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The CO 2 absorption flux while using monoethanolamide (MEA) solution in a spiral-wired channel was significantly enhanced by optimizing both the descending and ascending spiral ring pitch configurations within the filled channel. In this study, two distinct spiral ring pitch configurations were integrated into concentric circular membrane contactors to augment CO 2 absorption flux. Spiral rods were strategically inserted to mitigate concentration polarization effects, thereby reducing mass transfer boundary layers and increasing turbulence intensity. A theoretical one-dimensional model was developed to predict absorption flux and concentration distributions across varying MEA absorbent flow rates, CO 2 feed flow rates, and inlet CO 2 concentrations in the gas feed. Theoretical predictions of absorption flux improvement were validated against experimental results, demonstrating favorable agreement for both ascending and descending spiral ring pitch operations. Interestingly, the results indicated that descending spiral ring pitch operations achieved higher turbulent intensity compared to ascending configurations, thereby alleviating concentration polarization resistance and enhancing CO 2 absorption flux with reduced polarization effects. Specifically, under conditions of a 40% inlet CO 2 concentration and 5 cm 3 /s MEA feed flow rate, a notable 83.69% enhancement in absorption flux was achieved compared to using an empty channel configuration. Moreover, a generalized expression for the Sherwood number was derived to predict the mass transfer coefficient for CO 2 absorption in concentric circular membrane contactors, providing a practical tool for performance estimation. The economic feasibility of the spiral-wired module was also assessed by evaluating both absorption flux improvement and incremental power consumption. Overall, these findings underscore the effectiveness of optimizing spiral ring pitch configurations in enhancing CO 2 absorption flux, offering insights into improving the efficiency and economic viability of CO 2 capture technologies.

The CO 2 absorption by Monoethanolamine (MEA) solutions as chemical absorption was conducted in the membrane gas absorption module with inserting 3D mini-channel turbulence promoters of the present work. A mathematical modeling of CO 2 absorption flux was analyzed by using the chemical absorption theory based on mass-transfer resistances in series. The membrane absorption module with embedding 3D mini-channel turbulence promoters in the current study indicated that the CO 2 absorption rate improvement is achieved due to the diminishing concentration polarization effect nearby the membrane surfaces. A simplified regression equation of the average Sherwood number was correlated to express the enhanced mass-transfer coefficient of the CO 2 absorption. The experimental results and theoretical predictions showed that the absorption flux improvement was significantly improved with implementing 3D mini-channel turbulence promoters. The experimental results of CO 2 absorption fluxes were performed in good agreement with the theoretical predictions in aqueous MEA solutions. A further absorption flux enhancement up to 30.56% was accomplished as compared to the results in the previous work, which the module was inserted the promoter without mini channels. The influences of the MEA absorbent flow rates and inlet CO 2 concentrations on the absorption flux and absorption flux improvement are also illustrated under both concurrent- and countercurrent-flow operations.

Membrane dialysis is one of the membrane contactors applied to wastewater treatment. The dialysis rate of a traditional dialyzer module is restricted because the solutes transport through the membrane only by diffusion, in which the mass-transfer driving force across the membrane is the concentration gradient between the retentate and dialysate phases. A two-dimensional mathematical model of the concentric tubular dialysis-and-ultrafiltration module was developed theoretically in this study. The simulated results show that the dialysis rate improvement was significantly improved through implementing the ultrafiltration effect by introducing a trans-membrane pressure during the membrane dialysis process. The velocity profiles of the retentate and dialysate phases in the dialysis-and-ultrafiltration system were derived and expressed in terms of the stream function, which was solved numerically by the Crank-Nicolson method. A maximum dialysis rate improvement of up to twice that of the pure dialysis system (Vw=0) was obtained by employing a dialysis system with an ultrafiltration rate of Vw=2 mL/min and a constant membrane sieving coefficient of θ=1. The influences of the concentric tubular radius, ultrafiltration fluxes and membrane sieve factor on the outlet retentate concentration and mass transfer rate are also illustrated.

A novel design of an air gap membrane distillation (AGMD) module was proposed to enhance the permeate flux improvement for the desalination of pure water productivity. The modeling equations for predicting permeate flux in the AGMD module by inserting Λ-ribs carbon-fiber open slots under various hydrodynamic angles were developed theoretically and experimentally. The temperature distributions of both hot and cold feed streams were represented graphically with the hot saline flow rate, inlet saline temperature, and carbon-fiber hydrodynamic angles as parameters. The results showed a good agreement between the experimental results and theoretical predictions. Designed by inserting Λ-ribs carbon-fiber open slots into the flow channel, the membrane distillation module was implemented to act as an eddy promoter and yield an augmented turbulence flow. The effect of Λ-ribs carbon-fiber open slots not only assured the membrane stability by preventing vibration but also increased the permeate flux by diminishing the temperature polarization of the thermal boundary layer. The permeate flux improvement by inserting Λ-ribs carbon-fiber open slots in the AGMD module provided the maximum relative increment of up to 15.6% due to the diminution of the concentration polarization effect. The experimental data was incorporated with the hydrodynamic angle of Λ-ribs carbon-fiber open slots to correlate the enhancement factor with the Nusselt numbers to confirm the theoretical predictions. The accuracy derivation between the experimental results and theoretical predictions was pretty good, within 9.95≤E≤1.85. The effects of operating and designing parameters of hot saline flow rate, inlet saline temperature, and hydrodynamic angle on the permeate flux were also delineated by considering both the power consumption increment and permeate flux enhancement.

The use of microalgae for wastewater remediation and nutrient recovery answers the call for a circular bioeconomy, which involves waste resource utilization and ecosystem protection. The integration of microalgae cultivation and wastewater treatment has been proposed as a promising strategy to tackle the issues of water and energy source depletions. Specifically, microalgae-enabled wastewater treatment offers an opportunity to simultaneously implement wastewater remediation and valuable biomass production. As a versatile technology, membrane-based processes have been increasingly explored for the integration of microalgae-based wastewater remediation. This review provides a literature survey and discussion of recent progressions and achievements made in the development of membrane photobioreactors (MPBRs) for wastewater treatment and nutrient recovery. The opportunities of using microalgae-based wastewater treatment as an interesting option to manage effluents that contain high levels of nutrients are explored. The innovations made in the design of membrane photobioreactors and their performances are evaluated. The achievements pave a way for the effective and practical implementation of membrane technology in large-scale microalgae-enabled wastewater remediation and nutrient recovery processes.

Oxidative stress induces DNA damage which can be repaired by DNA repair proteins, such as Ku70/80. Excess reactive oxygen species (ROS) stimulate the activation of caspase-3, which degrades Ku 70/80. Cells with decreased Ku protein levels undergo apoptosis. Astaxanthin exerts antioxidant activity by inducing the expression of catalase, an antioxidant enzyme, in gastric epithelial cells. Therefore, astaxanthin may inhibit oxidative stress-induced DNA damage by preventing Ku protein degradation and thereby suppressing apoptosis. Ku proteins can be degraded via ubiquitination and neddylation which adds ubiquitin-like protein to substrate proteins. We aimed to determine whether oxidative stress decreases Ku70/80 expression through the ubiquitin-proteasome pathway to induce apoptosis and whether astaxanthin inhibits oxidative stress-induced changes in gastric epithelial AGS cells. We induced oxidative stress caused by the treatment of β-D-glucose (G) and glucose oxidase (GO) in the cells. As a result, the G/GO treatment increased ROS levels, decreased nuclear Ku protein levels and Ku-DNA-binding activity, and induced the ubiquitination of Ku80. G/GO increased the DNA damage marker levels (γ-H2AX; DNA fragmentation) and apoptosis marker annexin V-positive cells and cell death. Astaxanthin inhibited G/GO-induced alterations, including Ku degradation in AGS cells. MLN4924, a neddylation inhibitor, and MG132, a proteasome inhibitor, suppressed G/GO-mediated DNA fragmentation and decreased cell viability. These results indicated that G/GO-induced oxidative stress causes Ku protein loss through the ubiquitin-proteasome pathway, resulting in DNA fragmentation and apoptotic cell death. Astaxanthin inhibited oxidative stress-mediated apoptosis via the reduction of ROS levels and inhibition of Ku protein degradation. In conclusion, dietary astaxanthin supplementation or astaxanthin-rich food consumption may be effective for preventing or delaying oxidative stress-mediated cell damage by suppressing Ku protein loss and apoptosis in gastric epithelial cells.

Helicobacter pylori (H. pylori) increases production of reactive oxygen species (ROS) and activates signaling pathways associated with gastric cell invasion, which are mediated by matrix metalloproteinases (MMPs). We previously demonstrated that H. pylori activated mitogen-activated protein kinase (MAPK) and increased expression of MMP-10 in gastric epithelial cells. MMPs degrade the extracellular matrix, enhancing tumor invasion and cancer progression. The signaling pathway of phosphatidylinositol 3-kinase (PI3K)/serine/threonine protein kinase B (AKT)/mammalian target of rapamycin (mTOR) is associated with MMP expression. ROS activates PIK3/AKT/mTOR signaling in cancer. Astaxanthin, a xanthophyll carotenoid, shows antioxidant activity by reducing ROS levels in gastric epithelial cells infected with H. pylori . This study aimed to determine whether astaxanthin inhibits MMP expression, cell invasion, and migration by reducing the PI3K/AKT/mTOR signaling in H. pylori -infected gastric epithelial AGS cells. H. pylori induced PIK3/AKT/mTOR and NF-κB activation, decreased IκBα, and induced MMP (MMP-7 and -10) expression, the invasive phenotype, and migration in AGS cells. Astaxanthin suppressed these H. pylori -induced alterations in AGS cells. Specific inhibitors of PI3K, AKT, and mTOR reversed the H. pylori -stimulated NF-κB activation and decreased IκBα levels in the cells. In conclusion, astaxanthin suppressed MMP expression, cell invasion, and migration via inhibition of PI3K/AKT/mTOR/NF-κB signaling in H. pylori -stimulated gastric epithelial AGS cells.

Helicobacter pylori (H. pylori) is a Gram-negative bacterium that colonizes the gastric mucosa and triggers various stomach diseases. H. pylori induces reactive oxygen species (ROS) production and DNA damage. The heterodimeric Ku70/Ku80 protein plays an essential role in the repair of DNA double-strand breaks (DSB). Oxidative stress stimulate apoptosis and DNA damage that can be repaired by Ku70/80. However, excessive reactive oxygen species (ROS) can cause Ku protein degradation, resulting in DNA fragmentation and apoptosis. α-lipoic acid (α-LA), which is found in organ meats such as liver and heart, spinach, broccoli, and potatoes, quenches free radicals, chelates metal ions, and reduces intracellular DNA damage induced by oxidative stress. Here, we investigated whether H. pylori decreases Ku70/80 and induces apoptosis, and whether α-LA inhibits changes induced by H. pylori . We analyzed ROS, DNA damage markers (γ-H2AX, DNA fragmentation), levels of Ku70/80, Ku-DNA binding activity, Ku80 ubiquitination, apoptosis indices (Bcl-2, Bax, apoptosis-inducing factor (AIF), and caspase-3), and viability in a human gastric epithelial adenocarcinoma cell line (AGS). H. pylori increased ROS, DNA damage markers, Ku80 ubiquitination, and consequently induced apoptosis. It also decreased nuclear Ku70/80 levels and Ku-DNA-binding activity; increased Bax expression, caspase-3 cleavage, and truncated AIF; but decreased Bcl-2 expression. These H. pylori -induced alterations were inhibited by α-LA. The antioxidant N-acetylcysteine and proteasome inhibitor MG-132 suppressed H. pylori -induced cell death and decreased nuclear Ku70/80 levels. The results show that oxidative stress induced Ku70/80 degradation via the ubiquitin-proteasome system, leading to its nuclear loss and apoptosis in H. pylori -infected cells. In conclusion, α-LA inhibited apoptosis induced by H. pylori by reducing ROS levels and suppressing the loss of Ku70/80 proteins in AGS cells.

Theoretical predictions of carbon dioxide absorption flux were analyzed by developing one-dimensional mathematical modeling using the chemical absorption theory based on mass-transfer resistances in series. The CO 2 absorption into monoethanolamine (MEA) solutions was treated as chemical absorption, accompanied by a large equilibrium constant. The experimental work of the CO 2 absorption flux using MEA solution was conducted in double-unit flat-plate membrane contactors with embedded 3D turbulence promoters under various absorbent flow rates, CO 2 feed flow rates, and inlet CO 2 concentrations in the gas feed stream for both concurrent and countercurrent flow operations. A more compact double-unit module with embedded 3D turbulence promoters could increase the membrane stability to prevent flow-induced vibration and enhance the CO 2 absorption rate by overwhelming the concentration polarization on the membrane surfaces. The measured absorption fluxes with a near pseudo-first-order reaction were in good agreement with the theoretical predictions for the CO 2 absorption efficiency in aqueous MEA solutions, which was shown to be substantially larger than the physical absorption in water. By embedding 3D turbulence promoters in the MEA feed channel, the new design accomplishes a considerable CO 2 absorption flux compared with an empty channel as well as the single unit module. This demonstrates the value and originality of the present study regarding the technical feasibility. The absorption flux enhancement for the double-unit module with embedded 3D turbulence promoters could provide a maximum relative increase of up to 40% due to the diminution in the concentration polarization effect. The correlated equation of the average Sherwood number was obtained numerically using the fourth Runge-Kutta method in a generalized and simplified expression to calculate the mass transfer coefficient of the CO 2 absorption in the double-unit flat-plate membrane contactor with turbulence promoter channels.

Helicobacter pylori ( H. pylori ) causes gastric diseases by increasing reactive oxygen species (ROS) and interleukin (IL)-8 expression in gastric epithelial cells. ROS and inflammatory responses are regulated by the activation of nuclear factor erythroid-2-related factor 2 (Nrf2) and the expression of Nrf2 target genes, superoxide dismutase ( SOD ) and heme oxygenase-1 ( HO-1 ). We previously demonstrated that Korean red ginseng extract (RGE) decreases H. pylori -induced increases in ROS and monocyte chemoattractant protein 1 in gastric epithelial cells. We determined whether RGE suppresses the expression of IL-8 via Nrf2 activation and the expression of SOD and HO-1 in H. pylori -infected gastric epithelial AGS cells. H. pylori -infected cells were treated with RGE with or without ML385, an Nrf2 inhibitor, or zinc protoporphyrin (ZnPP), a HO-1 inhibitor. Levels of ROS and IL-8 expression; abundance of Keap1, HO-1, and SOD; levels of total, nuclear, and phosphorylated Nrf2; indices of mitochondrial dysfunction (reduction in mitochondrial membrane potential and ATP level); and SOD activity were determined. As a result, RGE disturbed Nrf2-Keap1 interactions and increased nuclear Nrf2 levels in uninfected cells. H. pylori infection decreased the protein levels of SOD-1 and HO-1, as well as SOD activity, which was reversed by RGE treatment. RGE reduced H. pylori -induced increases in ROS and IL-8 levels as well as mitochondrial dysfunction. ML385 or ZnPP reversed the inhibitory effect of RGE on the alterations caused by H. pylori . In conclusion, RGE suppressed IL-8 expression and mitochondrial dysfunction via Nrf2 activation, induction of SOD-1 and HO-1, and reduction of ROS in H. pylori -infected cells.

A new design of direct-contact membrane distillation (DCMD) modules with cross-diagonal carbon-fiber spacers of various hydrodynamic angles in flow channels to promote turbulence intensity was proposed to enhance pure water productivity. Attempts to reduce the temperature polarization coefficient were achieved by inserting cross-diagonal carbon-fiber spacers in channels, which create wakes and eddies in both heat and mass transfer behaviors to enhance the permeate flux enhancement. A simplified equation was formulated to obtain the theoretical predictions of heat transfer coefficients in the current DCMD device. The permeate fluxes and temperature distributions of both hot and cold feed streams are represented graphically with the inlet volumetric flow rate and inlet temperature of the hot saline feed stream as parameters. The higher distillate flux of countercurrent-flow operations for saline water desalination was accomplished as compared to the concurrent-flow operations of various hydrodynamic angles. The results show that the agreement between the theoretical predictions and experimental results is reasonably good. The effects of countercurrent-flow operations and inserting carbon fiber spacers have confirmed technical feasibility and device performance enhancement of up to 45%. The influences of operating and design parameters on the pure water productivity with the expense of energy consumption are also discussed.

Two geometric shape turbulence promoters (circular and square of same areas) of different array patterns using three-dimensional (3D) printing technology were designed for direct contact membrane distillation (DCMD) modules in the present study. The DCMD device was performed at middle temperature operation (about 45 °C to 60 °C) of hot inlet saline water associated with a constant temperature of inlet cold stream. Attempts to reduce the disadvantageous temperature polarization effect were made inserting the 3D turbulence promoters to promote both the mass and heat transfer characteristics in improving pure water productivity. The additive manufacturing 3D turbulence promoters acting as eddy promoters could not only strengthen the membrane stability by preventing vibration but also enhance the permeate flux with lessening temperature polarization effect. Therefore, the 3D turbulence promoters were individually inserted into the flow channel of the DCMD device to create vortices in the flow stream and increase turbulent intensity. The modeling equations for predicting the permeate flux in DCMD modules by inserting the manufacturing 3D turbulence promoter were investigated theoretically and experimentally. The effects of the operating conditions under various geometric shapes and array patterns of turbulence promoters on the permeate flux with hot inlet saline temperatures and flow rates as parameters were studied. The distributions of the fluid velocities were examined using computational fluid dynamics (CFD). Experimental study has demonstrated a great potential to significantly accomplish permeate flux enhancement in such new design of the DCMD system. The permeate flux enhancement for the DCMD module by inserting 3D turbulence promoters in the flow channel could provide a maximum relative increment of up to 61.7% as compared to that in the empty channel device. The temperature polarization coefficient (τtemp) was found in this study for various geometric shapes and flow patterns. A larger τtemp value (the less thermal resistance) was achieved in the countercurrent-flow operation than that in the concurrent-flow operation. An optimal design of the module with inserting turbulence promoters was also delineated when considering both permeate flux enhancement and energy utilization effectiveness.

Forward osmosis (FO) has been recognized as the preferred alternative membrane-based separation technology for conventional water treatment technologies due to its high energy efficiency and promising separation performances. FO has been widely explored in the fields of wastewater treatment, desalination, food industry and bio-products, and energy generation. The substrate of the typically used FO thin film composite membranes serves as a support for selective layer formation and can significantly affect the structural and physicochemical properties of the resultant selective layer. This signifies the importance of substrate exploration to fine-tune proper fabrication and modification in obtaining optimized substrate structure with regards to thickness, tortuosity, and porosity on the two sides. The ultimate goal of substrate modification is to obtain a thin and highly selective membrane with enhanced hydrophilicity, antifouling propensity, as well as long duration stability. This review focuses on the various strategies used for FO membrane substrate fabrication and modification. An overview of FO membranes is first presented. The extant strategies applied in FO membrane substrate fabrications and modifications in addition to efforts made to mitigate membrane fouling are extensively reviewed. Lastly, the future perspective regarding the strategies on different FO substrate layers in water treatment are highlighted.

We investigated the insertion of eddy promoters into a parallel-plate gas-liquid polytetrafluoroethylene (PTFE) membrane contactor to effectively enhance carbon dioxide absorption through aqueous amine solutions (monoethanolamide-MEA). In this study, a theoretical model was established and experimental work was performed to predict and to compare carbon dioxide absorption efficiency under concurrent- and countercurrent-flow operations for various MEA feed flow rates, inlet CO 2 concentrations, and channel design conditions. A Sherwood number's correlated expression was formulated, incorporating experimental data to estimate the mass transfer coefficient of the CO 2 absorption in MEA flowing through a PTFE membrane. Theoretical predictions were calculated and validated through experimental data for the augmented CO 2 absorption efficiency by inserting carbon-fiber spacers as an eddy promoter to reduce the concentration polarization effect. The study determined that a higher MEA feed rate, a lower feed CO 2 concentration, and wider carbon-fiber spacers resulted in a higher CO 2 absorption rate for concurrent- and countercurrent-flow operations. A maximum of 80% CO 2 absorption efficiency enhancement was found in the device by inserting carbon-fiber spacers, as compared to that in the empty channel device. The overall CO 2 absorption rate was higher for countercurrent operation than that for concurrent operation. We evaluated the effectiveness of power utilization in augmenting the CO 2 absorption rate by inserting carbon-fiber spacers in the MEA feed channel and concluded that the higher the flow rate, the lower the power utilization's effectiveness. Therefore, to increase the CO 2 absorption flux, widening carbon-fiber spacers was determined to be more effective than increasing the MEA feed flow rate.

Helicobacter pylori ( H. pylori ) infection leads to the massive apoptosis of the gastric epithelial cells, causing gastric ulcers, gastritis, and gastric adenocarcinoma. Autophagy is a cellular recycling process that plays important roles in cell death decisions and can protect cells by preventing apoptosis. Upon the induction of autophagy, the level of the autophagy substrate p62 is reduced and the autophagy-related ratio of microtubule-associated proteins 1A/1B light chain 3B (LC3B)-II/LC3B-I is heightened. AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) are involved in the regulation of autophagy. Astaxanthin (AST) is a potent anti-oxidant that plays anti-inflammatory and anti-cancer roles in various cells. In the present study, we examined whether AST inhibits H. pylori -induced apoptosis through AMPK-mediated autophagy in the human gastric epithelial cell line AGS (adenocarcinoma gastric) in vitro. In this study, H. pylori induced apoptosis. Compound C, an AMPK inhibitor, enhanced the H. pylori -induced apoptosis of AGS cells. In contrast, metformin, an AMPK activator, suppressed H. pylori -induced apoptosis, showing that AMPK activation inhibits H. pylori -induced apoptosis. AST inhibited H. pylori -induced apoptosis by increasing the phosphorylation of AMPK and decreasing the phosphorylation of RAC-alpha serine/threonine-protein kinase (Akt) and mTOR in H. pylori -stimulated cells. The number of LC3B puncta in H. pylori -stimulated cells increased with AST. These results suggest that AST suppresses the H. pylori -induced apoptosis of AGS cells by inducing autophagy through the activation of AMPK and the downregulation of its downstream target, mTOR. In conclusion, AST may inhibit gastric diseases associated with H. pylori infection by increasing autophagy through the activation of the AMPK pathway.

Helicobacter pylori (H. pylori) causes gastritis and gastric cancers. Oxidative stress is involved in the pathological mechanism of H. pylori -induced gastritis and gastric cancer induction. Therefore, reducing oxidative stress may be beneficial for preventing the development of H. pylori -associated gastric diseases. Nuclear factor erythroid-2-related factor 2 (Nrf2) is a crucial regulator for the expression of antioxidant enzyme heme oxygenase-1 (HO-1), which protects cells from oxidative injury. α-Lipoic acid (α-LA), a naturally occurring dithiol, shows antioxidant and anti-inflammatory effects in various cells. In the present study, we examined the mechanism by which α-LA activates the Nrf2/HO-1 pathway, suppresses the production of pro-inflammatory cytokine interleukine-8 (IL-8), and reduces reactive oxygen species (ROS) in H. pylori -infected AGS cells. α-LA increased the level of phosphorylated and nuclear-translocated Nrf2 by decreasing the amount of Nrf2 sequestered in the cytoplasm by complex formation with Kelch-like ECH1-associated protein 1 (KEAP 1). By using exogenous inhibitors targeting Nrf2 and HO-1, we showed that up-regulation of activated Nrf2 and of HO-1 results in the α-LA-induced suppression of interleukin 8 (IL-8) and ROS. Consumption of α-LA-rich foods may prevent the development of H. pylori -associated gastric diseases by decreasing ROS-mediated IL-8 expression in gastric epithelial cells.

Reactive oxygen species (ROS) contribute to the oncogenic phenotype of cancer cells by acting as signaling molecules for inducing proliferation. ROS are known to activate the epidermal growth factor receptor (EGFR), which causes the activation of the Ras/mitogen-activated protein kinases (MAPKs) pathway. The Ras-dependent pathway promotes the activation of nuclear factor-kappa-light-chain-enhancer of activated B cells (NF-κB), a transcriptional modulator of cyclooxygenase-2 (COX-2) that induces cell proliferation. Lycopene is a potent antioxidant carotenoid and is responsible for the red color of fruits and vegetables. This study aims to investigate whether lycopene inhibits proliferation and induces apoptosis in gastric cancer AGS cells by suppressing the EGFR/Ras/MAPK and NF-κB-COX-2 signaling axis. Lycopene decreased cell viability and increased apoptotic indices (DNA fragmentation, apoptosis inducing factor, cleavage of caspase-3 and caspase-9, Bax/Bcl-2 ratio). Lycopene reduced the level of intracellular and mitochondrial ROS and decreased the activation of the ROS-mediated EGFR/Ras/extracellular signal-regulated kinase (ERK) and p38 MAPK pathways, thus leading to attenuation of the DNA-binding activity of NF-κB p50/p50 and the level of COX-2 gene expression. These results show that lycopene-induced apoptosis and inhibition of proliferation occur via inhibition of ROS-activated EGFR/Ras/ERK and p38 MAPK pathways and NF-κB-mediated COX-2 gene expression in AGS cells. In conclusion, consumption of lycopene-enriched foods could decrease the incidence of gastric cancer.

Intracellular Ca 2+ homeostasis is commonly disrupted in acute pancreatitis. Sustained Ca 2+ release from internal stores in pancreatic acinar cells (PACs), mediated by inositol triphosphate receptor (IP3R) and the ryanodine receptor (RyR), plays a key role in the initiation and propagation of acute pancreatitis. Pancreatitis induced by cerulein, an analogue of cholecystokinin, causes premature activation of digestive enzymes and enhanced accumulation of cytokines and Ca 2+ in the pancreas and, as such, it is a good model of acute pancreatitis. High concentrations of the omega-3 fatty acid docosahexaenoic acid (DHA) inhibit inflammatory signaling pathways and cytokine expression in PACs treated with cerulein. In the present study, we determined the effect of DHA on key regulators of Ca 2+ signaling in cerulein-treated pancreatic acinar AR42 J cells. The results of RNA-Sequencing (RNA-Seq) analysis showed that cerulein up-regulates the expression of IP3R1 and RyR2 genes, and that pretreatment with DHA blocks these effects. The results of real-time PCR confirmed that DHA inhibits cerulein-induced IP3R1 and RyR2 gene expression, and demonstrated that DHA pre-treatment decreases the expression of the Relb gene, which encodes a component of the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) transcriptional activator complex, and the c-fos gene, which encodes a component of activator protein-1 (AP-1) transcriptional activator complex. Taken together, DHA inhibits mRNA expression of IP3R1, RyR2, Relb, and c-fos, which is related to Ca 2+ network in cerulein-stimulated PACs., Competing Interests: The authors declare no conflict of interest.

Generation of excess quantities of reactive oxygen species (ROS) caused by mitochondrial dysfunction facilitates rapid growth of pancreatic cancer cells. Elevated ROS levels in cancer cells cause an anti-apoptotic effect by activating survival signaling pathways, such as NF-κB and its target gene expression. Lycopene, a carotenoid found in tomatoes and a potent antioxidant, displays a protective effect against pancreatic cancer. The present study was designed to determine if lycopene induces apoptosis of pancreatic cancer PANC-1 cells by decreasing intracellular and mitochondrial ROS levels, and consequently suppressing NF-κB activation and expression of NF-κB target genes including cIAP1, cIAP2, and survivin. The results show that the lycopene decreased intracellular and mitochondrial ROS levels, mitochondrial function (determined by the mitochondrial membrane potential and oxygen consumption rate), NF-κB activity, and expression of NF-κB-dependent survival genes in PANC-1 cells. Lycopene reduced cell viability with increases in active caspase-3 and the Bax to Bcl-2 ratio in PANC-1 cells. These findings suggest that supplementation of lycopene could potentially reduce the incidence of pancreatic cancer.

The ω3-polyunsaturated fatty acid docosahexenoic acid (DHA) is known to induce apoptosis of cancer cells. In this study, DHA was shown to reduce viability of pancreatic cancer cells (PANC-1) by inducing DNA fragmentation, activating caspase-3, and increasing the ratio of Bax/Bcl-2. To determine the DHA mechanism of action, the impact of DHA on the activation of the key signaling proteins epidermal growth factor receptor (EGFR), signal transducer and activator of transcription factor 3 (STAT3), nuclear transcription factor-κB (NF-κB), and IκBα in PANC-1 cells was probed. The observed DHA suppression of NF-κB DNA-binding activity was found to result from reduced IκBα phosphorylation. The observed DHA-induced suppression of STAT3 activation was found to be the result of suppressed EGFR activation, which derives from the inhibitory effect of DHA on the integrity of localization of EGFR to cell membrane lipid rafts. Since the activation of STAT3 and NF-κB mediates the expression of survival genes cyclin D1 and survivin, DHA induced apoptosis by suppressing the STAT3/NF-κB-cyclin D1/survivin axis. These results support the proposal that DHA-induced apoptosis of pancreatic cells occurs via disruption of key pro-cell survival signaling pathways. We suggest that the consumption of DHA-enriched foods could decrease the incidence of pancreatic cancer.

Helicobacter pylori (H. pylori) infection leads to gastric inflammation, peptic ulcer and gastric carcinoma. H. pylori activates NADPH oxidase and increases reactive oxygen species (ROS), which induce NF-κB activation and IL-8 expression in gastric epithelial cells. Dysfunctional mitochondria trigger inflammatory cytokine production. Peroxisome proliferator-activated receptors-γ (PPAR-γ) regulate inflammatory response. Astaxanthin is a powerful antioxidant that protects cells against oxidative stress. The present study was aimed at determining whether astaxanthin inhibits H. pylori -induced mitochondrial dysfunction, NF-κB activation, and IL-8 expression via PPAR-γ activation in gastric epithelial cells. Gastric epithelial AGS cells were treated with astaxanthin, NADPH oxidase inhibitor apocynin and PPAR-γ antagonist GW9662, and infected with H. pylori. As a result, H. pylori caused an increase in intracellular and mitochondrial ROS, NF-κB activation and IL-8 expression, but decreased mitochondrial membrane potential and ATP level. Astaxanthin inhibited H. pylori -induced alterations (increased ROS, mitochondrial dysfunction, NF-κB activation, and IL-8 expression). Astaxanthin activated PPAR-γ and its target gene catalase in H. pylori -infected cells. Apocynin reduced ROS and inhibited IL-8 expression while astaxanthin did not affect NADPH oxidase activity. Inhibitory effects of astaxanthin on ROS levels and IL-8 expression were suppressed by addition of GW9662. In conclusion, astaxanthin inhibits H. pylori -induced mitochondrial dysfunction and ROS-mediated IL-8 expression by activating PPAR-γ and catalase in gastric epithelial cells. Astaxanthin may be beneficial for preventing oxidative stress-mediated gastric inflammation-associated H. pylori infection.

Alzheimer's disease (AD) is a fatal neurodegenerative disease. Brain amyloid-β deposition is a crucial feature of AD, causing neuronal cell death by inducing oxidative damage. Reactive oxygen species (ROS) activate NF-κB, which induces expression of Nucling. Nucling is a pro-apoptotic factor recruiting the apoptosome complex. Lycopene is an antioxidant protecting from oxidative stress-induced cell damage. We investigated whether lycopene inhibits amyloid-β-stimulated apoptosis through reducing ROS and inhibiting mitochondrial dysfunction and NF-κB-mediated Nucling expression in neuronal SH-SY5Y cells. We prepared cells transfected with siRNA for Nucling or nontargeting control siRNA to determine the role of Nucling in amyloid-β-induced apoptosis. The amyloid-β increased intracellular and mitochondrial ROS levels, apoptotic indices (p53, Bax/Bcl-2 ratio, caspase-3 cleavage), NF-kB activation and Nucling expression, while cell viability, mitochondrial membrane potential, and oxygen consumption rate decreased in SH-SY5Y cells. Lycopene inhibited these amyloid-β-induced alterations. However, amyloid-β did not induce apoptosis, determined by cell viability and apoptotic indices (p53, Bax/Bcl-2 ratio, caspase-3 cleavage), in the cells transfected with siRNA for Nucling. Lycopene inhibited apoptosis by reducing ROS, and by inhibiting mitochondrial dysfunction and NF-κB-target gene Nucling expression in neuronal cells. Lycopene may be beneficial for preventing oxidative stress-mediated neuronal death in patients with neurodegeneration., Competing Interests: The authors declare no conflicts of interest.

Oxidative stress is an important regulator in the pathogenesis of acute pancreatitis (AP). Reactive oxygen species induce activation of inflammatory cascades, inflammatory cell recruitment, and tissue damage. NF-κB regulates inflammatory cytokine gene expression, which induces an acute, edematous form of pancreatitis. Protein kinase C δ (PKCδ) activates NF-κB as shown in a mouse model of cerulein-induced AP. Docosahexaenoic acid (DHA), an ω-3 fatty acid, exerts anti-inflammatory and antioxidant effects in various cells and tissues. This study investigated whether DHA inhibits cerulein-induced AP in rats by assessing pancreatic edema, myeloperoxidase activity, levels of lipid peroxide and IL-6, activation of NF-κB and PKCδ, and by histologic observation. AP was induced by intraperitoneal injection (i.p.) of cerulein (50 μg/kg) every hour for 7 h. DHA (13 mg/kg) was administered i.p. for three days before AP induction. Pretreatment with DHA reduced cerulein-induced activation of NF-κB, PKCδ, and IL-6 in pancreatic tissues of rats. DHA suppressed pancreatic edema and decreased the abundance of lipid peroxide, myeloperoxidase activity, and inflammatory cell infiltration into the pancreatic tissues of cerulein-stimulated rats. Therefore, DHA may help prevent the development of pancreatitis by suppressing the activation of NF-κB and PKCδ, expression of IL-6, and oxidative damage to the pancreas., Competing Interests: The authors declare no conflicts of interest.