
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Tizoxanide induces autophagy by inhibiting PI3K/Akt/ mTOR pathway in RAW264.7 macrophage cells
Jiaoqin Shou,Mi Wang,Xiaolei Cheng,Xiaoyang Wang,Lifang Zhang,Yingchun Liu,Chenzhong Fei,Chunmei Wang,Feng Gu,Feiqun Xue,Juan Li,Keyu Zhang 대한약학회 2020 Archives of Pharmacal Research Vol.43 No.2
As the main metabolite of nitazoxanide, tizoxanide(TIZ) has a broad-spectrum anti-infective effect againstparasites, bacteria, and virus. In this study, we investigatedthe effects of TIZ on autophagy by regulating the PI3K/Akt/mTOR signaling pathway. RAW264.7 macrophage cellswere treated with various TIZ concentrations. Cell viabilityassay, transmission electron microscope, and immunofluorescencestaining were used to detect the biological functionof the macrophage cells, and the expression levels of theautophagy pathway-related proteins were measured by Westernblot. Results revealed that TIZ promoted the conversionof LC3-I to LC3-II, the formation of autophagy vacuoles,and the degradation of SQSTM1/p62 in a concentration- andtime-dependent manner in RAW264.7 cells. Treatment withTIZ increased the Beclin-1 expression level and inhibitedPI3K, Akt, mTOR, and ULK1 activation. These effects wereenhanced by pretreatment with rapamycin but attenuated bypretreatment with LY294002. In addition, the conversion ofLC3-I to LC3-II was observed in Vero, 293T, and HepG2cells treated with TIZ. These data suggested that TIZ mayinduce autophagy by inhibiting the Akt/mTOR/ULK1 signalingpathway in macrophages and other cells.
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