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2 results on '"Xiao-Fan Xiao"'

1. Inhibition of quorum sensing in drug-resistant Staphylococcus epidermidisbyflavaspidic acid BB.

Author

Xiao-Fan Xiao, Xiao-Feng Chen, Shi-Qian Zheng, Rong-Rong Deng, and Zhi-Bin Shen

Subjects
*QUORUM sensing, *MUPIROCIN, *STAPHYLOCOCCUS epidermidis, *STAPHYLOCOCCUS, *SCANNING electron microscopy, *GENE expression
Abstract

Background: To investigate the effect of flavaspidic acid BB (BB) on biofilms and quorumsensing-related genes of drug-resistant Staphylococcus epidermidis (SE) and to provideatheoretical basis for the development of BB as a new type of quorumsensing inhibitor. Methods: The microdilution method was applied to screen 15 clinical isolates of S. epidermidis for drug-resistant S. epidermidis to be used as the test strain. The effects of BBonthe biofilms of drug-resistant S. epidermidis at different growth stages were studied usingthecell counting kit-8 assay and scanning electron microscopy. The gene expression of sigB, sarA, and luxS, regulators involved in quorum sensing of biofilm formation, was measuredby PCR. Results: The minimum inhibitory concentrations of BB against 15 clinical strains of S. epidermidis ranged 11.67–66.67 µg/mL. BB significantly inhibited biofilmformationbydrug-resistant SE06 in the aggregation and maturation stages, with an activity superior tothose of mupirocin and fusidic acid (P < 0.05). At 40 µg/mL, BB reduced the secretionof extracellular polymers and promoted the disruption of biofilm structure. At 80 µg/mL, BBspecifically interfered with the quorum sensing system of drug-resistant SE06bydownregulating sarA and luxS, thereby inhibiting this microbe’s biofilmformation. Conclusion: BB exhibited strong inhibitory activity against SE06 by suppressing biofilmformation and downregulating quorum sensing-related genes and was identified as anewpotential quorum sensing inhibitor against S. epidermidis. [ABSTRACT FROM AUTHOR]

Published
2024
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2. Celastrol induce apoptosis of human multiple myeloma cells involving inhibition of proteasome activity

Author

Huang Sheng, Tai Yang, Jin Liu, Zhong Yueling, Xu Gaojie, Li Zhao, Yan Zeng, Jing-lin An, and Xiao-fan Xiao

Subjects
0301 basic medicine, Proteasome Endopeptidase Complex, Population, Apoptosis, Resting Phase, Cell Cycle, 03 medical and health sciences, chemistry.chemical_compound, Mice, 0302 clinical medicine, Cell Line, Tumor, medicine, Animals, Humans, education, IC50, Multiple myeloma, Cell Proliferation, Pharmacology, education.field_of_study, Severe combined immunodeficiency, Chemistry, Cell growth, medicine.disease, G1 Phase Cell Cycle Checkpoints, Xenograft Model Antitumor Assays, Triterpenes, 030104 developmental biology, Proteasome, Celastrol, Cancer research, Female, Multiple Myeloma, Pentacyclic Triterpenes, Proteasome Inhibitors, 030217 neurology & neurosurgery
Abstract

Celastrol exhibits anticancer activity and has a number of potential molecular targets. Among them, the proteasome has attracted particular attention. Although celastrol inhibits multiple myeloma (MM) cell proliferation, the induction of proteasome-inhibitory activity by celastrol in MM cells at the cellular level and in tumors of mice bearing xenografts has not been confirmed. In the present study, we found that celastrol inhibited the caspase-like (β1), trypsin-like (β2) and chymotrypsin-like (β5) proteasome activities of purified human 20S proteasomes, with half-maximal inhibitory concentration (IC50) values of 7.1, 6.3, and 9.3 μmol/L, respectively. Celastrol also inhibited human MM cellular β1, β2, and β5 proteasome activities, with IC50 values of 2.3, 2.1, and 0.9 μmol/L, respectively. After MM cells were treated with celastrol, a population of apoptotic cells and a population of cells in G0/G1 were observed. Celastrol also inhibited proteasome activity and induced apoptosis in tumor tissue. Treatment of MM.1S and RPMI 8226 tumor-bearing severe combined immunodeficiency (SCID) mice with celastrol reduced the tumor volume. In conclusion, our results reveal the effects of celastrol on proteasome activity in MM cells and shed light on the underlying mechanisms of its anticancer activity, providing a basis for developing celastrol as a potential therapeutic agent for MM.

Published
2018

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