An accurate, fast and sensitive method based on high performance liquid chromatography was established for the simultaneous determination of eleven ultra-violet absorbents in cosmetics. Eleven ultra-violet absorbents were baseline separated on an Acclaim C18 column within 11. 5 min using acetonitrile-0. 1%formic acid in water ( V/V) mobile phase, and detected at 361 nm with UV detection. Under the optimized conditions, the relative standard derivations ( RSDs) of the eleven ultra-violet absorbents were all less than 0. 1% for retention time, and less than 1. 2% for peak area; good linearity was obtained from 5 to and 500 mg/L with the correlation coefficients of above 0 . 9990 for these analytes; the recoveries spiked in a cosmetic sample were in the range of 77% -116%. Benzophenone-3, butylmethoxydibenzoylmethane, ethylhexylsalicylatec and homosalate were found in the detected cosmetic samples, and the concentration of homosalate was the highest. The results indicated that this method had potential for applications due to its convenience, accuracy and sensitivity. Oxybenzone, butylmethoxydibenzoylmethane, 2-ethylhexyl salicylatec and homosalate were found in the detected cosmetic samples, and the concentration of homosalate was the highest.

Objective:To investigate the effects of airborne fine particle on cell viability and inflammation in human bronchial epithelial cells.Methods:Atmospheric PM2.5 samples were collected by PM2.5 sampler.PM2.5 morphology was observed by scanning electron microscope (SEM).Human bronchial epithelial cells (BEAS-2B) were treated with PM2.5 at different concentrations (0,50,100,200,400,800 μg/mL) for 12,24 or 48 hours,and the cell activity were evaluated by cell counting kit-8 (CCK-8).The mRNA expression levels of (granulocyte-macrophage colony stimulating factor,GM-CSF) and TNF-α were detected by quantitative real-time PCR (qRT-PCR).Western blot was used to detect the protein expressions of GM-CSF and TNF-α.Results:According to SEM,the shape of PM2.5 varied,and the diameter was different and mostly equal to or less than 2.5 μm.CCK-8 assay showed that different concentrations of PM2.5 exposure for 12 hours,24 hours and 48 hours resulted in loss of cell viability of BEAS-2B cells (P＜0.05).Different concentrations of PM2.5 increased the mRNA and protein expression of GM-CSF and TNF-α,and the higher concentration of PM2.5 induced higher expression,which have statistical significant difference between the groups (P＜0.05).Conclusion:Atmospheric PM2.5 can cause inflammatory response in human bronchial epithelial cells.They can reduce cell viability,which may be related to the PM2.5 trigger and aggravation of bronchopulmonary inflammatory diseases.

Objective: To investigate the effect of PM2.5 exposure on nasal inflammatory cytokines and nasal mucosal pathology in a rat model of allergic rhinitis (AR). Methods: Twenty-four healthy female SD rats were randomly divided into 3 groups by random number table method, with 8 rats in each group: normal control group (NC group), ovalbumin (OVA) induced AR model (AR group), and AR model group inhaled to PM2.5 at 200 μg/m³, 3 h/d, for 30 d (ARE group). Nasal symptoms including sneezing, nasal rubs and nasal secretion were recorded. Levels of OVA specific IgE in serum, interleukin 6 (IL-6) and tumor necrosis factor-ɑ (TNF-ɑ) in nasal irrigating solution were measured by enzyme-linked immunosorbent assay (ELISA). The histopathological changes of nasal mucosa were observed by HE staining. SPSS 17.0 software was used to analyze the data. Results: The number of sneezing, nasal rubs and the amount of nasal secretion in the ARE group were significantly higher than that in the AR group and the NC group (number of sneezing (15.38±1.68) times/15 min vs (11.63±1.13) times/15 min vs (1.75±0.71) times/15 min, number of nasal rubs (27.75±2.12) times/15 min vs (21.25±2.96) times/15 min vs (5.25±1.04) times/15 min, amount of nasal secretion (18.90±2.07) mg vs (13.83±1.81) mg vs (3.78±0.41) mg, F values was 236.089, 224.139, 183.971, respectively, all P<0.001). Statistically significant differences in OVA specific IgE, IL-6 and TNF-ɑ levels were observed in ARE group exceeded AR group and NC group (OVA specific IgE (25.42±2.51) ng/ml vs (18.07±1.07) ng/ml vs (1.47±0.26) ng/ml, IL-6 (123.30±18.86) pg/ml vs (63.49±11.29) pg/ml vs (16.87±3.29) pg/ml, TNF-ɑ (162.50±38.15) pg/ml vs (72.96±11.28) pg/ml vs (27.52±4.15) pg/ml, F values was 481.604, 138.277, 63.938, respectively, all P<0.001). HE staining showed that the nasal epithelial cells of NC group were intact and neatly arranged. Nasal mucosa epithelial cells were arranged in disorder in AR group, with tissue structure swelling. Partial shedding of nasal epithelial cells, mucosal basement membrane thickening, submucosal tissue interstitial edema, vasodilation and gland hyperplasia were found in ARE group. Conclusion An increase inflammatory factors level such as IL-6 and TNF-ɑ aggravates pathological damage of nasal mucosa in a rat model of AR by exposure to PM2.5.

Objective: To explore the role of autophagy in PM2.5-induced inflammation in human nasal epithelial cells and related mechanism. Methods: Human nasal epithelial cells were exposed to different concentration of PM2.5 for different times, and the expression levels of microtubule-associated protein-1 light chain-3 Ⅱ (LC3 Ⅱ) and Beclin1 proteins were measured by Western blot. The typical autophagosome and autolysosome were observed by using transmission electron microscopy (TEM). To observe autophagic flux, mRFP-GFP-LC3 plasmid was transfected to nasal epithelial cells and the punctate staining of mRFP-GFP-LC3 were determined by confocal laser scanning microscope. The expression of inflammatory cytokines interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α) in cell culture supernatant were assessed by enzyme-linked immunosorbent assay (ELISA). To assess the role of autophagy in PM2.5-mediated inflammation, autophagy related gene Atg5 and Beclin-1 were silenced by siRNA knockdown, and inflammatory cytokines were analyzed.GraphPad Prism 6.0 was used for statistical analysis. Results: PM2.5 exposure increased the expression of LC3 Ⅱ and Beclin-1 proteins in a dose- (in PM2.5 group with concentration of 0, 15, 30, 60, 120 μg/ml, the expression of LC3 Ⅱ was 0.021±0.001(±s), 0.037±0.002, 0.058±0.005, 0.075±0.006, 0.085±0.004, respectively, F=126.8, P<0.05; the expression of Beclin-1 was 0.002±0.000, 0.003±0.000, 0.005±0.000, 0.007±0.001, 0.008±0.001, respectively, F=137.3, P<0.05) and time-dependent manner (in PM2.5 group with exposure time of 0, 3, 6, 12, 24 h, the expression of LC3Ⅱ was 0.160±0.007, 0.222±0.003, 0.251±0.015, 0.483±0.029, 0.585±0.035, respectively, F=215.3, P<0.05; the expression of Beclin-1 was 0.059±0.002, 0.080±0.002, 0.087±0.002, 0.183±0.007, 0.228±0.005, respectively, F=137.3, P<0.05) in human nasal epithelial cells. TEM analysis showed typical autophagosome and autolysosome in cells after PM2.5 exposure for 24 h. PM2.5 significantly increased the number of yellow and red dots representing autophagosomes and autolysosomes respectively, indicating autophagic flux was elevated. Moreover, PM2.5 enhanced the secretion of inflammatory cytokines such as IL-6 and TNF-α, which was dramatically prevented by Atg5-siRNA and Beclin-1-siRNA. Conclusion Autophagy plays an important role in PM2.5-caused inflammation response in nasal epithelial cells, which can induce release of inflammatory factors such as IL-6 and TNF-α and advance the inflammatory reaction.