Fabrication of EVOH/PANI Composite Nanofibrous Aerogels for the Removal of Dyes and Heavy Metal Ions.

Water pollution caused by the leakage and discharge of pollutants, such as dyes and heavy metal ions, can cause serious damage to the environment and human health. Therefore, it is important to design and develop adsorbent materials that are efficient and multifunctional for the removal of these pollutants. In this work, poly(vinyl alcohol-co-ethylene) (EVOH)/polyaniline (PANI) composite nanofibrous aerogels (NFAs) were fabricated via solution oxidation and blending. The aerogels were characterized by a scanning electron microscope, Fourier transform infrared spectrometry, a contact angle measuring instrument and a universal testing machine. The influences of the introduction of PANI nanorods on the structural properties of aerogels were investigated, and the adsorption performance of aerogels was also studied. The results showed that the introduction of PANI nanorods filled the fibrous network structure, reduced porosity, increased surface hydrophilicity and improved compressive strength. Furthermore, EVOH/PANI composite NFAs possess good adsorption performances for dyes and heavy metal ions: The adsorption capacities of methyl orange and chromium ions (VI) are 73.22 mg/g and 115.54 mg/g, respectively. Overall, the research suggests that EVOH/PANI NFAs have great potential as efficient and multifunctional adsorbent materials for the removal of pollutants from water.

Cucurbitacin B induces cell cycle arrest, apoptosis and autophagy associated with G actin reduction and persistent activation of cofilin in Jurkat cells.

AIM: The present study aimed to explore the antitumor effect and action mechanism of cucurbitacin B (CuB) on human T-cell leukemia Jurkat cells. METHODS: Cell proliferation was measured by the MTS assay. Cell cycle distribution, mitochondrial membrane potential and annexin V staining were analyzed using flow cytometry. Western blotting was used to determine the levels of apoptosis- and autophagy-related proteins. RESULTS: CuB inhibited the proliferation of Jurkat cells in a dose-dependent manner and induced G 2 /M phase arrest as well as formation of tetraploid cells. Accompanied with these effects, the actin dynamics was disrupted, and cofilin, a key regulator of actin dynamics, was persistently activated (dephosphorylated). Although CuB induced around 10% cells undergoing apoptosis, most of the cells were alive after CuB treatment for 24 h. Induction of autophagy was also evident by accumulation of LC3-II. CuB-induced autophagy seemed to be a prosurvival response, since suppression of CuB-induced autophagy significantly increased the activation of caspase-3. CONCLUSION: Our results demonstrated that CuB exhibited antitumor activity in Jurkat cells through induction of cell cycle arrest and apoptosis which was at least partly due to the disruption of actin dynamics.

Histone deacetylase inhibitor suberoylanilide hydroxamic acid exhibits anti-inflammatory activities through induction of mitochondrial damage and apoptosis in activated lymphocytes.

Suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor, has been proven to be an anti-cancer agent. Its anti-inflammatory activities have recently been observed both in in vitro and in vivo models. Yet its action on lymphocytes and the underlying mechanism are still not well known. In this study, in order to evaluate the anti-inflammatory function of SAHA, we analyzed the effects of SAHA on the proliferation, activation, cytokines secretion, cell cycle distribution and apoptosis of murine lymphocytes activated with concanavalin A (Con A). Our results demonstrated that SAHA inhibited the proliferation of Con A-activated lymphocytes in a dose-dependent manner. The expression of CD69 on CD3(+) T lymphocytes was significantly inhibited by SAHA. Intracellular cytokine staining analysis showed that SAHA could downregulate the expression of pro-inflammatory cytokines TNF-α, IL-6 and IFN-γ in T lymphocytes. Furthermore, analysis of sub-G(0)/G(1) peaks and annexin V binding populations revealed that SAHA induced apoptotic cell death in Con A-activated lymphocytes. Consistent with these results, SAHA treatment also induced a decrease of mitochondrial membrane potential and cleavage of caspase-3 and PARP in these cells. Moreover, SAHA caused an accumulation of phosphorylated histone H2A.X, indicating increased double strand DNA breaks. These findings suggest that induction of apoptosis through the mitochondrial pathway may contribute to the anti-inflammatory activities of SAHA on activated lymphocytes.