Effect of sodium nitroprusside on the microrheological properties of red blood cells in different media

Red blood cell(RBC)aggregation as well as their deformation significantly affects blood microrheology.These processes depend on various factors,one of which is concentration of the nitric oxide,one of the main signaling molecule in the bloodstream.The purpose of this study was to investigate the effect of nitric oxide on the microrheological properties of red blood cells(RBCs)in RBC samples of various media after the addition of nitric oxide donor sodium nitroprusside in vitro.Microrheological properties were measured using laser aggregometer and ektacytometer based on diffuse light scattering and diffraction of laser light on a suspension of RBCs,respectively.The study found that heparin-stabilized blood showed increased RBC aggregation and deformation with sodium nitroprusside concentrations of 100,and 200M,while EDTA-stabilized blood showed slightly decreased aggregation and unchanged deformation.With washed RBCs in dextran solution,the addition of sodium nitroprusside(in the concentrations of 100,and 200M)resulted in decreased aggregation and increased deformation.These-ndings aid in our understanding of nitric oxide's effect on RBC microrheological properties.

Inhibitory Effects of Sodium Ferulate on Proliferation of Rabbit Aortic Smooth Muscle Cells Induced by Oxidized LDL

The effects of sodium ferulate(SF), a water-soluble element of Chinese medicine Angelica sinensis diels, on cell-mediated oxidative modification of human low density lipoprotein(LDL) and proliferation of rabbit aortic smooth muscle cells(SMCs) were investigated. Using experimental models of proliferation of cultured rabbit aortic SMCs induced by oxidized LDL(ox-LDL), the extent of oxidation was determined by thiobarbituric acid reactive substances(TBARS) method, MTT colorimetry and 3H-thymidine(3H-TdR) incorporation were used to observe proliferation of SMCs. It showed that SF effectively inhibited cell-mediated oxidation induced by Cu2+ in a concentration-dependent manner. At the final concentration of 40, 80, 120 gmL-1, SF could significantly inhibit 3H-TdR incorporation and cell Proliferation in a dose-dependent manner. The results indicated that SF could, in vitro protect LDL against oxidative modification and inhibit the proliferation of SMC, which might be due to its free radical scavenging capacity.

Bone marrow-derived mesenchymal stem cells ameliorate sodium nitrite-induced hypoxic brain injury in a rat model

Sodium nitrite（Na NO2） is an inorganic salt used broadly in chemical industry. Na NO2 is highly reactive with hemoglobin causing hypoxia. Mesenchymal stem cells（MSCs） are capable of differentiating into a variety of tissue specific cells and MSC therapy is a potential method for improving brain functions. This work aims to investigate the possible therapeutic role of bone marrow-derived MSCs against Na NO2 induced hypoxic brain injury. Rats were divided into control group（treated for 3 or 6 weeks）, hypoxic（HP） group（subcutaneous injection of 35 mg/kg Na NO2 for 3 weeks to induce hypoxic brain injury）, HP recovery groups N-2 w R and N-3 w R（treated with the same dose of Na NO2 for 2 and 3 weeks respectively, followed by 4-week or 3-week self-recovery respectively）, and MSCs treated groups N-2 w SC and N-3 w SC（treated with the same dose of Na NO2 for 2 and 3 weeks respectively, followed by one injection of 2 × 106 MSCs via the tail vein in combination with 4 week self-recovery or intravenous injection of Na NO2 for 1 week in combination with 3 week self-recovery）. The levels of neurotransmitters（norepinephrine, dopamine, serotonin）, energy substances（adenosine monophosphate, adenosine diphosphate, adenosine triphosphate）, and oxidative stress markers（malondialdehyde, nitric oxide, 8-hydroxy-2′-deoxyguanosine, glutathione reduced form, and oxidized glutathione） in the frontal cortex and midbrain were measured using high performance liquid chromatography. At the same time, hematoxylin-eosin staining was performed to observe the pathological change of the injured brain tissue. Compared with HP group, pathological change of brain tissue was milder, the levels of malondialdehyde, nitric oxide, oxidized glutathione, 8-hydroxy-2′-deoxyguanosine, norepinephrine, serotonin, glutathione reduced form, and adenosine triphosphate in the frontal cortex and midbrain were significantly decreased, and glutathione reduced form/oxidized glutathione and adenosine monophosphate/adenosine triphosphate ratio were significantly increased in the MSCs treated groups. These findings suggest that bone marrow-derived MSCs exhibit neuroprotective effects against Na NO2-induced hypoxic brain injury through exerting anti-oxidative effects and providing energy to the brain.

Highly efficient solution-processed CZTSSe solar cells based on a convenient sodium-incorporated post-treatment method

In CZTSSe solar cells,a simple sodium-incorporation post-treatment method toward solution-processed Cu2Zn Sn S4precursor films is presented in this work.An ultrathin NaCl film is deposited on Cu2Zn Sn S4precursor films by spin-coating NaCl solution.In subsequent selenization process,the introduction of Na Cl is found to be benefacial for the formation of Cu2-xSe,which can further facilitate the element transportation,leading to dense and smooth CZTSSe films with large grains and less impurity Cu2Sn(S,Se)3phase.SIMS depth profiles confirm the gradient distribution of the sodium element in Na-doped absorbers.Photoluminescence spectra show that the introduction of appropriate sodium into the absorber can inhibit the band tail states.As high as 11.18% of power conversion efficiency(PCE)is achieved for the device treated with 5 mg mL^-1 NaCl solution,and an average efficiency of Na-doped devices is 10.71%,13%higher than that of the control groups(9.45%).Besides,the depletion width and the charge recombination lifetime can also have regular variation with sodium treatment.This work offers an easy modification method for high-quality Na-doped CZTSSe films and high-performance devices,in the meantime,it can also help to further understand the effects of sodium in CZTSSe solar cells.

The expression of glucose regulated protein-94 in colorectal carcinoma cells treated by sodium butyrate

The expression of glucose regulated protein 94 (GRP94)during the treatment of human colorectal carcinoma cell lineClone A cells with sodium butyrate was studied. Sodium butyrate (SB) can cause functional and morphological effects on Clone A cells including growth arrest at Go/G1 stage and cell differentiation as observed by morphological changes, MTT and flow cytometry assays, as well as reduced Grp94 gene expression as shown by Northern blot and Western blot assays. The possible mechanism of the correlation between Grp94 gene expression and tumor growth inhibition and cell differentiation is briefly discussed.

Effects of Sodium Salicylate on the Expression of HSP27 Protein during Oxidative Stress in Tissue-cultured Human Lens Epithelial Cells

The effects of sodium salicylate on the expression of heat shock protein 27 （HSP27） during oxidative stress in tissue-cultured human lens epithelial cells were investigated. Cultured human lens epithelial cells （HLB-3） were divided into 3 groups： control group （group A）, oxidation injury group （group B） and sodium salicylate group （group C）. Apoptosis of human lens epithelial cells cultured in vitro was induced in the presence of 150 μmol/L H2O2. Cells viability and the expression of HSP27 were analyzed. Viability of the cells was measured by methyl thiazole tetrazolium （MTT） chromatometry. The expression of HSP27 in HLB-3 cells was detected by using immunohistochemistry and image analysis system, Sodium salicylate could induce the expression of HSP27, and the cells viability in group C was significantly higher than in group B （0.2667±0.01414 vs 0.2150±0.01080, P=0.012〈0.05）. The average gray value of HSP27 in group B was less than that in group C （P=0.000〈0.05）. The increased expression of HSP27 by sodium salicylate might play an important role in the protection of hydrogen peroxide-induced injury of human lens epithelial cells, suggesting that sodium salicylate could suppress, at least in part, the apoptosis of human lens epithelial cells.

Calcitriol analog ZK191784 ameliorates acute and chronic dextran sodium sulfate-induced colitis by modulation of intestinal dendritic cell numbers and phenotype

AIM: To investigate the effects of ZK1916784, a low calcemic analog of calcitriol on intestinal inflammation. METHODS: Acute and chronic colitis was induced by dextran sodium sulfate (DSS) according to standard procedures. Mice were treated intraperitoneally with ZK1916784 or placebo and colonic inflammation was evaluated. Cytokine production by mesenterial lymph node (MLN) cells was measured by ELISA. Immunohistochemistry was performed to detect intestinal dendritic cells (DCs) within the colonic tissue, and the effect of the calcitriol analog on DCs was investigated. RESULTS: Treatment with ZK191784 resulted in significant amelioration of disease with a reduced histological score in acute and chronic intestinal inflammation. In animals with acute DSS colitis, down- regulation of colonic inflammation was associated with a dramatic reduction in the secretion of the proinflammatory cytokine interferon (IFN)-γ and a significant increase in intereleukin (IL)-10 by MLN cells. Similarly, in chronic colitis, IL-10 expression in colonic tissue increased 1.4-fold when mice were treated with ZK191784, whereas expression of the Th1-specific transcription factor T-beta decreased by 81.6%. Lower numbers of infiltrating activated CD11c+ DCs were found in the colon in ZK191784-treated mice with acute DSScolitis, and secretion of proinflammatory cytokines by primary mucosal DCs was inhibited in the presence of the calcitriol analog. CONCLUSION: The calcitriol analog ZK191784 demonstrated significant anti-inflammatory properties in experimental colitis that were at least partially mediated by the immunosuppressive effects of the derivate on mucosal DCs.

Simulation of thermal and sodium expansion stress in aluminum reduction cells

Two finite element(FE) models were built up for analysis of stress field in the lining of aluminum electrolysis cells.Distribution of sodium concentration in cathode carbon blocks was calculated by one FE model of a cathode block.Thermal stress field was calculated by the other slice model of the cell at the end of the heating-up.Then stresses coupling thermal and sodium expansion were considered after 30 d start-up.The results indicate that sodium penetrates to the bottom of the cathode block after 30 d start-up.The semi-graphitic carbon block has the largest stress at the thermal stage.After 30 d start-up the anthracitic carbon has the greatest sodium expansion stress and the graphitized carbon has the lowest sodium expansion stress.Sodium penetration can cause larger deformation and stress in the cathode carbon block than thermal expansion.

Effects of Mitogen-activated Protein Kinase Signal Pathway on Heat Shock Protein 27 Expression in Human Lens Epithelial Cells Exposed to Sodium Salicylate in vitro

The roles of mitogen-activated protein kinase （MAPK） signal pathway in sodium salieylate-induced expression of heat shock protein 27 （HSP27） in human lens epithelial cells （HLECs-B3） in vitro were investigated. HLECs-B3 were incubated in the fresh media containing sodium salicylate at different concentrations for different durations, and allowed to be recovered in fresh medium without sodium salicylate for different durations with or without pretreatment with p38MAPK inhibitor （SB203580）, ERK1/2 inhibitor （PD98059） and JNK/SAPK inhibitor （SP600125）. The expression of P38MAPK, ERK1/2, JNK/SAPK, phosphorylated P38MAPK, phosphorylated ERK1/2, phosphorylated JNK/SAPK and HSP27 was detected by Western blot. The expression of HSP27 mRNA and protein was detected by RT-PCR and immunohistochemistry respectively. It was found there was only weak expression of HSP27 in normal HLECs. The expression of HSP27 was not detectable in HLECs-B3 that were exposed to sodium salicylate （55 retool/L） for 1-5 h. It was indicated that recovery from sodium salicylate （〉35 mmol/L） significantly increased the synthesis of HSP27. The expression of HSP27 was up-regulated in HLECs-B3 under sodium salicylate recovery for 3 h, reached the peak level for 6 h, and returned to the level of control cells by 24 h. Activation of P38MAPK from sodium salicylate stimulation occurred at 30th rain, and increased significantly at 1st h, then declined and renamed to baseline level at 3rd h under sodium salicylate recovery. Activation of ERK1/2 occurred at 1st h and reached the peak level at 6th h under sodium salicylate recovery. However, JNK/SAPK was inactivated by sodium salicylate. The expression of HSP27 could be down-regulated with the pretreatment of SB203580 and PD98059 jointly. It is concluded that sodium salicylate can induce the expression of HSP27 in HLECs-B3. The effects are mediated, at least in part, through the activation of P38MAPK and ERK1/2 signaling pathway.

Anti-proliferation and apoptosis-inducing effects of sodium aescinate on retinoblastoma Y79 cells

AIM:To investigate the anti-proliferation and apoptosisinducing effects of sodium aescinate(SA)on retinoblastoma Y79 cells and its mechanism.METHODS:Y79 cells were cultured at different drug concentrations for different periods of time(24,48,and 72 h).The inhibitory effect of SA on proliferation of Y79 cells was detected by the cell counting kit-8(CCK-8)assay,and the morphology of Y79 cells in each group was observed under an inverted microscope.An IC50 of 48 h was selected for subsequent experiments.After pretreatment with SA for 24 and 48 h,cellular DNA distribution and apoptosis were detected by flow cytometry.Real-time qunatitative polymerase chain reaction(RT-qPCR)and Western blot were used to assess changes in related genes(CDK1,CyclinB1,Bax,Bcl-2,caspase-9,caspase-8,and caspase-3).RESULTS:SA inhibited proliferation and induced apoptosis of Y79 cells in a time-dependent and concentrationdependent manner.Following its intervention in the cell cycle pathway,SA can inhibit the expression of CDK1 and Cyclin B1 at the mRNA and protein levels,and block cells in the G2/M phase.In caspase-related apoptotic pathways,up-regulation of Bax and down-regulation of Bcl-2 caused caspase-9 to self-cleave and further activate caspase-3.What’s more,the caspase-8-mediated extrinsic apoptosis pathway was activated,and the activated caspase-8 was released into the cytoplasm to activate caspase-3,which as a member of the downstream apoptotic effect group,initiates a caspase-cascade reaction that induces cell apoptosis.CONCLUSION:SA inhibits the proliferation of Y79 cells by arresting the cell cycle at the G2/M phase,and induces apoptosis via the caspase-related apoptosis pathway,indicating that SA may have promising potential as a chemotherapeutic drug.

Inhibitory Effect of Diclofenac Sodium on the Proliferation of Rabbit Corneal Epithelial Cells in vitro

<Abstract>Purpose:To investigate the inhibitory effect of diclofenac sodium on rabbit corneal epithelial cells (RCECs) in vitro and explore its pharmacological mechanism. Methods: The fresh rabbit cornea was cultured to get the primary RCECs,and RCECs of passage 2 were used for the research. The cells were divided into experimental groups,the cells in which were incubated with different concentrations(18.18, 27.27, 36.36, 45.45, 54.55 μg/ml) of diclofenac sodium, and control group. The effect of diclofenac sodium on the proliferation of cells was measured by methyl thiazolyl thiazolium (MTT) assay 24, 48 and 72 h after incubation. While the RCECs were divided into experimental groups, the cells in which were incubated with 9 and 12.5 μg/ml diclofenac sodium, and control group. The cell cycle and apoptotic rate were observed by flow cytometer. Results:MTT assay showed that diclofenac sodium had obvious inhibitory effect on RCECs,and the inhibition rate was increasing along with the increase of the concentration of diclofenac sodium and the incubation time(P<0.05). Flow cytometer showed that after incubation with diclofenac sodium, the cells in G0/G1 phase were obviously increased, the apoptosis cusp and apoptotic rate were increased. Conclusion: Diclofenac sodium has obvious inhibitory effect on RCECs, which was dosage-dependent,and it may function by inducing cell apoptosis and ceasing cells cycles.

Sodium chloride methanol solution spin-coating process for bulk-heterojunction polymer solar cells

The sodium chloride methanol solution process is conducted on the conventional poly（3-hexylthiophene）（P3HT）/[6,6]-phenyl-C61-butyric acid methyl ester（PC_（61）BM） polymer bulk heterojunction solar cells. The device exhibits a power conversion efficiency of up to 3.36%, 18% higher than that of the device without the solution process. The measurements of the active layer by x-ray photoelectron spectroscopy（XPS）, atomic force microscopy（AFM）, and ultraviolet photoelectron spectroscopy（UPS） indicate a slight phase separation in the vertical direction and a sodium chloride distributed island-like interface between the active layer and the cathode. The capacitance–voltage（C–V） and impedance spectroscopy measurements prove that the sodium chloride methanol process can reduce the electron injection barrier and improve the interfacial contact of polymer solar cells. Therefore, this one-step solution process not only optimizes the phase separation in the active layers but also forms a cathode buffer layer, which can enhance the generation, transport, and collection of photogenerated charge carriers in the device simultaneously. This work indicates that the inexpensive and non-toxic sodium chloride methanol solution process is an efficient one-step method for the low cost manufacturing of polymer solar cells.

Increasein the Activity of Human Breast CancerCells to Induce Cytotoxic T Lymphocytes by Sodium Phenylacetate

The effects of differentiation inducer sodium phenylacetate on antigen expression of human breas cancer MDA-453 cells and their activity to induce allospecific cytotoxic T lymphocytes (CTL) in peripheral blood mononuclear cells (PBMC) were investigated. The results showed that sodium phenylacetate could the expression of HLA-A2 molecules, intercellular adhesion molecule-1 (ICAW-1) and protein HER-2/neu on the surface of MDA-453 cells. In mixed allogenic PBMC/MDA-453 cell (shared the same HLA-A2 locus) culture in vitro, MDA-453 cells could stimulate PBMC growth in the presence of low dose of interleukin-2 (IL-2 ), but sodium phenylacetate-treated MDA-453 cells were more potent for stimulating PBMC growth than the untreated cells. PBMC obtained from frow culture at 7th day could kill MDA-453 cells. The cytotoxicity of PBMC obtained form the culture at 21st day was restricted to MDA-453 cells (PBMC could hardly kill K562 and Raji cells), so the PBMC at this time could be called allospecific CTL. Sodium phenylacetate-treated MDA-453 cells were more potent for inducing allospecific CTL than the untreated cells in mixed allogenic PBMC/MDA-453 cell culture. In summary, sodium phenylacetate could increase the activity of breast cancer MDA-453 cells to induce allospecific CTL with a corresponding effect on antigen expression.

Possible Role of Mast Cells and Neuropeptides in the Recovery Process of Dextran Sulfate Sodium-induced Colitis in Rats

Objective To clarify the role of mast cells and neuropeptides substance P （SP）, somatostatin （SS）, and vasoactive intestinal peptide （VIP） in dextran sulfate sodium （DSS）-induced colitis in rats. Methods Experimental colitis was induced in Sprague-Dawley rats （180-200 g, n=20） by oral in- gestion of 4% （w/v） DSS in drinking water for 7 days. Control rats （n=5） drank water and were sacrificed on day 0. Mast cell number, histamine levels in whole blood and tissue, tissue levels of SP, SS and, VIP in the dis- tal colon of the rats were measured on day 8, day 13, and day 18 of experimentation. Results Oral administration of 4% DSS solution for 7 days resulted in surface epithelial loss and crypt loss in the distal colon. Mast cell count increased on day 8 （1.75±1.09/mm vs. 0.38±0.24/mm, P〈0.05） and day 13 （1.55±1.01/mm vs. 0.38±0.24/mm, P〈0.05） after DSS treatment. Whole blood his- tamine levels were increased on day 8 （266.93±35.62 ng/mL vs. 76.87±32.28 ng/mL, P〈0.01） and gradu- ally decreased by clay 13 and day 18 after DSS treatment. Histamine levels in the distal colon were decreased on day 8 （1.77±0.65 ng/mg vs. 3.06±0.87 ng/mg, P〈0.05） and recovered to control levels by day 13 after DSS treatment. SP level in the distal colon gradually increased and were raised significantly by day 13 （8777.14±3056.14 pg/mL vs. 4739.66±3299.81 pg/mL, P〈0.05） after DSS treatment. SS and VIP levels in the distal colon were not changed. Conclusions Mast cell degranulation followed by histamine release may play an important role in the pathogenesis of colitis induced by DSS. SP may be a significant substance in the progression of inflamma- tion and the recovery process of DSS-induced colitis.

The Effect of Sodium Nitrite on Induction of Apoptosis in Human Gastric Adenocarcinoma Epithelia (AGS) Cells

To examine the cytocidal effect of sodium nitrite on the cancer cell, we subjected human gastric adenocarcinoma epithelia (AGS) cells to various experimentation following exposure to sodium nitrite, and measured the resulting changes in the levels of cell death, lactate dehydrogenase (LDH) release, and caspase-3, -6, -8, and -9 activities. Our data revealed that, in AGS cells, treatment with ≥6.25 mM sodium nitrite for 8 h resulted in an obvious increase in cell death. LDH release was also markedly increased following sodium nitrite treatment, but at a concentration of ≥6.25 mM for 24 h. This increasing trend showed a positive correlation (r = 0.9564, P < 0.05). In addition, we detected pronounced increases in caspase activities with various concentrations of sodium nitrite: caspase-3 at ≥25 mM for 1 h, ≥12.5 mM for 3 h and 6 h;caspase-9 at 50 mM for 1 h and 3 h, and ≥6.25 mM for 6 h;and caspase-6 at 50 mM for 1 h and 3 h. We did not however, detect any observable increase in the activity of caspase-8 following sodium nitrite treatment at any concentration or for any duration of treatment in this study. This data demonstrates that, in AGS cells, higher concentrations or longer durations of treatment with sodium nitrite could exhibit a cytocidal effect, and that sodium nitrite could induce apoptosis via activation of the caspase-9, caspase-3 cascade (intrinsic pathway) and caspase-6.

Effects of Nano-sustained Release Sodium Butyrate on Growth and Intestinal Cell Proliferation of Grass Carps

Taking grass carps with the initial weight of about 20g as the research object,the basic feeds of grass carps were added with0.0%,0.1%,0.3%,0.6%,0.8%,and 1% of nano-sustained release sodium butyrate to prepare 6 types of experimental feeds with equal nitrogen and energy.The effects of different concentrations of nano-sustained release sodium butyrate were surveyed on growth and intestinal cell proliferation of grass carps.The experiment was carried out in cages with 50 carps per cage,and each treatment was repeated 3 times for60 days.Experimental results indicated that the addition of nano-sustained release sodium butyrate significantly promoted the growth of grass carps and significantly increased the ratio of intestinal villus to crypt depth.When the addition of nano-sustained release sodium butyrate was0.6%,the weight increase rate,specific growth rate,fullness and intestinal villus height of grass carps were the highest,which was significantly higher than that of the control group(P < 0.05).The study results indicated that addition of appropriate amount of nano-sustained release sodium butyrate can promote the growth of grass carps through increasing the intestinal villus height,and the suitable addition dosage was0.6%.

Rechargeable Na-MnO_(2) battery with modified cell chemistry

High voltage,high energy density,nominal cycle life,and low cost are the most critical requirements of rechargeable batteries for their widespread energy storage applications in electric vehicles and renewable energy technologies.Na-MnO_(2) battery could be a low-cost contender,but it suffers extensively from its low cell voltage and poor rechargeability.In this study,we modified the conventional cell structure of Na-MnO_(2) battery and established altered cell chemistry through a hybrid electrochemical process consisting of Na striping/plating at the anode and Zn^(2+) insertion/de-insertion along with MnO_(2) dissolution/deposition at the cathode.After the modification,Na-MnO_(2) battery exhibits a discharge capacity of 267.10 mA h/g and a cell voltage of 3.30 V(vs.Na/Na^(+)),resulting in a high specific energy density of 881.43 Wh/kg.After 300 cycles,the battery retains 98% of its first-cycle discharge capacity with100% coulombic efficiency.Besides,Na metal-free battery assembled using sodium biphenyl as a safer anode also delivers an excellent energy density of 810.0 Wh/kg.This work could provide a feasible method to develop an advanced Na-MnO_(2) battery for real-time energy storage applications.

Observations on the Function of Mucous Cells in the Epidermis of the Cat-fish Clarias batrachus Exposed to Sodium Dodecyl Sulfate

Response of mucous cells, in the epidermis of the catfish Clarias batrachus, to a sublethal concentration of sodium dodecyl sulfate was studied and correlated with the alteration in the status of their secretory activity after different durations of the treatment. At 4h, 8h, 24h,48h and 72h of the detergent treatment, most mucous cells attained voluminous dimensions and appeared closely approximating to or even overlapping the adjacent ones. At 12h, 36h, and 60h, in contrast, the mucous cells appeared small and slender, and seemed to be located at greater intervals. These changes in dimensions were responsible for the apparent increase or decrease in the density of mucous cells after different durations of detergent treatment. Statistically, however, no significant change was observed in the total number of the mucous cells throughout the experiment.The mucous cells appeared enlarged towards the end of the experiment signifying increased mucus production. This is considered as an adaptation, for protection, assisting the fish to adjust to the changed environment.A shift in the histochemical nature of the secretory contents at the middle and basal parts of the mucous cells, from a mixture of neutral and acid glycoproteins to neutral glycoproteins, during the early stages of the treatment suggests that acid moities could not simultaneously be synthesized as an immediate response to enhanced mucous secretion. The apical parts of the mucous cells, however, showed no histochemical change throughout the experiment.

Combinatorial effect of diclofenac with piperine and D-limonene on inducing apoptosis and cell cycle arrest of breast cancer cells

Objective:To investigate the potential synergistic activity of diclofenac with piperine and D-limonene in inducing apoptosis and cell cycle arrest in breast cancer MCF-7 cells.Methods:Molecular docking study was conducted to evaluate the binding affinity of diclofenac with piperine and D-limonene against p53,Bax,and Bcl-2.The MTT assay was used to determine IC50,and the Chou-Talay method was used to determine the synergistic concentration of the combination treatment of diclofenac plus piperine and diclofenac plus D-limonene.Apoptosis detection,cell cycle arrest,reactive oxygen species production,and mitochondrial membrane potential were also investigated.Results:Diclofenac,piperine,and D-limonene showed potent binding affinity for p53,Bax,and Bcl-2.Diclofenac plus piperine and diclofenac plus D-limonene enhanced the formation of reactive oxygen species,which also had an effect on the mitochondrial membrane’s integrity and caused DNA fragmentation.Diclofenac plus piperine and diclofenac plus D-limonene arrested the cells in the sub-G0phase while drastically lowering the percentage of cells in the G2/M phase.Furthermore,the elevated apoptosis in the combined therapy was confirmed by annexin V/propidium iodide staining.Conclusions:The combined therapy prominently enhanced the antiproliferative and apoptotic effects on MCF-7 cells compared with treatment with diclofenac,piperine,and D-limonene alone.

Sodium Diffuses from Glass Substrates through P1 Lines and Passivates Defects in Perovskite Solar Modules

Most thin-film photovoltaic modules are constructed on soda-lime glass(SLG)substrates containing alkali oxides,such as Na_(2)O.Na may diffuse from SLG into a module's active layers through P1 lines,an area between a module's constituent cells where the substrate-side charge transport layer(CTL)is in direct contact with SLG.Na diffusion from SLG is known to cause several important effects inⅡ-Ⅵand chalcogenide solar modules,but it has not been studied in perovskite solar modules(PSMs).In this work,we use complementary microscopy and spectroscopy techniques to show that Na diffusion occurs in the fabrication process of PSMs.Na diffuses vertically inside P1 lines and then laterally from P1 lines into the active area for up to 360 pm.We propose that this process is driven by the high temperatures the devices are exposed to during CTL and perovskite annealing.The diffused Na preferentially binds with Br,forming Br-poor,l-rich perovskite and a species rich in Na and Br(Na-Br)close to P1 lines.Na-Br passivates defect sites,reducing non-radiative recombination in the perovskite and boosting its luminescence by up to 5×.Na-Br is observed to be stable after 12 weeks of device storage,suggesting long-lasting effects of Na diffusion.Our results not only point to a potential avenue to increase PSM performance but also highlight the possibility of unabated Na diffusion throughout a module's lifetime,especially if accelerated by the electric field and elevated temperatures achievable during device operation.