Antiallergic effects of ethanol extract of Cnidium monnieri (L.) Cuss. on DNCB-induced atopic dermatitis in mice

Purpose: To study the anti-allergic effects of ethanol extract of Cnidium monnieri (L.) Cuss. on 2, 4-dinitrochlorobenzene (DNCB)-induced atopic dermatitis in mice.Method: Atopic dermatitis (AD) was induced by DNCB in Balb/c mice, and the mice randomly divided into normal group, negative control group, hydrocortisone group, and ethanol extract of Cnidium monnieri (L.) Cuss. (EECM) group. Ear swelling was determined by measuring the thicknesses of the left and right ears of each mouse. Spleen and thymus indices were calculated from spleen, thymus and body weight values. The levels of TNF-α and IgE in serum were determined by enzyme-linked immunosorbent assay (ELISA). Hematoxylin-eosin (H & E) staining and toluidine blue staining were used to evaluate pathological changes in ear tissue, while high performance liquid chromatography (HPLC) was performed to ascertain the bioactive compounds in EECM.Results: Compared with the negative control group, EECM significantly alleviated skin lesions, reduced thickness of ear swelling, and decreased spleen and thymus indexes of mice (p < 0.05). Moreover, EECM significantly reduced epidermal thickness (p < 0.01). However, EECM did not significantly alter the number of mast cells (p > 0.05). The expressions of TNF-α and IgE in serum were also significantly down-regulated (p < 0.01, p < 0.05). Results from HPLC revealed that the contents of bergapten, imperatorin and osthole in EECM were 0.73, 3.69 and 9.40 mg/g, respectively.Conclusion: EECM ameliorates AD in mice via inhibition of inflammation and by a mechanism that might be related to the regulation of TNF-α and IgE levels. The major bioactive constituents of EECM are osthole, imperatorin and bergapten. Thus, this plant extract has a potential to be developed for the treatment of of atopic dermatitis

Resveratrol ameliorates necrotizing enterocolitis in neonatal rats through regulation of inflammatory and apoptotic pathways

Purpose: To determine the efficacy of resveratrol in mitigating necrotizing enterocolitis (NEC) in neonatal rats.Methods: Necrotizing enterocolitis (NEC) was induced in neonatal rats using hypoxia and hypothermia. At the completion of treatment, the intestinal tissues of the rats were isolated for evaluation of various biochemical parameters.Results: There was significant increase in the levels of proinflammatory cytokines (TNF-α, IL-6 and IL-1β) and oxidative stress markers (MDA, xanthine oxidase and nitric oxide) in intestinal tissues of NEC rats (p < 0.05). However, resveratrol treatment led to significant decrease in the levels of cytokines and oxidative stress parameters, relative to the NEC group (p < 0.05). Furthermore, Western blotting resultsshowed up-regulation in protein expressions of inflammatory cytokines in NEC rats. However, the protein expressions of inflammatory cytokines were down-regulated in the NEC rats on treatment with resveratrol. Moreover, resveratrol reversed the NEC-induced up-regulations of Bax and caspase-3, as well as NEC-mediated down-regulation of Bcl-2.Conclusion: These results demonstrate that resveratrol mitigates NEC-induced intestinal damage in neonatal rats via anti-inflammatory, anti-apoptotic and antioxidant mechanisms of action. Therefore, resveratrol is a potential therapeutic agent for NEC

NOx Emission Trends over Chinese Cities Estimated from OMI Observations During 2005 to 2015

Satellite NO2 observations have been widely used to evaluate emission changes. To determine trends in NOx emission over China, we used a method independent of chemical transport models to quantify the NOx emissions from 48 cities and 7 power plants over China, on the basis of Ozone Monitoring Instrument (OMI) NO2 observations during 2005 to 2015. We found that NOx emissions over 48 Chinese cities increased by 52 from 2005 to 2011 and decreased by 21 from 2011 to 2015. The decrease since 2011 could be mainly attributed to emission control measures in power sector; while cities with different dominant emission sources (i.e. power, industrial and transportation sectors) showed variable emission decline timelines that corresponded to the schedules for emission control in different sectors. The time series of the derived NOx emissions was consistent with the bottom-up emission inventories for all power plants (r = 0.8 on average), but not for some cities (r = 0.4 on average). The lack of consistency observed for cities was most probably due to the high uncertainty of bottom-up urban emissions used in this study, which were derived from downscaling the regional-based emission data to cities by using spatial distribution proxies

Berberine inhibits the malignant cell phenotype by inactivating PI3K/AKT/mTOR signaling in laryngeal squamous cell carcinoma

Background. Berberine is an active compound found in different herbs used in Chinese medicine and is well-known for its potential anticancer properties. The study aimed to figure out the role of berberine in regulating the malignant behavior of laryngeal squamous cell carcinoma (LSCC) cells. Methods. LSCC cell lines (SNU-899 and AMC-HN-8) were treated with different concentrations of berberine (0-200 μM) to determine its cytotoxicity. The migration, invasion, and apoptosis of LSCC cells were measured by wound healing assays, Transwell assays, and flow cytometry. Western blot was performed for the quantification of proteins involved in PI3K/AKT/mTOR signaling. Results. The viability of LSCC cells was dose-dependently reduced by berberine. Berberine dampened LSCC cell migration and invasion while augmenting cell apoptosis, as evidenced by a reduced wound closure rate, a decrease in invaded cell number, and a surge in cell apoptosis in the context of berberine stimulation. Importantly, the effects of berberine on the cancer cell process were enhanced by LY294002 (an inhibitor for PI3K) treatment. Moreover, the protein levels of phosphorylated PI3K, AKT, and mTOR were markedly reduced in response to berberine treatment. Conclusion. Berberine inhibits cell viability, migration, and invasion but augments cell apoptosis by inactivating PI3K/AKT/mTOR signaling in LSCC

Chitosan/Silver Nanoparticle/Graphene Oxide Nanocomposites with Multi-Drug Release, Antimicrobial, and Photothermal Conversion Functions

In this work, we designed and fabricated a multifunctional nanocomposite system that consists of chitosan, raspberry-like silver nanoparticles, and graphene oxide. The room temperature atmospheric pressure microplasma (RT-APM) process provides a rapid, facile, and environmentally-friendly method for introducing silver nanoparticles into the composite system. Our composite can achieve a pH controlled single and/or dual drug release. Under pH 7.4 for methyl blue loaded on chitosan, the drug release profile features a burst release during the first 10 h, followed by a more stabilized release of 70–80% after 40–50 h. For fluorescein sodium loaded on graphene oxide, the drug release only reached 45% towards the end of 240 h. When the composite acted as a dual drug release system, the interaction of fluorescein sodium and methyl blue slowed down the methyl blue release rate. Under pH 4, both single and dual drug systems showed a much higher release rate. In addition, our composite system demonstrated strong antibacterial abilities against E. coli and S. aureus, as well as an excellent photothermal conversion effect under irradiation of near infrared lasers. The photothermal conversion efficiency can be controlled by the laser power. These unique functionalities of our nanocomposite point to its potential application in multiple areas, such as multimodal therapeutics in healthcare, water treatment, and anti-microbials, among others

Impacts of climate change on future air quality and human health in China.

In recent years, air pollution has caused more than 1 million deaths per year in China, making it a major focus of public health efforts. However, future climate change may exacerbate such human health impacts by increasing the frequency and duration of weather conditions that enhance air pollution exposure. Here, we use a combination of climate, air quality, and epidemiological models to assess future air pollution deaths in a changing climate under Representative Concentration Pathway 4.5 (RCP4.5). We find that, assuming pollution emissions and population are held constant at current levels, climate change would adversely affect future air quality for >85% of China's population (∼55% of land area) by the middle of the century, and would increase by 3% and 4% the population-weighted average concentrations of fine particulate matter (PM2.5) and ozone, respectively. As a result, we estimate an additional 12,100 and 8,900 Chinese (95% confidence interval: 10,300 to 13,800 and 2,300 to 14,700, respectively) will die per year from PM2.5 and ozone exposure, respectively. The important underlying climate mechanisms are changes in extreme conditions such as atmospheric stagnation and heat waves (contributing 39% and 6%, respectively, to the increase in mortality). Additionally, greater vulnerability of China's aging population will further increase the estimated deaths from PM2.5 and ozone in 2050 by factors of 1 and 3, respectively. Our results indicate that climate change and more intense extremes are likely to increase the risk of severe pollution events in China. Managing air quality in China in a changing climate will thus become more challenging

Pyrotinib and chrysin synergistically potentiate autophagy in HER2-positive breast cancer

Human epidermal growth factor receptor 2 (HER2)-positive breast cancer (BC) has been the most challenging subtype of BC, consisting of 20% of BC with an apparent correlation with poor prognosis. Despite that pyrotinib, a new HER2 inhibitor, has led to dramatic improvements in prognosis, the efficacy of pyrotinib monotherapy remains largely restricted due to its acquired resistance. Therefore, identifying a new potential antitumor drug in combination with pyrotinib to amplify therapeutic efficacy is a pressing necessity. Here, we reported a novel combination of pyrotinib with chrysin and explored its antitumor efficacy and the underlying mechanism in HER2-positive BC. We determined that pyrotinib combined with chrysin yielded a potent synergistic effect to induce more evident cell cycle arrest, inhibit the proliferation of BT-474 and SK-BR-3 BC cells, and repress in vivo tumor growth in xenograft mice models. This may be attributed to enhanced autophagy induced by endoplasmic reticulum stress. Furthermore, the combined treatment of pyrotinib and chrysin induced ubiquitination and glucose-6-phosphate dehydrogenase (G6PD) degradation by upregulating zinc finger and BTB/POZ domain-containing family protein 16 (ZBTB16) in tumorigenesis of BC. Mechanistically, we identified that miR-16-5p was a potential upstream regulator of ZBTB16, and it showed a significant inverse correlation with ZBTB16. Inhibition of miR-16-5p overexpression by restoring ZBTB16 significantly potentiated the overall antitumor efficacy of pyrotinib combined with chrysin against HER2-positive BC. Together, these findings demonstrate that the combined treatment of pyrotinib and chrysin enhances autophagy in HER2-positive BC through an unrecognized miR-16-5p/ZBTB16/G6PD axis.</p