Tea polyphenols and catechins postpone evolution of antibiotic resistance genes and alter microbial community under stress of tetracycline.

Relying on the high mobility of water flow, the dissemination of antibiotic resistance genes (ARGs) in the water tends to be exacerbated and enlarged. It caused negative impacts on a wider scope of the environment. The ARGs dissemination monitoring and the methods efficiently reducing their concentration in water became the focus of interest. Green chemicals with antibacterial effects such as tea polyphenols (TPs) and catechins (CA) have been considered as auxiliary disinfectants for ARGs removal in the water environment. However, the antibacterial performance of TPs and CA under the stress of external antibiotics still lacks sufficient research. The results show that more operational taxonomic units can be observed in water samples with TPs and CA than in those without the ingredients under pressure of tetracycline. An unexpected increase along with the increase of ARGs concentrations and the diversity of microbial communities under the low-concentration TPs or CA (1 mg/L). Besides, under the stress of tetracycline, the inhibition of TPs was detected to be strengthened for increase of inti1 and tetC but weakened towards for the increase of tetA. Whilst CA substantially diminished abundances of tetC and tetA under tetracycline pressure. This research demonstrated that TPs and CA are able to assuage development of ARGs under the pressure of antibiotic in water system.

Puerarin suppresses LPS-induced breast cancer cell migration, invasion and adhesion by blockage NF-κB and Erk pathway.

BACKGROUND: Chronic inflammation is a major risk factor for the development and metastatic progression of breast cancer. Puerarin has long been used as traditional Chinese medicine, which possesses manifold physiological activities, including anti-inflammation and anti-cancer activities. However, its anti-cancer metastasis activity in breast cancer cell inflammation-mediated have not been studied. METHODS: Cell viability was detected with Cell Counting Kit (CCK)-8. Transwell migration and invasion assay were performed to evaluate cell migration and invasion, respectively. Enzyme-linked immunosorbent assay (ELISA) was conducted to analysis the expression of inflammatory factor. In addition, mRNA and protein levels of related cytokines were determined by qRT- PCR assay and western blot analysis, respectively. RESULTS: In this study, puerarin significantly inhibited lipopolysaccharide (LPS)-induced MCF-7 and MDA-MB-231 cell migration, invasion and adhesion. The mRNA and protein levels revealed that puerarin treatment effectively negated the expression of CCR7, CXCR4, MMP-2, MMP-9, ICAM and VCAM in LPS- activated MCF-7 and MDA-MB-231 cells. Further, the expression of inflammatory factor TNF-α and IL-6 in cell culture supernatant remarkably reduced. Finally, the result indicated that puerarin abrogated the NF-κB activation in breast cancer cells stimulated by LPS, which is mediated through inhibition of phosphorylation of p65 and IκBα. Also, puerarin inhibited phosphorylation of Erk in breast cancer cells LPS-induced. CONCLUSIONS: This present study revealed that puerarin might be a novel therapeutic drug for breast cancer treatment.