Acid-induced tubular g-C3N4 for the selective generation of singlet oxygen by energy transfer: Implications for the photocatalytic degradation of parabens in real water environments.

Parabens are widely present in aquatic environments and pose potential health risk. Although great progress has been made in the field of the photocatalytic degradation of parabens, the powerful Coulomb interactions between electrons and holes are the major limitations to photocatalytic performance. Hence, acid-induced tubular g-C3N4 (AcTCN) was prepared and applied for the removal of parabens from a real water environment. AcTCN not only increased the specific surface area and light absorption capacity, but also selectively generated 1O2 via an energy transfer-mediated oxygen activation pathway. The 1O2 yield of AcTCN was 11.8 times higher than that of g-C3N4. AcTCN exhibited remarkable removal efficiencies for parabens depending on the length of the alkyl group. Furthermore, the rate constants (k values) of parabens in ultrapure water were higher than those in tap and river water because of the presence of organic and inorganic species in real water environments. Two possible pathways for the photocatalytic degradation of parabens are proposed based on the identification of intermediates and theoretical calculations. In summary, this study offers theoretical support for the efficient enhancement of the photocatalytic performance of g-C3N4 for the removal of parabens in real water environments.

Solar-induced efficient propylparaben photodegradation by nitrogen vacancy engineered reticulate g-C3N4: Morphology, activity and mechanism.

Propylparaben (PrP) has attracted extensive concerns due to its wide occurrence in wastewater and potential health risk. Herein, nitrogen vacancy engineered reticulate g-C3N4 (Nv-RCN) was successfully synthesized for the photodegradation of PrP. Nv-RCN exhibited larger specific surface area, greater light absorption ability, higher transfer and separation efficiency of charge carriers in comparison with bulk g-C3N4 (CN). According to the characterization results and DFT calculation, nitrogen vacancy could capture electrons and facilitate oxygen adsorption. The Nv-RCN exhibited an outstanding PrP removal efficiency of 94.3 %, and the corresponding apparent rate constant of Nv-RCN was 3.37 times higher than that of CN. High O2 concentration (8 mg/L) and low pH value (pH = 3) promoted PrP photodegradation based on Box-Behnken Design. The O2- was the major radical during PCOP of Nv-RCN, and could oxidize PrP by decarbonylation and dealkylation. This study provided new insights to the improvement of photodegradation performance of g-C3N4 for parabens removal and related environmental remediation.

Qualitative and quantitative detection and identification of two benzodiazepines based on SERS and convolutional neural network technology.

Drug abuse is a global social issue of concern. As the drug market expands, there is an urgent need for technological methods to rapidly detect drug abuse to meet the needs of different situations. Here, we present a strategy for the rapid identification of benzodiazepines (midazolam and diazepam) using surface-enhanced Raman scattering (SERS) combined with neural networks (CNN). The method uses a self-assembled silver nanoparticle paper-based SERS substrate for detection. Then, a SERS spectrum intelligent recognition model based on deep learning technology was constructed to realize the rapid and sensitive distinction between the two drugs. In this work, a total of 560 SERS spectra were collected, and the qualitative and quantitative identification of the two drugs in water and a beverage (Sprite) was realized by a trained convolutional neural network (CNN). The predicted concentrations for each scenario could reach 0.1-50 ppm (midazolam in water), 0.5-50 ppm (midazolam in water and diazepam in Sprite), and 5-150 ppm (diazepam in Sprite), with a strong coefficient of determination (R2) larger than 0.9662. The advantage of this method is that the neural network can extract data features from the entire SERS spectrum, which makes up for information loss when manually identifying the spectrum and selecting a limited number of characteristic peaks. This work clearly clarifies that the combination of SERS and deep learning technology has become an inevitable development trend, and also demonstrates the great potential of this strategy in the practical application of SERS.

Incorporation of gelatin improves toughness of collagen films with a homo-hierarchical structure.

In this study, gelatin (type A and type B) with/without transglutaminase (TGase) were added to collagen fiber films to form hierarchical structure and its effects on the film were investigated. The analysis of mechanical properties indicate that gelatin significantly increased the toughness of the collagen film, where the 10 wt% type A gelatin -contained films had highest tensile strength, elongation at break and work of fracture. However, TGase crosslinking compromised the benefits of type A gelatin greatly, while type B gelatin showed a slight improvement, due to the difference in crosslinking activity between them. In the meantime, the hydrogen bonds were formed between the collagen and gelatin according to the results of the Fourier transformation infrared. In general, it is expected that the hierarchical structure formed in the collagen/gelatin films can be used as an effective strategy to enhance the collagen matrix films' mechanical properties.

Using Flammulina velutipes derived chitin-glucan nanofibrils to stabilize palm oil emulsion:A novel food grade Pickering emulsifier.

We herein report chitin-glucan nanofibrils from edible mushroom Flammulina velutipes (CGNFs) as a novel stabilizer for palm oil Pickering emulsion (o/w, 30:70, v:v). Generally, these CGNFs being composed of glucose and glucosamine, are threadlike with 4.9 ± 1.2 nm wide and 222.6 ± 91.9 nm long. They were easily absorbed on the oil-water interface to form a compact layer around the oil droplets referring to Pickering emulsion. This emulsion presented shear-thinning and gel-like behaviors, wherein CGNFs concentration had a profound influence on the emulsion volume, droplet size, and stabilization index. Moreover, CGNFs showed an ability to stabilize the emulsion with a minimum of surface coverage approximately 30%. It indicated that moderate concentration of NaCl improved the emulsification effect, and the emulsion were stable in a large range of pH. These CGNFs are easy to prepare, eco-friendly and sustainable, which provides a potential for large-scale application of Pickering emulsion in food and nutraceuticals fields.

Using cellulose nanofibers to reinforce polysaccharide films: Blending vs layer-by-layer casting.

Based on the electrostatic interaction mechanism, cellulose nanofiber (CNF) was utilized as reinforcing additives to fabricate polysaccharide films (alginate (Alg) or chitosan (CH)) by two methods: blending and layer-by-layer (LbL). Results showed that the addition of CNF led to higher tensile strength for all films than those without CNF addition, except for the blending CH film due to CNF agglomeration. The highest TS reached 140 MPa for the blending Alg film at 7 wt% CNF. Moreover, all CNF-reinforced films generally had lower water vapor permeability. The addition of CNF aggravated the opacity of all films, especially for the blending ones. Microstructure indicated that CNF were well dispersed in Alg-based films while aggregates were evident in the blending CH films. Interactions between CNF and Alg (or CH) and their relations on film performance were supported by FTIR and DSC of the resultant films, zeta-potential and turbidity of the film-forming solutions.

A top-down approach to improve collagen film's performance: The comparisons of macro, micro and nano sized fibers.

The severe reduction of mechanical strength of collagen once it is extracted or dissociated from animal tissues and no additional crosslinking approaches are conducted, impede its application in biodegradable and edible food packaging. Here, for the first time, high pressure homogenization (HPH) was used to prepare diverse sized fibers and the related fibers-composed films' performance were investigated. These fibers have a diversity of effects on film performance. The films prepared with smaller sized fibers had a more uniform and denser structure. The mechanical and the water barrier properties of the films improved significantly as the fiber size decreased. No obvious change in FTIR and thermal properties suggests that the improved film performance is mainly attributed to the physical entanglement and non-covalent bonds. Given the forementioned benefits of the films, control of fiber size can be a potential industrial approach for producing collagenous materials in edible food packaging.

Activation of transient receptor potential vanilloid 3 channel (TRPV3) aggravated pathological cardiac hypertrophy via calcineurin/NFATc3 pathway in rats.

Cardiac hypertrophy is a compensatory response to mechanical stimuli and neurohormonal factors, ultimately progresses to heart failure. The proteins of some transient receptor potential (TRP) channels, Ca2+ -permeable nonselective cation channel, are highly expressed in cardiomyocytes, and associated with the occurrence of cardiac hypertrophy. Transient receptor potential vanilloid 3 (TRPV3) is a member of TRP, however, the functional role of TRPV3 in cardiac hypertrophy remains unclear. TRPV3 was elevated in pathological cardiac hypertrophy, but not in swimming exercise-induced physiological cardiac hypertrophy in rats. TRPV3 expression was also increased in Ang II-induced cardiomyocyte hypertrophy in vitro, which was remarkably increased by carvacrol (a nonselective TRPV channel agonist), and reduced by ruthenium red (a nonselective TRPV channel antagonist). Interestingly, we found that activated TRPV3 in Ang II-induced cardiomyocyte hypertrophy was accompanied with increasing intracellular calcium concentration, promoting calcineurin, and phosphorylated CaMKII protein expression, and enhancing NFATc3 nuclear translocation. However, blocking or knockdown of TRPV3 could inhibit the expressions of calcineurin, phosphorylated CaMKII and NFATc3 protein by Western blot. In conclusion, the activation of TRPV3 aggravated pathological cardiac hypertrophy through calcineurin/NFATc3 signalling pathway and correlated with the protein expression levels of calcineurin, phosphorylated CaMKII and NFATc3, revealing that TRPV3 might be a potential therapeutic target for cardiac hypertrophy.

Metal ions increase mechanical strength and barrier properties of collagen-sodium polyacrylate composite films.

From the previous experiment, it was confirmed that the incorporation of 0.3 wt% sodium polyacrylate (PAAS) into collagen (Co) fibers can improve the mechanical properties and thermal stability of the composite films. In this study, Ca2+, Fe3+ and Ag+ ranging 0.001-0.004 mol/g were used to improve the properties of Co-PAAS blend films based on the rationale of their potential electrostatic interaction with these biopolymers. As expected, Zeta-potential film-forming solutions was decreased to some extent with the addition of metal ions. SEM images presented that the surface of the composites became coarser and internal structure became more stratified as metal ion contents increased. Tensile strength was increased by the addition of these ions with a varied optimal concentration: Ca2+ (0.003 mol/g), Fe3+ (0.002 mol/g) and Ag+ (0.001 mol/g). Water vapor permeability (WVP), solubility and light transmission value of films while causing film thickness no obvious change. In addition, the differential scanning calorimetry (DSC) and thermo-gravimetric analysis (TGA) results indicated that the metal ions improved the thermal stability of the composite film. Therefore, Ca2+, Fe3+ and Ag+ with an appropriate addition amount can be used as a potential alternative to reinforce collagenous composite materials.

MiRNA-409-3p enhances cisplatin-sensitivity of ovarian cancer cells by blocking the autophagy mediated by Fip200.

Background: Efficacy of chemotherapy for ovarian cancer (OC) is usually affected by various factors,especially the chemoresistance of ovarian cancer cells. Downregulation of miR-409-3p has been found in a variety of tumors. However, the role of miR-409-3p in chemo-resistant OC cells still remains unknown. The aim of this study was to investigate the effect of miR-409-3p on cisplatin-resistant OC cells and to elucidate the mechanism by which enhances cisplatin-sensitivity of OC cells. Methods: Expression of miR-409-3p in OC cells was assessed by qRT-PCR. MTS and clone formation assays were used to validate cell proliferation. Flow cytometry was performed for apoptosis analysis. Western blot assay was used to assess the alterations of signaling pathway related proteins. BALB/c nude mouse xenograft model was used to evaluate the role of miR-409-3p in cisplatin-resistant OC cells in vivo. Results: We found that miR-409-3p was apparently downregulated in the OC cells compared with normal ovarian cells. Results also showed that compared with the cisplatinsensitive cells, in cisplatin-resistant cells, miR-409-3p was decreased with an obvious increasing autophagic activity. In addition, based on the bioinformatics analysis, miR-409-3p was supposed to bind with Fip200. Our results demonstrated that in miR-409-3p overexpression cells, significant decreases were seen in protein expression of Fip200 and autophagic activity, which might be caused by conjugation between overexpressed miR-409-3p and 3'-UTR in Fip200 mRNA. Moreover, under the miR-409-3p overexpression, we found that cisplatin-sensitive and cisplatin-resistant ovarian cancer cells were more sensitive to the chemotherapeutics, which could be reversed by Fip2000. Further, we found that chemosensitivity in tumor cells was augmented by miR-409-3p overexpression, and Fip200 acted as a key link in interrupting the chemotherapy-induced autophagy. Conclusions: Results mentioned above revealed that miR-409-3p can ameliorate cisplatin-sensitivity of ovarian cancer cells through blocking the autophagy mediated by Fip200.

Transient receptor potential vanilloid-3 (TRPV3) activation plays a central role in cardiac fibrosis induced by pressure overload in rats via TGF-ß1 pathway.

Cardiac fibrosis is a common pathologic change along with pressure overload. Recent studies indicated that transient receptor potential (TRP) channels played multiple roles in heart. However, the functional role of transient receptor potential vanilloid-3 (TRPV3) in cardiac fibrosis remained unclear. The present study was designed to investigate the relationship between TRPV3 activation and pressure overload-induced cardiac fibrosis. Pressure overload rats were successfully established by abdominal aortic constriction (AAC), and cardiac fibrosis was simulated by 100 nM angiotensin II (Ang II) in neonatal cardiac fibroblasts. Echocardiographic parameters, cardiac fibroblast proliferation, cell cycle, intracellular calcium concentration ([Ca2+] i ), and the protein expressions of collagen I, collagen III, transforming growth factor beta 1 (TGF-ß1), cyclin E, and cyclin-dependent kinase 2 (CDK2) were measured. Echocardiographic and histological measurements suggested that the activation of TRPV3 exacerbated the cardiac dysfunction and increased interstitial fibrosis in pressure overload rats. Further results showed that TRPV3 activation upregulated the expressions of collagen I, collagen III, TGF-ß1, cyclin E, and CDK2 in vivo and in vitro. At the same time, blocking TGF-ß1 pathway could partially reverse the effect of TRPV3 activation. These results suggested that TRPV3 activation exacerbated cardiac fibrosis by promoting cardiac fibroblast proliferation through TGF-ß1/CDK2/cyclin E pathway in the pressure-overloaded rat hearts.

Activation of AMPK Attenuated Cardiac Fibrosis by Inhibiting CDK2 via p21/p27 and miR-29 Family Pathways in Rats.

Cardiac fibrosis is pathological damage associated with nearly all forms of heart disease. AMP-activated protein kinase (AMPK) is an evolutionary conserved energy-sensing enzyme. Emerging evidences indicate that AMPK plays an important role in cardiac fibrosis and cell proliferation. However, less is known about the detailed mechanism of AMPK activation on cardiac fibrosis. In this study, we found the AMPK activation improved the impaired cardiac function of cardiac fibrosis rats and decreased interstitial fibrosis. Further results indicated AMPK activation promoted p21 and p27 and inhibited CDK2 and cyclin E protein expressions both in vivo and in vitro. Moreover, AMPK activation repressed downstream transcription factor hepatocyte nuclear factor 4 alpha (HNF-4α) expression and decreased the binding of HNF-4α to TGF-ß1 promoters, which eventually resulted in TGF-ß1 downregulation and miR-29 family upregulation. Furthermore, miR-29, in turn, inhibited the progression of cardiac fibrosis through suppressing its target CDK2. Taken together, activation of AMPK, on the one hand, upregulated p21 and p27 expression, further inhibited CDK2 and cyclin E complex, and finally suppressed the progression of cardiac fibrosis, and, on the other hand, repressed HNF-4α expression, further downregulated the activity of TGF-ß1 promoter, promoted miR-29 expression, and finally prevented the development of cardiac fibrosis.

Role of carvacrol in cardioprotection against myocardial ischemia/reperfusion injury in rats through activation of MAPK/ERK and Akt/eNOS signaling pathways.

Carvacrol (CAR) is a compound isolated from some essential oils, many studies have demonstrated its therapeutic potential on different diseases. This study aims to evaluate the protective effect of CAR against myocardial ischemia/reperfusion (I/R) injury in rats. Male adult rats underwent ligation of the left anterior descending coronary artery (LAD) in I/R models. Rats were treated with CAR after LAD. The levels of I/R- induced infarct size, cardiomyocyte apoptosis and cardiac functional impairment were examined. Levels of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) were detected by western blotting. Cardiomyocytes induced by hypoxic reperfusion (H/R) injury were tested by Hoechst 33258. Our results revealed that CAR administration significantly protected the heart function, attenuated myocardial infarct size, increased SOD and CAT levels, reduced MDA level and especially decreased cardiomyocytes apoptosis. Western blotting showed that CAR treatment up-regulated phosphorylated ERK (p-ERK), while producing no impact onp38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK). The cardioprotection of CAR was reversed by the ERK inhibitor PD-98059, demonstrating the involvement of the MAPK/ERK pathway in the anti-apoptotic mechanisms of CAR. Besides, the results in vitro also showed the protective efficiency of CAR on cardiomyocytes H/R injury. Furthermore, pretreatment with CAR markedly increased the activation of Akt/eNOS pathway in cardiomyocytes subjected to H/R, and the protective effects of CAR were abolished in the presence of the Akt inhibitor LY294002. Therefore, the cardioprotective effects of CAR may be attributed to its antioxidant and antiapoptotic activities through activations of the MAPK/ERK and Akt/eNOS signaling pathways.

Activation of peroxisome proliferator-activated receptor γ (PPARγ) through NF-κB/Brg1 and TGF-ß1 pathways attenuates cardiac remodeling in pressure-overloaded rat hearts.

BACKGROUND/AIMS: Cardiac remodeling is a common pathophysiological change along with chronic hypertension and myocardial infarction. Recent evidence indicated that cardiac tissue expressed peroxisome proliferator-activated receptor γ (PPARγ). However, the functional role of PPARγ in cardiac remodeling remained unclear. The present study was designed to investigate the relationship between PPARγ activation and pressure overload-induced cardiac remodeling. METHODS: Cardiac remodeling model was successfully established by abdominal aorta ligation. Cardiac fibrosis and cardiomyocyte hypertrophy were simulated by 100 nM angiotensin II (Ang II) in vitro. Haemodynamic parameters, the expressions of Brg1, α-MHC, ß-MHC, transforming growth factor beta 1 (TGF-ß1), collagen-I, collagen-III and NF-κB were examined. RESULTS: Morphological and haemodynamic measurements showed that the activation of PPARγ improved the impaired cardiac function and decreased interstitial fibrosis in cardiac remodeling rats. Further results also showed that the activation of PPARγ inhibited the expressions of Brg1 and TGF-ß1 in the cardiac remodeling hearts. The activation of PPARγ also inhibited the proliferation and collagen production of cardiac fibroblasts, and down-regulated the activity of Brg1 and the expression of TGF-ß1 induced by Ang II in cultured neonatal rat cardiomyocytes and cardiac fibroblasts, respectively, through NF-κB pathway. CONCLUSIONS: These results suggested that PPARγ activation effectively inhibited cardiac remodeling processes by suppression of Brg1 and TGF-ß1 expressions through NF-κB pathway in the pressure-overloaded hearts induced by abdominal aorta ligation in rats.

[A random control study of indomethacin-containing MYCu intrauterine contraceptive device for 60 months].

OBJECTIVE: To explore the clinical efficacy and safety of MYCu intrauterine contraceptive device (IUD) containing indomethacin. METHODS: From October 1 to December 31, 2004, women of child-bearing age requiring IUD for contraception were chosen from the Outpatient Departments of China-Japan Friendship Hospital of Jilin University, Peking University First Hospital, Peking University Third Hospital, Jilin University Second Hospital and Affiliated Shengjing Hospital of China Medical University. They were randomly inserted with MYCuIUD and control TCu380A IUD each for 1000 cases and followed up at 1, 3, 6, 12, 24, 36, 48 and 60 months post-insertion. RESULTS: When MYCu IUD group and TCu380A group 60 months post-insertion were compared, the cumulative pregnancy rates with IUD in situ were 2.38/100 women per year and 2.84/100 women per year respectively. And the difference had no statistical significance (P > 0.05); the cumulative expulsion rates, mostly of partial expulsion and downward movement, were 0.87/100 women per year and 2.94/100 women per year respectively. And the difference had statistical significance (P < 0.05); the cumulative termination rates due to bleeding/pain were 3.57/100 women per year and 4.83/100 women per year respectively. And the difference had no statistical significance (P > 0.05); Side effects in MYCu group were less pronounced than those in TCu group. And the inter-group differences had statistical significance (P < 0.05). CONCLUSION: As a comparatively ideal medicated medical device, MYCu IUD has an excellent contraceptive efficacy, a low rate of expulsion and side effects and good reversibility. Particularly a low occurrence rate of bleeding and pain during early insertion is recommended. Its life expectancy is 15 years. And its contraceptive effectiveness and safety after 5 years should be examined during further follow-ups.

Activation of cholinergic anti-inflammatory pathway contributes to the protective effects of 100% oxygen inhalation on zymosan-induced generalized inflammation in mice.

BACKGROUND: The 100% oxygen inhalation has been demonstrated to have a protective effect on mice with zymosan-induced generalized inflammation. However, the underlying mechanism is largely unknown. The present study was designed to explore the role of the cholinergic anti-inflammatory pathway in this animal model. METHODS: Oxygen inhalation was given to mice at 4 and 12 h after zymosan injection. One group of mice underwent vagotomy 7 d before zymosan injection. The other two groups of mice either received nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine, or α7 nicotinic acetylcholine receptor (α7nAChR) antagonist methyllycaconitine 30 min before oxygen was given. RESULTS: The 100% oxygen treatment significantly decreased the serum level of TNF-α and increased the serum level of IL-10. The pathologic changes of the heart, lung, liver, and kidney were attenuated, as well as the dysfunction of liver and kidney. The 7-d survival rate of zymosan-challenged mice was also improved. Conversely, all these protective effects caused by pure oxygen treatment were abolished in those animals that received anti-cholinergic treatments. CONCLUSIONS: The cholinergic anti-inflammatory pathway may be involved in the 100% oxygen protective mechanism against zymosan-induced generalized inflammation in mice.

Topiramate attenuates cerebral ischemia/reperfusion injury in gerbils via activating GABAergic signaling and inhibiting astrogliosis.

Impaired GABAergic inhibitory synaptic transmission plays an essential role in the pathogenesis of selective neuronal cell death following transient global ischemia. GABA(A) receptor (GABA(A)R), K⁺-Cl⁻ co-transporter 2 (KCC2), Na⁺-K⁺-Cl⁻ co-transporter 1 (NKCC1) and astrocytes are of particular importance to GABAergic transmission. The present study was designed to explore whether the neuroprotective effect of topiramate (TPM) was linked with the alterations of GABAergic signaling and astrocytes. The bilateral carotid arteries were occluded, and TPM (80 mg/kg/day (divided twice daily), i.p.) was injected into gerbils. At day 1, 3 and 7 post-ischemia, neurological deficit was scored and changes in hippocampal neuronal cell death were evaluated by Nissl staining. The apoptosis-related regulatory proteins (procaspase-3, caspase-3, Bax and Bcl-2) and GABAergic signal molecules (GABA(A)R α1, GABA(A)R γ2, KCC2 and NKCC1) were also detected using western blot assay. In addition, the fluorescent intensity and protein level of glial fibrillary acidic protein (GFAP), a major component of astrocyte, were examined by confocal and immunoblot analysis. Our results showed that TPM treatment significantly decreased neurological deficit scores, attenuated the ischemia-induced neuronal loss and remarkably decreased the expression levels of procaspase-3, caspase-3 as well as the ratio of Bax/Bcl-2. Besides, treatment with TPM also resulted in the increased protein expressions of GABA(A)R α1, GABA(A)R γ2 and KCC2 together with the decreased protein level of NKCC1 in gerbils hippocampus. Furthermore, fluorescent intensity and protein level of GFAP were evidently reduced in TPM-treated gerbils. These findings suggest that the therapeutic effect of TPM on global ischemia/reperfusion injury appears to be associated with the enhancement of GABAergic signaling and the inhibition of astrogliosis in gerbils.

Effects of reactive oxygen species scavenger on the protective action of 100% oxygen treatment against sterile inflammation in mice.

Sepsis/multiple organ dysfunction syndrome (MODS) is a major cause of high mortality in the intensive care unit. We have recently reported that 100% oxygen treatment is beneficial to mice with zymosan-induced sterile inflammation by increasing antioxidant enzymatic activities. Yet, the use of hyperoxia is hindered by concerns that it could exacerbate organ injury by increasing free radical formation. It is believed that systemic inflammation and overproduction of reactive oxygen species (ROS) contribute to the mechanism underlying sepsis/MODS. A ROS scavenger has been proven to protect against sepsis/MODS in some animal models. Therefore, we hypothesized that ROS scavenger pretreatment might enhance the protective action of 100% oxygen treatment against zymosan-induced sterile inflammation in mice. In the present study, we showed that 100% oxygen treatment prevented the abnormal changes in serum biochemical parameters, tissue oxygenation, and organ histopathology, and improved the 14-day survival rate in zymosan-stimulated mice, indicating that 100% oxygen treatment had a protective action on sterile inflammation. We found that pretreatment with a ROS scavenger (N-acetylcysteine, vitamin C, or dimethylthiourea) abolished this protective action of 100% oxygen treatment. We also showed that 100% oxygen treatment decreased the levels of serum proinflammatory cytokines (TNF-alpha, IL-6, and high-mobility group box 1), increased the level of serum anti-inflammatory cytokine (IL-10), and upregulated the activities of serum and tissue antioxidant enzymes (superoxide dismutase, catalase, and glutathione peroxidase) in zymosan-stimulated mice, which were reversed by the pretreatment with a ROS scavenger (N-acetylcysteine, vitamin C, or dimethylthiourea). We thus conclude that ROS scavenger pretreatment partly abolishes the protective effects of 100% oxygen treatment on sterile inflammation in mice by regulating inflammatory cytokines as well as antioxidant enzymes.

Effect of dopamine and metaraminol on the renal function of patients with septic shock.

BACKGROUND: Vasoactive drugs are often necessary for reversing hypotension in patients with severe infection. The standard for evaluating effects of vasoactive drugs should not only be based on the increase of arterial blood pressure, but also on the blood flow perfusion of internal organs. The effects of dopamine and metaraminol on the renal function of the patients with septic shock were investigated retrospectively in this study. METHODS: Ninety-eight patients with septic shock were divided into three groups according to the highest infusing rate of metaraminol, with the lightest infusing rate of (0.1 - 0.5, 0.6 - 1.0, > 1.0) microgxkg(-1)xmin(-1) in group A, B and C respectively. Urine output, mean arterial blood pressure (MAP), heart rate (HR), urine output, blood urea nitrogen (BUN), creatinine (CRE), urine albumin (U-ALB), urine beta(2)-microglubulin (Ubeta(2)-MG) and Apache III scores were recorded. RESULTS: Before antishock therapy, hypotension, tachycardia and oliguria occurred to all the 98 patients with septic shock and CRE, BUN, U-ALB, Ubeta(2)-MG and Apache III scoring were abnormal in most cases. With the antishock therapy, MAP, HR, urine output, BUN and CRE in all patients returned gradually to normal (P < 0.05 or < 0.01 compared to those before antishock therapy). U-ALB, Ubeta(2)-MG output and Apache III scoring also reverted but remained abnormal (P < 0.01 compared to those before antishock therapy). No statistically significant differences in the changes of these indices with the time existed among the three groups (P > 0.05). CONCLUSION: Dopamine and metaraminol when applied to the patients with septic shock could effectively maintain the circulatory stability and promote restoration of renal function.