[Pollution Characteristics and Multilevel Risk Assessments of Antibiotics in the Urban Rivers of Beijing, China].

To comprehensively assess the pollution characteristics and ecological risks of antibiotics in the rivers in Beijing, the concentrations of 35 common antibiotics belonging to four categories were quantified by using solid phase extraction combined with high-performance liquid chromatography-tandem mass spectrometry. The ecological risks of antibiotics were evaluated using the methods of risk quotient (RQ) and joint probability curves (JPCs). The results showed that a total of 33 antibiotics were detected in the surface water of ten rivers in Beijing, and the total concentrations of antibiotics ranged from N.D. to 1 573.57 ng·L-1. Sulfamethoxazole showed the highest concentration (N.D.-160.04 ng·L-1), followed by sulfadiazine (0.09-147.90 ng·L-1) and ofloxacin (0.28-94.72 ng·L-1). There were 16 antibiotics with a detection frequency greater than 50.0 %. The RQ method showed that there were 12 antibiotics with potential ecological risks. Tetracycline, clarithromycin, and trimethoprim showed the highest risks, with RQs of 3.99, 1.86, and 1.01, respectively. The risks of antibiotics at the outlets of wastewater treatment plants were higher than those in mainstream rivers. The PNEC exceedance rates of tetracycline, clarithromycin, and trimethoprim were above 2.3 %. Based on JPCs, the maximum risk product of clarithromycin was 1.66 %, and it showed low risks to 0.3 %-7.0 % of species. The risks of other antibiotics could be ignored. The detection frequency, distribution of concentrations, most sensitive species, and species sensitivity distribution of antibiotics had important impacts on the ecological risk assessment. Using the multilevel ecological risk assessment strategy can effectively avoid inadequate protection and overprotection and is also conducive to the hierarchical and zoning management of antibiotics throughout the region.

Notoginsenoside R1 protects human keratinocytes HaCaT from LPS-induced inflammatory injury by downregulation of Myd88.

Burn injury is a gigantic challenge in public health which brings multiple negative effects to patients both in physical and spiritual aspects. Inflammation plays vital roles in the progression of burn injury, and our study investigated whether notoginsenoside R1 (NGR1) alleviated lipopolysaccharide (LPS)-induced human keratinocyte HaCaT cell inflammatory injury. Inflammatory injury was induced by LPS in HaCaT cells. Stimulated cells were then treated by NGR1 in different concentrations. Cell viability and cell apoptosis were detected by Cell Counting Kit-8 and flow cytometry, respectively. The concentration of tumor necrosis factor α (TNF-α) and interleukin-6 (IL-6) was measured by enzyme-linked immunosorbent assay (ELISA). The accumulated levels of apoptosis-related proteins (caspase-3 and caspase-9), nuclear factor κB (NF-κB), p38 mitogen-activated protein kinase (p38MAPK) signal pathways-related proteins (p65, IκBα, and p38MAPK), and myeloid differentiation primary response 88 (MyD88) were examined by western blot. Transfection was used to alter the expression of MyD88. We found that LPS stimulated HaCaT cells and induced cell inflammation, evidenced by decreasing cell viability, increasing cell apoptosis, and elevating TNF-α and IL-6 expressions. Then, we found that NGR1 reversed the results by enhancing cell viability, inhibiting cell apoptosis, and reducing TNF-α and IL-6 expressions. In addition, NGR1 decreased the phosphorylation of p65, IκBα, and p38MAPK, which increased by LPS. Moreover, NGR1 negatively regulated the expression of MyD88, and transfection with pMyD88 led to the opposite results with what showed by NGR1 in LPS-stimulated HaCaT cells. To sum up, NGR1 alleviates LPS-induced HaCaT cell inflammatory injury by downregulation of MyD88, as well as inactivation of NF-κB and p38MAPK signal pathways.