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Calcium oxide incorporated porous carbon materials were synthesized by the impregnation method to study CO2 adsorption and separation of CO2/CH4. The X-ray diffraction, Raman analysis, N2 isotherms...

The biocomposites of polypyrrole (PPY), polyaniline (PANI) and sodium alginate (NaAlg) with cellulosic biomass barley husk (BH) were prepared and employed for the removal of 2,4-dichlorophenol (2,4-DCP) form aqueous media. The sorption of 2,4-DCP was studied using native and biocomposites (PPY/BH, PANI/BH and NaAlg/BH) as function of various process variables. The maximum sorption (qe, 7.55–24.57 mg/g) of 2,4-DCP was achieved in the range of 7–10 pH, 0.05 g composite dose, 25 mg/L initial concentration of 2,4-DCP and 120 min contact time at 30 °C. The FTIR analysis revealed the involvement of amino, hydroxyl and carboxylic groups for the binding of 2,4-DCP on the surface of biocomposites. The Freundlich and pseudo second order kinetics models best explained the 2,4-DCP adsorption on to the biocomposites. The ∆G, ∆H and ∆S parameters were also computed, which revealed the favorable and exothermic adsorption nature of 2,4-DCP. Presence of salts affected the 2,4-DCP adsorption negatively. HCl found to be efficient desorbing agent for 2,4-DCP from composites and up to 65.12% was eluted using 0.5 N solution. In view of promising efficiency, the biocomposites have potential to remove 2,4-DCP form industrial effluents.

Rapid industrialization is polluting the water resources and is becoming a serious environmental issue. In present study, the adsorption-desorption behavior of Direct Orange-26 (DO-26), Direct Red-31 (DR-31), Direct Blue-67 (DB-67) and Ever direct Orange-3GL (EDO-3) dyes on to native, modified rice husk (MRH), polyvinyl alcohol (PVA), carboxymethyl cellulose (CMC) and alginate (ALG) immobilized biomasses were investigated under different experimental conditions. For adsorbent modification, physical and chemical treatments were performed. The results showed that HCl pre-treatment considerably increased the sorption capacity of dyes versus native biomass. The sorption data were optimized using pseudo 1st order, intra-particle diffusion, pseudo 2nd order and Elovich models. The results revealed that the two-step rate equation was followed for the desorption kinetics of dyes. The involvement of -OH (hydroxyl), -COOH (carboxylic) and -NH2 (amino) groups in the adsorption of dyes onto biomasses was shown by FTIR analysis. Studies exhibited that among adsorbents employed, the MRH has the excellent potential for the dyes degradation from textile effluents.

Metal chelation-enhanced changes in surface plasmon resonance (SPR) band of gallic acid-functionalized AgNP solution to monitor aluminum ions (Al3+) is reported herein. In aqueous solution, Al3+ selectively induced a strong absorbance with large shifts up to ∼125 nm from the SPR band with color changing from orange to red. This study illustrates that hydroxyl groups of phenol affect the response of a probe that tunes the absorbance maxima to a longer wavelength at 525 nm. Moreover, the rapid formation of a AgNP-Al3+ coordination complex was demonstrated by real-time monitoring, adsorptive removal, and energy dispersive spectroscopy mapping.

Seedlings of alfalfa (Medicago sativa L.) were exposed to different concentrations of atmospheric ozone (20–30 (control), 40–60, 65–80, and 85–120 ppb) in four distinct areas in the Riyadh region, so as to decide how ozone affected some of the seedling cellular organelles. Results acquired utilizing transmission electron microscopy demonstrated certifiable impacts to exist on the cell organelles in the tissues of both the leaf mesophyll and stem cortex; contrasted with control plants, the chloroplasts seemed enlarged, irregular, different sizes, decomposed, and possibly dissolved, while the plastoglobules seemed deformed, more widely spaced, and enlarged, also the vacuoles contained no clear non-living components. Moreover, some parts of the cytoplasmic membranes were ruptured, with only a few vesicles created at all concentrations, particularly in plants exposed to concentrations of 65–80 and 85–120 ppb, while no effects were noted in these organelles in control plants or plants exposed to 40–60 ppb. High concentrations (85–120 ppb) led to enlarged, irregularly shaped nuclei and chromatin intensification; however, no clear effects of ozone were noted on the shapes of chloroplast starch grains or the mitochondria in leaf mesophyll and cortex cells in the stem. The high ozone concentrations can cause negative effects on the growth of alfalfa seedlings, leading to imbalances in their vital functions and acceleration of aging, thus potentially decreasing the total plant yield. The discoveries hence propose that alfalfa plants should not be planted near polluted areas, and that they can be utilized as bioindicators of air pollution by ozone. Keywords: Alfalfa, Cell wall, Organelles, Nucleus, Chloroplasts, TEM

The untreated systemic chronic inflammation leads to autoimmune diseases, hyperglycemia, cardiovascular diseases, type 2 diabetes, hypertension, osteoporosis, and so on. Phytochemicals effectively inhibit the inflammation, and numerous studies have proved that the phytocomponents possess anti-inflammatory property via inhibiting the cyclooxygenase and lipoxygenase signaling pathways. Rhaponticin is one such phytochemical obtained from the perennial plant Rheum rhaponticum L. belonging to Polygonaceae family. We assessed the anti-inflammatory potency of rhaponticin in endothelial cells induced with lipopolysaccharides (LPS). Four different endothelial cells induced with LPS were treated with rhaponticin and assessed for the nitric oxide generation. The cytotoxic potency of rhaponticin was evaluated in endothelial cells using the 3-(4,5-dimethylthizaol-2yl)-2,5-diphenyl tetrazolium bromide assay. The tumor necrosis factor-α (TNF-α) synthesis was quantified using the commercially available assay kit. The inflammatory signaling protein gene expression of TNF-α, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX2), and interleukin-1β (IL-1β) was analyzed with quantitative polymerase chain reaction (PCR) analysis. The gene expression of NADPH oxidase (NOX) cytoplasmic catalytic subunits gp91phox , p47phox , and p22phox was assessed with real-time PCR analysis. Finally, to confirm the anti-inflammatory potency of rhaponticin, the nuclear factor kappa B (NFκB) and mitogen-activated protein kinase (MAPK) signaling protein expression was analyzed with immunoblotting analysis. Rhaponticin treatment significantly decreased the levels of nitric oxide and TNF-α synthesis in LPS-induced endothelial cells. It significantly decreased the gene expression of inflammatory proteins and NOX signaling protein. The protein expression of NFκB and MAPK signaling proteins was drastically decreased in rhaponticin-treated endothelial cells induced with LPS. Overall, our results confirm that rhaponticin effectively inhibited the inflammation triggered by LPS in endothelial cells via downregulating iNOS, COX2, and NFκB and MAPK signaling pathways.

The present study aimed to explore the possible radioprotective effects of celastrol and relevant molecular mechanisms in an in vitro cell and in vivo mouse models exposed to gamma radiation. Human keratinocytes (HaCaT) and foreskin fibroblast (BJ) cells were exposed to gamma radiation of 20Gy, followed by treatment with celastrol for 24 h. Cell viability, reactive oxygen species (ROS), nitric oxide (NO) and glutathione (GSH) production, lipid peroxidation, DNA damage, inflammatory cytokine levels, and NF-&kappa, B pathway activation were examined. The survival rate, levels of interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-&alpha, ) in blood, and p65 and phospho-p65 expression were also evaluated in mice after exposure to gamma radiation and celastrol treatment. The gamma irradiation of HaCaT cells induced decreased cell viability, but treatment with celastrol significantly blocked this cytotoxicity. Gamma irradiation also increased free radical production (e.g., ROS and NO), decreased the level of GSH, and enhanced oxidative DNA damage and lipid peroxidation in cells, which were effectively reversed by celastrol treatment. Moreover, inflammatory responses induced by gamma irradiation, as demonstrated by increased levels of IL-6, TNF-&alpha, and IL-1&beta, were also blocked by celastrol. The increased activity of NF-&kappa, B DNA binding following gamma radiation was significantly attenuated after celastrol treatment. In the irradiated mice, treatment with celastrol significantly improved overall survival rate, reduced the excessive inflammatory responses, and decreased NF-&kappa, B activity. As a NF-&kappa, B pathway blocker and antioxidant, celastrol may represent a promising pharmacological agent with protective effects against gamma irradiation-induced injury.

Background Cycloastragenol (CAG), a triterpene aglycone is commonly prescribed for treating hypertension, cardiovascular disease, diabetic nephropathy, viral hepatitis, and various inflammatory-linked diseases. Hypothesis We investigated CAG for its action on signal transducer and activator of transcription 3 (STAT3) activation cascades, and its potential to sensitize gastric cancer cells to paclitaxel-induced apoptosis. Methods The effect of CAG on STAT3 phosphorylation and other hallmarks of cancer was deciphered using diverse assays in both SNU-1 and SNU-16 cells. Results We observed that CAG exhibited cytotoxic activity against SNU-1 and SNU-16 cells to a greater extent as compared to normal GES-1 cells. CAG predominantly caused negative regulation of STAT3 phosphorylation at tyrosine 705 through the abrogation of Src and Janus-activated kinases (JAK1/2) activation. We noted that CAG impaired translocation of STAT3 protein as well as its DNA binding activity. It further decreased cellular proliferation and mediated its anticancer effects predominantly by causing substantial apoptosis rather than autophagy. In addition, CAG potentiated paclitaxel-induced anti-oncogenic effects in gastric tumor cells. Conclusions Our results indicate that CAG can function to impede STAT3 activation in human gastric tumor cells and therefore it may be a suitable candidate agent for therapy of gastric cancer.

Osteosarcoma or osteogenic sarcoma is the most common and prevalent cancerous tumor of bone and occurs especially in children and teens. Recent treatment strategy includes a combination of both chemotherapy and surgeries. Although, the use of single drug-based chemotherapy treatment remains unsatisfactory. Therefore, combinatorial therapy has emerged as a potential strategy for treatment with limited side- effects. Here, we evaluated the combinatorial anticancerous effect of cisplatin (CIS) and doxorubicin (DOX) bioconjugated bromelain encapsulated gold nanoparticles (B-AuNPs conjugated CIS and DOX) in the treatment of osteosarcoma. The synthesized B-AuNPs conjugated CIS and DOX were characterized by various characterization techniques like UV-vis spectroscopy, TEM, DLS and zeta potential to ensure the synthesis, size, shape, size distribution and stability. Drug loading efficiency bioconjugation of CIS and DOX was ensured by UV-vis spectroscopy. Bioconjugation of CIS and DOX was further confirmed using UV-vis spectroscopy, TEM, DLS, Zeta potential and FT-IR analysis. The combinatorial effect of CIS and DOX in B-AuNPs conjugated CIS and DOX showed highly improved potency against MG-63 and Saos-2 cells at a very low concentration where primary osteoblasts didn-t show any cytotoxic effect. The apoptotic effect of B-AuNPs conjugated CIS and DOX on osteosarcoma and primary osteoblasts cells were analyzed by increased permeability of the cell membrane, condensed chromatin and deep blue fluorescent condensed nucleus. The results clearly showed that B-AuNPs conjugated CIS and DOX significantly improved the potency of both the chemotherapeutic drugs by delivering them specifically into the nucleus of cancer cells through caveolae-dependent endocytosis. Thus, the greater inhibitory effect of combinatorial drugs (B-AuNPs conjugated CIS and DOX) over single drug based chemotherapy would be of great advantage during osteosarcoma treatment. (C) 2017 Published by Elsevier B.V.

Glioma is the prime cause of cancer allied mortality in adolescent people and it accounts about 80% of all malignant tumours. Eugenol is a major bioactive constituent present in the essential oils with numerous pharmacological benefits including nueroprotective activity. The major drawback of eugenol is its extreme volatile property and oxygen sensitivity therefore we increased the efficacy of drug; eugenol by encapsulating with chitosan polymer. Eugenol loaded chitosan polymer (EuCs) was characterized using FTIR, XRD, SEM, HR-TEM analysis and the encapsulation, drug release efficacy was assessed at in vitro condition. The induction of autophagy and anticancer efficacy of EuCs on glioma cells was evaluated with rat C6 glioma cells using MTT assay, acridine orange staining, immunocytochemical analysis of NFκβ protein expression and FLOW cytometric analysis. The anti-metastatic property of Eu-CS was assessed by immunoblotting and RT-PCR analysis of epithelial mesenchymal transition protein expression in EuCs treated rat C6 glioma cells. Our characterization analysis proves that EuCs possess essential physical and functional properties of copolymer to be utilized as a drug. Further the MTT analysis and AO staining confirms even in the presence of oncogenic inducer and autophagic inhibitors, EuCs exhibits apoptotic potency on rat C6 glioma cells. The result of immunocytochemical studies depicts the inhibition of NFκβ protein expression and flow cytometry studies confirm apoptosis induction by EuCs. The inhibition of metastasis by EuCs was proven by the decrease in epithelial mesenchymal transition protein expression in Eu-Cs treated rat C6 glioma cells. Over all our results authentically confirms eugenol loaded chitosan nanopolymer persuasively induces apoptosis and inhibits metastasis in rat C6 glioma cells.

Epithelial mesenchymal transition (EMT) refers to a phenomenon through which epithelial cells develop the metastatic and invasive potential, which are closely related to carcinogenesis. Farnesol (FOH) obtained from the oils of diverse plants can exhibit significant therapeutic actions against obesity, diabetes, inflammatory conditions and cancers. Here, we evaluated the potential effects of FOH on growth and metastasis and it was observed that FOH significantly abrogated cell proliferation in lung cancer cells. Moreover, FOH inhibited cell repair movement by wound healing assay and reduced cell adhesion. It suppressed the expression of mesenchymal genes such as fibronectin, vimentin, N-cadherin, twist, and snail, and increased expression of epithelial genes such as occludin and E-cadherin. It also attenuated the migration and invasion through the inhibition of the PI3K/Akt/mTOR signaling pathway. Furthermore, FOH inhibited the tumor growth of xenograft mouse lung cancer model, and modulated the expression of mesenchymal and epithelial markers. The results suggest that FOH may block the PI3K/Akt/mTOR signaling pathway and thus exhibit anti-proliferative and anti-metastatic activity against lung cancer cells.