[Effect of Baicalin on Pyroptosis of Diffuse Large B-Cell Lymphoma Cell Lines DB and Its Mechanism].

OBJECTIVE: To investigate the effect of Baicalin on the proliferation and pyroptosis of diffuse large B-cell lymphoma cell line DB and its mechanism. METHODS: DB cells were treated with baicalin at different concentrations (0, 5, 10, 20, 40 µmol/L). Cell proliferation was detected by CCK-8 assay and half maximal inhibitory concentration (IC50) was calculated. The morphology of pyroptosis was observed under an inverted microscope, the integrity of the cell membrane was verified by LDH content release assay, and the expressions of pyroptosis-related mRNA and protein (NLRP3, GSDMD, GSDME, N-GSDMD, N-GSDME) were detected by real-time fluorescence quantitative PCR and Western blot. In order to further clarify the relationship between baicalin-induced pyroptosis and ROS production in DB cells, DB cells were divided into control group, baicalin group, NAC group and NAC combined with baicalin group. DB cells in the NAC group were pretreated with ROS inhibitor N-acetylcysteine (NAC) 2 mmol/L for 2 h. Baicalin was added to the combined treatment group after pretreatment, and the content of reactive oxygen species (ROS) in the cells was detected by DCFH-DA method after 48 hours of culture. RESULTS: Baicalin inhibited the proliferation of DB cells in a dose-dependent manner (r=-0.99), and the IC50 was 20.56 µmol/L at 48 h. The morphological changes of pyroptosis in DB cells were observed under inverted microscope. Compared with the control group, the release of LDH in the baicalin group was significantly increased (P<0.01), indicating the loss of cell membrane integrity. Baicalin dose-dependently increased the expression levels of NLRP3, N-GSDMD, and N-GSDME mRNA and protein in the pyroptosis pathway (P<0.05). Compared with the control group, the level of ROS in the baicalin group was significantly increased (P<0.05), and the content of ROS in the NAC group was significantly decreased (P<0.05). Compared with the NAC group, the content of ROS in the NAC + baicalin group was increased. Baicalin significantly attenuated the inhibitory effect of NAC on ROS production (P<0.05). Similarly, Western blot results showed that compared with the control group, the expression levels of pyroptosis-related proteins was increased in the baicalin group (P<0.05). NAC inhibited the expression of NLRP3 and reduced the cleavage of N-GSDMD and N-GSDME (P<0.05). Compared with the NAC group, the NAC + baicalin group had significantly increased expression of pyroptosis-related proteins. These results indicate that baicalin can effectively induce pyroptosis in DB cells and reverse the inhibitory effect of NAC on ROS production. CONCLUSION: Baicalin can inhibit the proliferation of DLBCL cell line DB, and its mechanism may be through regulating ROS production to affect the pyroptosis pathway.

[Regulation of Baicalin on Growth of Extranodal NK/T Cell Lymphoma Cells through FOXO3/CCL22 Signaling Pathway].

OBJECTIVE: To investigate the effect of baicalin on the growth of extranodal NK/T cell lymphoma (ENKTCL) cells and its related mechanism. METHODS: Normal NK cells and human ENKTCL cells lines SNK-6 and YTS were cultured, then SNK-6 and YTS cells were treated with 5, 10, 20 µmol/L baicalin and set control. Cell proliferation and apoptosis was detected by Edu method and FCM method, respectively, and expressions of BCL-2, Bax, FOXO3 and CCL22 proteins were detected by Western blot. Interference plasmids were designed and synthesized. FOXO3 siRNA interference plasmids and CCL22 pcDNA overexpression plasmids were transfected with PEI transfection reagent. Furthermore, animal models were established for validation. RESULTS: In control group and 5, 10, 20 µmol/L baicalin group, the proliferation rate of SNK-6 cells was (56.17±2.96)%, (51.92±4.63)%, (36.42±1.58)%, and (14.60±2.81)%, respectively, while that of YTS cells was (58.85±2.98)%, (51.38±1.32)%, (34.75±1.09)%, and (15.45±1.10)%, respectively. In control group and 5, 10, 20 µmol/L baicalin group, the apoptosis rate of SNK-6 cells was (5.93±0.74)%, (11.78±0.34)%, (28.46±0.44)%, and (32.40±0.37)%, respectively, while that of YTS cells was (7.93±0.69)%, (16.29±1.35)%, (33.91±1.56)%, and (36.27±1.06)%, respectively. Compared with control group, the expression of BCL-2 protein both in SNK-6 and YTS cells decreased significantly (P<0.001), and the expression of Bax protein increased in SNK-6 cells only when the concentration of baicalin was 20 µmol/L (P<0.001), while that in YTS cells increased in all three concentrations(5, 10, 20 µmol/L) of baicalin (P<0.001). The expression of FOXO3 protein decreased while CCL22 protein increased in ENKTCL cell lines compared with human NK cells (P<0.001), but the expression of FOXO3 protein increased (P<0.01) and CCL22 protein decreased after baicalin treatment (P<0.001). Animal experiments showed that baicalin treatment could inhibit tumor growth. The expression of CCL22 protein in ENKTCL tissue of nude mice treated with baicalin decreased compared with control group (P<0.01), while the FOXO3 protein increased (P<0.05). In addition, FOXO3 silencing resulted in the decrease of FOXO3 protein expression and increase of CCL22 protein expression (P<0.01, P<0.001). CONCLUSION: Baicalin can inhibit proliferation and promote apoptosis of ENKTCL cell lines SNK-6 and YTS, up-regulate the expression of Bax protein, down-regulate the expression of BCL-2 protein, and down-regulate the expression of CCL22 protein mediated by FOXO3. Animal experiment shown that the baicalin can inhibit tumor growth. Baicalin can inhibit the growth and induce apoptosis of ENKTCL cells through FOXO3/CCL22 signaling pathway.

Effects of driving behavior on real-world emissions of particulate matter, gaseous pollutants and particle-bound PAHs for diesel trucks.

This study employed a portable emissions measurement system to investigate the effects of vehicle attributes, driving behavior, and road grade on real-world emissions of particulate matter (PM), regulated gaseous pollutants, and particle-bound polycyclic aromatic hydrocarbons (PAHs) for old-model diesel trucks (model year 1995-2006, 6.7-35.0 metric ton) with little to no tailpipe emission control. The rated power of engines was a major determinant of the distance-specific emission factors of PM, particle-bound PAHs, and most gaseous pollutants. However, the engine size was unrelated to the total hydrocarbon emission factor and the benzo[a]pyrene equivalent (BaPeq) emission factor of PAHs. Aggressive (AG) and normal (NR) driving behaviors were quantitatively defined with a relative positive acceleration. The emission factors of PM, CO2, and THC were significantly different (p < 0.05) between the AG and NR driving modes. AG driving caused an average increase in emissions of PM, CO2, NOx, and particle-bound PAHs by 122%, 56%, 15%, and 128%, respectively, compared to the respective emissions under the NR mode. The BaPeq emission factor of PAHs in the AG mode was more than 10 times that in the NR mode. The road gradient (ranging from -9.3% to 9.0% over the test route) had significant impacts on the emissions of PM, CO2, and NOx. PM, CO2, and NOx emission factors increased by 109%, 168%, and 160%, respectively, in the >6% grade bin and decreased by 95%, 91%, and 90%, respectively, in the equivalent negative-grade bin, implying that the decrease in emissions on negative road slopes may not compensate for the increase in emissions on the equivalent positive road slopes despite the road slope being compensated. The findings of this study will be valuable for developing air quality management strategies and furthering scientific knowledge on the complex interplay of different variables that affect real-world emissions of on-road vehicles.

Adsorption of Cadmium Ions from an Aqueous Solution on a Highly Stable Dopamine-Modified Magnetic Nano-Adsorbent.

Magnetic nanomaterials were functionalized with dopamine hydrochloride as the functional reagent to afford a core-shell-type Fe3O4 modified with polydopamine (Fe3O4@PDA) composite, which was used for the adsorption of cadmium ions from an aqueous solution. In addition, the effects of environmental factors on the adsorption capacity were investigated. Furthermore, the adsorption kinetics, isotherm, and thermodynamics of the adsorbents were discussed. Results revealed that the adsorption of cadmium by Fe3O4@PDA reaches equilibrium within 120 min, and kinetic fitting data are consistent with the pseudo-second-order kinetics (R2 > 0.999). The adsorption isotherm of Cd2+ on Fe3O4@PDA was in agreement with the Freundlich model, with the maximum adsorption capacity of 21.58 mg/g. The thermodynamic parameters revealed that adsorption is inherently endothermic and spontaneous. Results obtained from the adsorption-desorption cycles revealed that Fe3O4@PDA exhibits ultra-high adsorption stability and reusability. Furthermore, the adsorbents were easily separated from water under an enhanced external magnetic field after adsorption due to the introduction of an iron-based core. Hence, this study demonstrates a promising magnetic nano-adsorbent for the effective removal of cadmium from cadmium-containing wastewater.

Combination of S-1 and gefitinib increases the sensitivity to radiotherapy in lung cancer cells.

OBJECTIVE: To investigate the potential radiosensitization of S-1 and gefitinib in human non-small cell lung cancer (NSCLC) in vitro and in vivo. METHODS: The impact of radiation, 5-fluorouracil (5-Fu), and gefitinib on the proliferation and apoptosis of human NSCLC A549, H1299, H1975, and HCC827 cells was examined by MTT and flow cytometry. The effect of radiation, 5-Fu, and gefitinib on the clonogenicity of H1975 and HCC827 cells was determined by colony formation assay. The effect of radiation, 5-fluorouracil (5-Fu), and gefitinib on the EGFR, AKT, and ERK1/2 activation in H1975 cells was determined by Western blot. The therapeutic efficacy of radiation, S-1, and gefitinib in the growth of implanted H1975 tumors and the AKT activation in the tumors were examined in vivo and immunohistochemistry, respectively. RESULTS: Combination of radiation, 5-Fu, and gefitinib significantly inhibited the proliferation of H1975 cells and triggered their apoptosis, but not other NSCLC cells tested. The combination therapy significantly mitigated the clonogenicity and attenuated the activation of EGFR and AKT signaling in H1975 cells. Furthermore, combination of S-1, gefitinib, and radiation significantly inhibited the growth of implanted H1975 tumors in mice and remarkably reduced the AKT phosphorylation in the tumors. CONCLUSIONS: Our data indicated that combination of S-1 and gefitinib significantly increased radiosensitivity of H1975 cells. The triple combination therapies may benefit patients with the EGFR T790M mutant NSCLC.

[Arsenic removal by coagulation process and the field expanding experiments for Yangzonghai Lake].

Yangzonghai Lake is the third largest plateau lake in Yunnan province. In June 2008, arsenic contamination was detected in Yangzonghai Lake and the water quality worsens dramatically from standard grade II to worse than grade V. Since Yongzonghai Lake is so large with the area of 31 km2 and the storage capacity of 6.04 x 10(8) m3, those pretreatment operations of the traditional arsenic removal methods, such as pre oxidation, adjusting pH value, are not applicable. In this study, a facile remediation strategy for arsenic removal by coagulation process, in which ferric chloride was directly sprayed into the contaminated water without any pretreatment, was reported. The results showed that the arsenic removal percentage was up to 95.1%-96.7% for 50 L raw water with reagent dosage of 1.62-3.20 mg x L(-1). Furthermore, the pH value of the lake kept constant in the coagulation process, which was beneficial for fish survival. Re-dissolved arsenic from precipitation was not detected in 954 days. The strategy of ferric chloride coagulation were applied to field experiments for lake water with volumes of 1 x 10(4) m3 and 25 x 10(4) m3, in which arsenic was also removed effectively. The reported strategy was of great advantage for simple operation, low cost and ecological safety, therefore it provides a representative example for arsenic contamination treatment of large lake.

[Mechanism of gold solid extraction from aurocyanide solution using D3520 resin impregnated with TRPO].

Trialkyphosphine oxides (TRPO) was successfully used for the impregnation of D3520 resin to prepare an extractant-impregnated resin (EIR). Solid extraction of Au(I) from alkaline cyanide solution was studied using this extractant-impregnated resin (EIR), with addition of cetyltrimethylammonium bromide (CTMAB), directly into the aurous aqueous phase in advance. The mechanism of solid extraction was further investigated by means of FTIR, XPS and SEM. The column separation studies have shown that cationic surfactant CTMAB played a key role in the solid phase extraction, and the resin containing TRPO were effective for the extraction of gold when the molar ratio of CTMAB: Au( I ) reached 1:1. FTIR spectroscopy of gold loaded EIR showed that the frequency of C[triple bond]N stretching vibration was at 2144 cm(-1), and the frequency of P=O stretching vibration shifted to lower frequency from 1153 to 1150 cm(-1). The XPS spectrum of N(1s), Au(4f7/2) and Au(4f5/2) sugges- ted that the coordination environment of gold did not change before and after extraction, and gold was still as the form of Au (CN)2(-) anion exiting in the loaded resin; O(1s) spectrum showed that the chemically combined water significantly increased after solid extraction from 30.74% to 42.34%; Comparing to the P(2p) spectrum before and after extraction, the binding energy increased from 132. 15 to 132. 45 eV, indicating there maybe existing hydrogen-bond interaction between P=O and water molecule, such as P=O...H-O-H. The above results obtained established that in the solid extraction process, the hydrophobic ion association [CTMA+ x Au(CN)] diffused from the bulk solution into the pores of the EIR, and then be solvated by TRPO adsorbed in the pores through hydrogen bonding bridged by the water molecules.

Features of left ventricular hypertrophy in patients with metabolic syndrome with or without comparable blood pressure: a meta-analysis.

The prevalence of metabolic syndrome (MS) has been on the rise over the past few decades, and this is associated with an increased incidence of target organ damage such as left ventricular hypertrophy (LVH). This meta-analysis aims to evaluate the features of LVH in MS patients with or without high blood pressure (BP). PubMed, Cochrane Library, Embase, Science Citation Index, and China Biology Medicine Disc, WanFang data, China National Knowledge Infrastructure database, and VIP were searched. Cross-sectional studies which directly compared LVH in hypertensive patients with MS and those with hypertension alone were identified. The following parameters were analyzed: systolic blood pressure (SBP), diastolic blood pressure (DBP), left ventricular mass (LVM), left ventricular mass index (LVMI), left ventricular mass/height(2.7) (LVM/h(2.7)), interventricular septum thickness (IVSt), left ventricular end-diastolic diameter (LVEDd), left ventricular posterior wall (LVPW), ratio of early to late diastolic peak flow velocity (E/A), and relative wall thickness (RWT). Data were extracted and analyzed by Cochrane Collaboration's RevMan 5.0 software. 14 studies involving 5,994 patients were included. In four studies, MS patients with comparable level of BP had higher SBP (mmHg) [Mean Difference (MD) = 2.28, 95 % confidence intervals (CI): -0.58 to 5.13], DBP (mmHg) (MD = 1.32, 95 % CI: -0.23 to 2.87), LVM (g) (MD = 42.10, 95 % CI: 6.92-77.28), LVMI (g/m(2)) (MD = 8.93, 95 % CI: 5.29-12.57), LVM/h(2.7) (g/m(2.7)) (MD = 5.40, 95 % CI: 2.51-8.29), IVSt (mm) (MD = 0.49, 95 % CI: 0.28-0.71), LVEDd (mm) (MD = 1.04, 95 % CI: -1.10 to 3.18), LVPW (mm) (MD = 0.75, 95 % CI: 0.13-1.37), RWT (MD = 0.06, 95 % CI: -0.00 to 0.12), and lower E/A (MD = -0.08, 95 % CI: -0.18 to 0.02) when compared to the patients with hypertension alone. In other ten studies, the hypertensive patients with MS exhibited higher levels of SBP (mmHg) (MD = 4.67, 95 % CI: 2.72-6.62), DBP (mmHg) (MD = 2.03,95 % CI: 1.40-2.65), LVM (g) (MD = 24.79, 95 % CI: 20.21-29.36), LVMI(g/m(2)) (MD = 9.22, 95 % CI: 2.81-15.64), LVM/h(2.7) (g/m(2.7)) (MD = 5.97, 95 % CI: 4.14-7.80), IVSt (mm) (MD = 0.63, 95 % CI: 0.58-0.69), LVEDd (mm) (MD = 1.11, 95 % CI: 0.42-1.80), LVPW (mm) (MD = 0.63, 95 % CI: 0.31-0.94), RWT (MD = 0.02, 95 % CI: 0.01-0.03), as compared to patients with hypertension alone (P < 0.05). In addition, the MS patients combining with hypertension showed a lower E/A (MD = -0.07, 95 % CI: -0.10 to -0.04) when compared to those with hypertension alone. This study suggests that MS plays an important role in the development of LVH. MS seems to amplify hypertension-related cardiac changes. Furthermore, MS combining with higher level of BP will aggravate LVH and damage the diastolic function of left ventricle.