One-Step Synthesis of Multifunctional Bacterial Cellulose Film-Based Phase Change Materials with Cross-Linked Network Structure for Solar-Thermal Energy Conversion, Storage, and Utilization.

As one of the important directions of solar energy utilization, the construction of composite photothermal phase change materials (PCM) with reasonable network support and low leakage in the simple method is important to solve the transient availability of solar energy and achieve long-lasting energy output. Here, a multifunctional silylated bacterial cellulose (BC)/hydroxylated carbon nanotube (HCNT)/polyethylene glycol (PEG) (SBTP) photothermal film-based PCM with cross-linked network structure is prepared by simple one-step synthesis. The formation of the cross-linked network structure achieves the enhancement of BC support network, prominent dispersion of HCNT and the direct introduction and perfect interlocking of PEG. Therefore, the optimal SBTP film exhibits high thermal enthalpy of 145.1 J g-1, enthalpy efficiency of over 94%, robust shape stability and low leakage of <1.2%. It also displays high photothermal conversion of over 80 °C, photothermal storage of 394 s g-1 and excellent stability. Thus, it can demonstrate a maximum output voltage of 423 mV and high power density of 30.26 W m-2 under three solar irradiations when applied in the solar-thermal-electric energy conversion field. Meanwhile, it also can apply in the thermal management of solar cell and light-emitting diode (LED) chip, and convert the waste heat into electricity, demonstrating multi-scene application capability.

Electrocatalytic Valorization of Nitrate and Polyester Plastic for Simultaneous Production of Ammonia and Glycolic Acid.

Electrochemical upcycling of nitrate and polyester plastic into valuable products is an ideal solution to realize the resource utilization. Here, the co-production of ammonia (NH3) and glycolic acid (GA) via electrochemical upcycling of nitrate and polyethylene terephthalate (PET) plastics over mesoporous Pd3Au film on Ni foam (mPd3Au/NF), which is synthesized by micelle-assisted replacement method, is proposed. The mPd3Au/NF with well-developed mesoporous structure provides abundant active sites and facilitated transfer channels and strong electronic effect. As such, the mPd3Au/NF exhibits high Faraday efficiencies of 97.28% and 95.32% at 0.9 V for the formation of NH3 and GA, respectively. Theoretical results indicate that the synergistic effect of Pd and Au can optimize adsorption energy of key intermediates *NOH and *OCH2-CH2OH on active sites and increase bond energy of C─C band, thereby improving the activity and selectivity for the formation of NH3 and GA. This work proposes a promising strategy for the simultaneous conversation of nitrate and PET plastic into high-value NH3 and GA.

Quasi-Solid-State All-V2O5 Battery.

Solid-state symmetrical battery represents a promising paradigm for future battery technology. However, its development is hindered by the deficiency of high-performance bipolar electrodes and compatible solid electrolytes. Herein, a quasi-solid-state all-V2O5 battery constructed by a binder-free carbon fabric-V2O5 nanowires@graphene (CVOG) bipolar electrode and a softly cross-linked polyethylene oxide-based solid polymer electrolyte (SPE) is reported. The synergetic effect of nano-structuring of V2O5, hierarchical conductive network, and graphene wrapping endows the CVOG electrode with boosted reaction kinetics and suppressed vanadium dissolution. The cathodic and anodic reactions of CVOG are decoupled by electrochemical analysis, conceiving the feasibility of constructing all-V2O5 full battery. In manifesting the solid-state all-V2O5 battery, the robust and elastic SPE exhibits high ionic conductivity, tight/self-adaptable electrolyte-electrode contact, and a low charge-transfer barrier. The resultant solid-state full battery exhibits a high reversible capacity of 158 mAh g-1 at 0.1 C, good capacity retention of over 61% from 0.1 C to 2 C, and remarkable cycling stability of 77% capacity retention after 1000 cycles at 1 C, which surpass other solid-state symmetrical batteries. Hence, this work provides a practice of high-performance solid-state batteries with symmetrical configuration and is constructive for next-generation battery technology.

Anesthesia/surgery-induced learning and memory dysfunction by inhibiting mitophagy-mediated NLRP3 inflammasome inactivation in aged mice.

Postoperative cognitive dysfunction (POCD) is a common postoperative complication, not only affects the quality of life of the elderly and increases the mortality rate, but also brings a greater burden to the family and society. Previous studies demonstrated that Nod-like receptor protein 3 (NLRP3) inflammasome participates in various inflammatory and neurodegenerative diseases. However, possible mitophagy mechanism in anesthesia/surgery-elicited NLRP3 inflammasome activation remains to be elucidated. Hence, this study clarified whether mitophagy dysfunction is related to anesthesia/surgery-elicited NLRP3 inflammasome activation. POCD model was established in aged C57BL/6 J mice by tibial fracture fixation under isoflurane anesthesia. Morris Water Maze (MWM) was used to evaluate learning and memory abilities. We found that in vitro experiments, lipopolysaccharide (LPS) significantly facilitated NLRP3 inflammasome activation and mitophagy inhibition in BV2 cells. Rapamycin restored mitophagy and improved mitochondrial function, and inhibited NLRP3 inflammasome activation induced by LPS. In vivo experiments, anesthesia and surgery caused upregulation of hippocampal NLRP3, caspase recruitment domain (ASC) and interleukin-1ß (IL-1 ß), and downregulation of microtubule-associated protein light chain 3II (LC3II) and Beclin1 in aged mice. Olaparib inhibited anesthesia/surgery-induced NLRP3, ASC, and IL-1ß over-expression in the hippocampus, while upregulated the expression of LC3II and Beclin1. Furthermore, Olaparib improved cognitive impairment in older mice. These results revealed that mitophagy was involved in NLRP3 inflammasome-mediated anesthesia/surgery-induced cognitive deficits in aged mice. Overall, our results suggested that mitophagy was related in NLRP3 inflammasome-induced cognitive deficits after anesthesia and surgery in aged mice. Activating mitophagy may have clinical benefits in the prevention of cognitive impairment induced by anesthesia and surgery in elderly patients.

Multi-omics analysis reveals BDE47 induces depression-like behaviors in mice by interfering with the 2-arachidonoyl glycerol-associated microbiota-gut-brain axis.

2,2',4,4'-tetrabromodiphenyl ether (BDE47) is a foodborne environmental risk factor for depression, but the pathogenic mechanism has yet to be fully characterized. In this study, we clarified the effect of BDE47 on depression in mice. The abnormal regulation of the microbiome-gut-brain axis is evidenced closely associated with the development of depression. Using RNA sequencing, metabolomics, and 16s rDNA amplicon sequencing, the role of the microbiome-gut-brain axis in depression was also explored. The results showed that BDE47 exposure increased depression-like behaviors in mice but inhibited the learning memory ability of mice. The RNA sequencing analysis showed that BDE47 exposure disrupted dopamine transmission in the brain of mice. Meanwhile, BDE47 exposure reduced protein levels of tyrosine hydroxylase (TH) and dopamine transporter (DAT), activated astrocytes and microglia cells, and increased protein levels of NLRP3, IL-6, IL-1ß, and TNF-α in the brain of mice. The 16 s rDNA sequencing analysis showed that BDE47 exposure disrupted microbiota communities in the intestinal contents of mice, and faecalibaculum was the most increased genus. Moreover, BDE47 exposure increased the levels of IL-6, IL-1ß, and TNF-α in the colon and serum of mice but decreased the levels of tight junction protein ZO-1 and Occludin in the colon and brain of mice. In addition, the metabolomic analysis revealed that BDE47 exposure induced metabolic disorders of arachidonic acid and neurotransmitter 2-Arachidonoyl glycerol (2-AG) was one of the most decreased metabolites. Correlation analysis further revealed gut microbial dysbiosis, particularly faecalibaculum, is associated with altered gut metabolites and serum cytokines in response to BDE47 exposure. Our results suggest that BDE47 might induce depression-like behavior in mice through gut microbial dysbiosis. The mechanism might be associated with the inhibited 2-AG signaling and increased inflammatory signaling in the gut-brain axis.

Eco-Friendly Fabrication of Transparent Superhydrophobic Coating with Excellent Mechanical Robustness, Chemical Stability, and Long-Term Outdoor Durability.

Surfaces that possess both superhydrophobicity and high transparency at the same time recently have attracted extensive attention in outdoor applications. However, fabrication and application of transparent superhydrophobic coating usually face following challenges: the micro-nano hierarchical structure required for superhydrophobicity usually leads to a decrease in the light transmittance due to its light trapping effect; fluorine-containing materials used in the preparation of superhydrophobic surfaces are potentially harmful to humans and the environment; and the superhydrophobic surface is easily destroyed by external factors. In this work, a transparent superhydrophobic coating was fabricated via an inexpensive and eco-friendly two-step method, that is, dipping glass substrate into the polydimethylsiloxane/SiO2 suspension followed by calcination treatment. The prepared coating showed superhydrophobicity with a water contact angle of 164° and a sliding angle less than 1.0°. In the visible light region with the wavelength range of 300-900 nm, the maximal transmittance of the superhydrophobic coating was ∼91.4%, which is higher than that of the untreated glass substrate (∼90.9%). Moreover, the coating can maintain superhydrophobicity and high transmittance after sandpaper abrasion, water flow impact, immersion in strong acid/alkaline solution, UV irradiation, and long-term outdoor exposure. We believing that the coating has huge potential value in outdoor applications.

Positive effect of compound amino acid chelated calcium from the shell and skirt of scallop in an ovariectomized rat model of postmenopausal osteoporosis.

BACKGROUND: Osteoporosis has become an important public health issue with the increase of aging population, and afflicts millions of people worldwide, particularly elderly or postmenopausal women. In the present study, we prepared compound amino acid chelated calcium (CAA-Ca) from processing by-products of Chlamys farreri, and evaluated its effect on postmenopausal osteoporosis with an ovariectomized (OVX) rat model. RESULTS: A 60-day treatment of OVX rats with CAA-Ca significantly enhanced the bone mineral density (BMD) and the bone calcium content. Meanwhile, some bone morphometric parameters, trabecular bone number (Tb.N), trabecular bone volume fraction (BV/TV), trabecular bone thickness (Tb.Th) and cortical bone wall thickness (Ct.Th), were also increased by 8.20%, 118.18%, 32.99% and 19.10%, respectively. In addition, the alkaline phosphatase (ALP) levels in serum were significantly reduced after CAA-Ca treatment, while the blood calcium levels were increased. Mechanistically, CAA-Ca down-regulated the levels of receptor activator of nuclear factor-κB (RANK) and receptor activator of nuclear factor-κB ligand (RANKL), and up-regulated osteoprotegerin (OPG) levels in osteoclasts, inhibiting bone resorption and bone loss. Meanwhile, CAA-Ca treatment raised ß-catenin levels and lowered Dickkopf1 (DKK1) levels in the Wnt signaling pathway of osteoblasts, which can promote calcium absorption and bone formation. CONCLUSION: The results suggested that CAA-Ca promoted bone formation, inhibited bone resorption and improved bone microstructure. Therefore, this study contributes to the potential application of CAA-Ca as a functional food resource in the treatment of postmenopausal osteoporosis. © 2021 Society of Chemical Industry.

Sinapic Acid Alleviated Inflammation-Induced Intestinal Epithelial Barrier Dysfunction in Lipopolysaccharide- (LPS-) Treated Caco-2 Cells.

The integrity and permeability of the intestinal epithelial barrier are important indicators of intestinal health. Impaired intestinal epithelial barrier function and increased intestinal permeability are closely linked to the onset and progression of various intestinal diseases. Sinapic acid (SA) is a phenolic acid that has anti-inflammatory, antihyperglycemic, and antioxidant activities; meanwhile, it is also effective in the protection of inflammatory bowel disease (IBD), but the specific mechanisms remain unclear. Here, we evaluated the anti-inflammatory of SA and investigated its potential therapeutic activity in LPS-induced intestinal epithelial barrier and tight junction (TJ) protein dysfunction. SA improved cell viability; attenuated epithelial permeability; restored the protein and mRNA expression of claudin-1, ZO-1, and occludin; and reversed the redistribution of the ZO-1 and claudin-1 proteins in LPS-treated Caco-2 cells. Moreover, SA reduced the inflammatory response by downregulating the activation of the TLR4/NF-κB pathway and attenuated LPS-induced intestinal barrier dysfunction by decreasing the activation of the MLCK/MLC pathway. This study demonstrated that SA has strong anti-inflammatory activity and can alleviate the occurrence of high intercellular permeability in Caco-2 cells exposed to LPS.

A preliminary study on the mechanism of the neurosteroid-mediated ionotropic receptor dysfunction in neurodevelopmental toxicity induced by decabromodiphenyl ether.

The mechanism of neurodevelopmental toxicity of decabromodiphenyl ether (BDE209) remains unclear. Recent evidence suggests that neurosteroids disorders play a vital role in BDE209 induced-neurodevelopmental toxicity. To explore the mechanism of it, pregnant ICR mice were orally gavaged with 0, 225, and 900 mg kg-1 BDE209 for about 42 days. Spatial learning and memory abilities of offspring were tested on postnatal day (PND) 21. Offspring were euthanized at PND26, the neuronal structure, neurosteroids level, and related proteins including neurosteroids synthase, ionotropic receptors and cAMP-response element binding protein (CREB) pathway were evaluated, as well as Ca2+ concentration and the mitochondrial membrane potential (Mmp). Our results showed that BDE209 impaired learning and memory abilities and disrupted neuronal structure. Meanwhile, BDE209 decreased the pregnenolone (PREG), dehydroepiandrosterone (DHEA), progesterone (PROG) and allopregnanolone (ALLO) levels in the serum and brain, as well as the mRNA and protein levels of cholesterol-side-chain cleavage enzyme (P450scc), steroid 17α-hy-droxylase (P450C17), 3ß-hydroxysteroid dehydrogenase (3ß-HSD) and steroid 5α-reductase of type I (5α-R) in the hippocampi. Also, BDE209 suppressed mRNA and protein levels of NR1, NR2A and NR2B subunits of the N-methyl-D-aspartic acid receptor (NMDAR) and α1 subunit of the Gamma-amino butyric acid A receptor (GABAAR), but increased the levels of ß2 and γ2 subunits of the GABAAR in the hippocampi. Moreover, BDE209 increased the Ca2+ concentration and phosphorylation extracellular regulated protein kinases (P-ERK) 1/2 level, but decreased the P-CREB and Mmp level in the hippocampi. These results indicate that BDE209 exposure during pregnancy and lactation is possible to affect learning and memory formation of offspring by the neurosteroid-mediated ionotropic receptors dysfunction.

Neurotoxicity and related mechanisms of flame retardant TCEP exposure in mice.

Objective: To explore the neurotoxicity and mechanism of tris(2-chloroethyl) phosphate (TCEP) exposure in mice.Methods: Total 30 adult Kunming mice were randomly divided into normal control group (0 mg/kg·d), low-dose TCEP group (10 mg/kg·d), and high-dose TCEP group (100 mg/kg·d), and administered continuously by gavage for 30 days.Results: Compared with the control group, the water intake of high-dose TCEP group was declined significantly (p < 0.05), and the organ index of liver and spleen were increased significantly (p < 0.05). In addition, the escape latency of TCEP exposed mice were longer than that in the control group in water maze test (p < 0.05), while the total swimming course of high-dose TCEP group was elevated and the swimming time in target quadrant was obviously shortened compared with the control group (p < 0.05). The serum levels of total-triiodothyronine (TT3) and free triiodothyronine (FT3) were significantly higher in the high-dose TCEP group than in the control group (p＜0.05). Compared with the control group, the activities of glutathione transferase (GST) and super oxide dismutase (SOD) in the high-dose TCEP group were increased, and GST in the low-dose TCEP group were decreased, while the content of malonaldehyde (MDA) in both groups was increased (p＜0.05). In the CCK8 assay, the viability of PC12 cells decreased with an increase of TCEP concentration, indicating a concentration dependent neurotoxicity.Conclusion: TCEP exposure can cause neurotoxicity by increasing thyroid hormones and inducing oxidative damage in mice.

Lactobacillus plantarum YS2 (yak yogurt Lactobacillus) exhibited an activity to attenuate activated carbon-induced constipation in male Kunming mice.

The present study investigated the effects of Lactobacillus plantarum YS2 (LP-YS2) that was isolated from yak yogurt on activated carbon-induced constipation in Kunming (KM) mice. The KM mice were orally administered LP-YS2 and reference strain Lactobacillus delbrueckii ssp. bulgaricus. Administration of LP-YS2 [1.0 × 109 cfu/kg of body weight (BW)] promoted gastrointestinal peristalsis and reduced the first black stool defecation time (129 min), which clearly defines attenuation of the voiding difficulty in mice with constipation. The LP-YS2 treatment also increased the serum level of motilin (MTL; 178.2 pg/mL), gastrin (69.4 pg/mL), acetylcholine (Ach; 30.1 pg/mL), substance P (SP; 57.6 pg/mL), and vasoactive intestinal peptide (VIP; 53.2 pg/mL) and reduced the somatostatin (SS, 32.6 pg/mL) levels compared with the L. delbrueckii ssp. bulgaricus treatment (MTL, 139.7 pg/mL; gastrin, 43.1 pg/mL; Ach, 15.9 pg/mL; SP, 43.6 pg/mL; VIP, 32.3 pg/mL; SS, 55.1 pg/mL) and the control (MTL, 105.3 pg/mL; gastrin, 26.7 pg/mL; Ach, 9.7 pg/mL; SP, 30.2 pg/mL; VIP, 21.0 pg/mL; SS, 70.5 pg/mL). The LP-YS2 treatment significantly increased the colonic mRNA and protein expression of c-Kit (CD117, cluster of differentiation 117; 2.87 times mRNA expression of the control group), stem cell factor (30.40 times mRNA expression of the control group), and glial cell-derived neurotrophic factor (29.97 times mRNA expression of the control group) in mice with constipation. In addition, LP-YS2 reduced the expression of transient receptor potential vanilloid 1 (0.42 times mRNA expression of the control group) and nitric oxide synthase (0.49 times mRNA expression of the control group) in constipated mice. These results demonstrate that LP-YS2 was able to attenuate the activated carbon-induced constipation in KM mice.

Preventive effect of Lactobacillus plantarum KSFY02 isolated from naturally fermented yogurt from Xinjiang, China, on d-galactose-induced oxidative aging in mice.

Yogurt from Xinjiang, China, is a traditional and naturally fermented food, and abundant microorganisms are produced during its fermentation process. In this study, we carried out in vivo animal experiments to explore the effect of a newly isolated lactic acid bacterial strain, Lactobacillus plantarum KSFY02 (LP-KSFY02), on oxidative aging. We used d-galactose to induce oxidative aging in mice and analyzed the serum and tissues of those mice using molecular biology detection methods. The results showed that LP-KSFY02 could inhibit the decreases in the thymic, cerebral, cardiac, liver, spleen, and kidney indices of mice caused by oxidative aging. The LP-KSFY02 strain increased activity of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) and reduced levels of nitric oxide (NO) and malondialdehyde in the serum, liver, and spleen of the oxidative aging mice. Pathological observation demonstrated that LP-KSFY02 alleviated damage to the liver and spleen of oxidative aging mice. Quantitative PCR showed that LP-KSFY02 effectively upregulated mRNA expression of neuronal nitric oxide synthase (Nos1), endothelial nitric oxide synthase (Nos3), copper/zinc superoxide dismutase (Sod1), manganese superoxide dismutase (Sod2), catalase (Cat), heme oxygenase-1 (Hmox1), nuclear factor erythroid 2 related factor 2 (Nfe2l2), γ-glutamylcysteine synthetase (Gclm), and quinone oxidoreductase 1 (Nqo1) in mouse liver and spleen and downregulated expression of inducible nitric oxide synthase (Nos2). Western blot analysis revealed that LP-KSFY02 effectively upregulated protein expression of SOD1, SOD2, CAT, GSH1, and GSH2 in mouse liver and spleen tissues. Therefore, LP-KSFY02 can effectively prevent d-galactose-induced oxidative aging in mice. Its efficacy was superior to that of Lactobacillus delbrueckii ssp. bulgaricus (LDSB) and vitamin C, which are commonly used in the medical field as antioxidants. Thus, LP-KSFY02 is a high-quality strain with probiotic potential.

Effects of maternal exposure to BDE209 on neuronal development and transcription of iodothyronine deiodinase in offspring mice.

The present study investigated the alterations in nerve function and its potential mechanism of offspring result from the decabromodiphenyl ether (BDE209) orally gavage (0, 1.5, and 225 mg/kg.d body weight) in pregnant and lactating mice. Weight gain and litter size of maternal mice and body weight of offspring were examined. Learning and memory abilities of offspring were tested by the Morris water maze experiment. Thyroid hormones (THs) concentrations in peripheral blood of offspring were detected by the chemiluminescence enzyme immunoassay. Relative mRNA expression of type 1 iodothyronine deiodinase (dio1), type 2 iodothyronine deiodinase (dio2), and type 3 iodothyronine deiodinase (dio3) in the livers and brains of offspring were measured by QRT-PCR (quantitative real-time polymerase chain reaction). Protein expression of dio3 in the livers and brains of offspring was measured by Western blot. All indexes of offspring were tested at postnatal day (PND) 21 and PND 60, respectively. As a result, administration of BDE209 decreased weight gain and litter size of maternal mice, and reduced body weight of offspring mice, prolonged escape latency and declined guardant time of offspring in the Morris water maze experiment. Moreover, BDE209 elevated serum levels of total thyroxine (T4), total triiodothyronine (T3), free T4, and free T3 in offspring. In addition, maternal exposure to BDE209 inhibited dio1, dio2, dio3 mRNA expression in the livers of offspring, while elevated dio1 mRNA expression and reduced dio3 mRNA expression in the brains of offspring. BDE209 also inhibited the protein expression of dio3 in the livers and brains of offspring. These results indicate that BDE209 exposure to pregnant and lactating mice can cause disruption in serum THs of offspring by altering mRNA and protein expression of iodothyronine deiodinases, which might consequently result in neurologic impairment of offspring mice.

Effect of Breviscapine on Recovery of Viable Myocardium and Left Ventricular Remodeling in Chronic Total Occlusion Patients After Revascularization: Rationale and Design for a Randomized Controlled Trial.

BACKGROUND How to speed the recovery of viable myocardium in chronic total occlusion (CTO) patients after revascularization is still an unsolved problem. Breviscapine is widely used in cardiovascular diseases. However, there has been no study focused on the effect of breviscapine on viable myocardium recovery and left ventricular remodeling after CTO revascularization. MATERIAL AND METHODS We propose to recruit 78 consecutive coronary artery disease (CAD) patients with CTO during a period of 12 months. They will be randomly assigned to receive either breviscapine (40 mg) or placebo in the following 12 months. Blood tests, electrocardiogram, and Major Adverse Cardiac Events (MACE) will be collected at baseline and the follow-up visits at 1, 3, 6, 9, and 12 months. Low-dose dobutamine MRI will be applied for the assessment of viable myocardium, microcirculation perfusion, and left ventricular remodeling, and the concentrations of angiogenic cytokine, vascular endothelial growth factor (VEGF), and basic fibroblast growth factor (bFGF) will be investigated at baseline and at 1- and 12-month follow-up. The recovery of viable myocardium after revascularization in CTO patients was the primary endpoint. Improvement of microcirculation perfusion, left ventricular remodeling, peripheral concentrations of VEGF and bFGF as well as MACE will be the secondary endpoints. RESULTS Breviscapine treatment obviously improve the recovery of viable myocardium, myocardial microcirculation perfusion, and left ventricular remodeling after revascularization in CTO patients, and reduce the occurrence of MACE. We also will determine if breviscapine increases the peripheral blood angiogenic cytokine concentrations of VEGF and bFGF. CONCLUSIONS This study will aim to demonstrate the effect of breviscapine on the recovery of viable myocardium and left ventricular remodeling in CTO patients after revascularization.

Lactobacillus paracasei ssp. paracasei YBJ01 reduced d-galactose-induced oxidation in male Kuming mice.

We investigated in vitro and in vivo antioxidant activity of Lactobacillus paracasei ssp. paracasei YBJ01 (LPSP-YBJ01) isolated and identified from fermented yogurt. Strain LPSP-YBJ01 had stress tolerance against acidity, bile salt, and osmotic pressure. Five in vitro antioxidant assays were used to evaluate antioxidant activity of LPSP-YBJ01, which could scavenge free radicals (2,2-diphenyl-1-picrylhydrazyl and hydroxyl) and superoxide anion in vitro. In addition, strain LPSP-YBJ01 had stronger antilipid peroxidation activity and weak reducing power in vitro. We measured in vivo antioxidant activity of LPSP-YBJ01 in an oxidation mouse model induced by d-galactose injection. Strain LPSP-YBJ01 significantly increased serum superoxide dismutase (SOD), glutathione peroxidase, and total-antioxidant capability, and inhibited generation of malondialdehyde in a dose-dependent manner. In addition, strain LPSP-YBJ01 also increased the hepatic and splenic protein expressions of some antioxidant enzymes such as catalase, Cu/Zn-SOD, and Mn-SOD in mice treated with d-galactose. Thus, LPSP-YBJ01 had antioxidant activity in vitro and in vivo and may be a useful probiotic.

Comparison of Antioxidative Effects of Insect Tea and Its Raw Tea (Kuding Tea) Polyphenols in Kunming Mice.

Kudingcha is a traditional Chinese tea, and insect tea is a special drink produced by the metabolism of insect larvae using the raw Kuding tea. Insect tea polyphenols (ITP) and its raw tea (Kuding tea) polyphenols (KTP) are high-purity polyphenols extracted by centrifuge precipitation. The present study was designed to compare the antioxidative effects of insect tea polyphenols (ITP) and its raw tea (Kuding tea) polyphenols (KTP) on d-galactose-induced oxidation in Kunming (KM) mice. KM mice were treated with ITP (200 mg/kg) and KTP (200 mg/kg) by gavage, and vitamin C (VC, 200 mg/kg) was also used as a positive control by gavage. After determination in serum, liver and spleen, ITP-treated mice showed higher superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and glutathione (GSH) activities and lower nitric oxide (NO), malonaldehyde (MDA) activities than VC-treated mice, KTP-treated mice and untreated oxidation mice (control group). By H&E section observation, the mice induced by d-galactose-induced oxidation showed more changes than normal mice, and oxidative damage appeared in liver and spleen tissues; ITP, VC and KTP improved oxidative damage of liver and spleen tissues, and the effects of ITP were better than VC and KTP. Using quantitative polymerase chain reaction (qPCR) and western blot experiments, it was observed that ITP could increase the mRNA and protein expression of neuronal nitric oxide synthase (nNOS), endothelial nitric oxide synthase (eNOS), manganese superoxide dismutase (Mn-SOD), cupro/zinc superoxide dismutase (Cu/Zn-SOD), catalase (CAT), heme oxygenase-1 (HO-1), nuclear factor erythroid 2 related factor 2 (Nrf2), gamma glutamylcysteine synthetase (γ-GCS), and NAD(P)H:quinone oxidoreductase 1 (NQO1) and reduce inducible nitric oxide synthase (iNOS) expression in liver and spleen tissues compared to the control group. These effects were stronger than for VC and KTP. Both ITP and KTP had good antioxidative effects, and after the transformation of insects, the effects of ITP were better than that of KTP and even better than VC. Thus, ITP can be used as an antioxidant and anti-ageing functional food.

Lactobacillus casei Strain Shirota Enhances the In Vitro Antiproliferative Effect of Geniposide in Human Oral Squamous Carcinoma HSC-3 Cells.

This study investigated the enhanced antiproliferative effect of Lactobacillus casei strain Shirota (LcS) on geniposide actions in human oral squamous carcinoma HSC-3 cells. An MTT assay, flow cytometry, qPCR assay, western blot and HPLC were used for this study. The concentration of 1.0 × 106 CFU/mL of LcS had no effect on the HOK normal oral epithelial cells and HSC-3 cancer cells. The 25 and 50 µg/mL geniposide concentrations also had no impact on HOK normal oral epithelial cells, but they had remarkable inhibitory effects on the growth of HSC-3 cancer cells, which are enhanced in the presence of LcS. By the flow cytometry assay, the LcS-geniposide-H (1.0 × 106 CFU/mL LcS and 50 µg/mL geniposide)-treated HSC-3 cancer cells had the largest number of cells undergoing apoptosis compared to cells treated with other combinationsand obviously more than cells treated with only geniposide-H (50 µg/mL geniposide). Geniposide-H could increase the mRNA and protein expressions of caspase-3, caspase-8, caspase-9, Bax, p53, p21, IκB-α, Fas, FasL, TIMP-1, and TIMP-2 as well as decrease those of Bcl-2, Bcl-xL, HIAP-1, HIAP-2, NF-κB, COX-2, iNOS, MMP-2, and MMP-9 compared to other groups of cells, and LcS further enhanced these changes, with results that are greater than for the cells treated with only a high concentration of geniposide. The results of this study show thatLcS enhanced the antiproliferative effect of geniposide in HSC-3 cancer cells.

Activation of liver X receptor attenuates lysophosphatidylcholine-induced IL-8 expression in endothelial cells via the NF-κB pathway and SUMOylation.

The liver X receptor (LXR) is a cholesterol-sensing nuclear receptor that has an established function in lipid metabolism; however, its role in inflammation is elusive. In this study, we showed that the LXR agonist GW3965 exhibited potent anti-inflammatory activity by suppressing the firm adhesion of monocytes to endothelial cells. To further address the mechanisms underlying the inhibition of inflammatory cell infiltration, we evaluated the effects of LXR agonist on interleukin-8 (IL-8) secretion and nuclear factor-kappa B (NF-κB) activation in human umbilical vein endothelial cells (HUVECs). The LXR agonist significantly inhibited lysophosphatidylcholine (LPC)-induced IL-8 production in a dose-dependent manner without appreciable cytotoxicity. Western blotting and the NF-κB transcription activity assay showed that the LXR agonist inhibited p65 binding to the IL-8 promoter in LPC-stimulated HUVECs. Interestingly, knockdown of the indispensable small ubiquitin-like modifier (SUMO) ligases Ubc9 and Histone deacetylase 4 (HDAC4) reversed the increase in IL-8 induced by LPC. Furthermore, the LPC-induced degradation of inhibitory κBα was delayed under the conditions of deficient SUMOylation or the treatment of LXR agonist. After enhancing SUMOylation by knockdown SUMO-specific protease Sentrin-specific protease 1 (SENP1), the inhibition of GW3965 was rescued on LPC-mediated IL-8 expression. These findings indicate that LXR-mediated inflammatory gene repression correlates to the suppression of NF-κB pathway and SUMOylation. Our results suggest that LXR agonist exerts the anti-atherosclerotic role by attenuation of the NF-κB pathway in endothelial cells.

Safety and efficacy of autologous thymosin ß4 pre-treated endothelial progenitor cell transplantation in patients with acute ST segment elevation myocardial infarction: A pilot study.

BACKGROUND: Experimental studies and clinical trials suggest that endothelial progenitor cell (EPC) transplantation can repair "broken" heart. However, transplantation of autologous EPCs has numerous limitations, including the limited supply of expanded EPCs, the impaired function and activity of the transplanted cells and so on. Therefore, we investigated the feasibility, safety and initial clinical outcome of autologous thymosin ß4 (Tß4) pre-treated EPC transplantation in patients with acute ST segment elevation myocardial infarction (STEMI). METHODS: Ten patients with STEMI were included; they were randomized to 2 groups: EPC transplantation group (control group; n = 5) and Tß4-pre-treated EPC transplantation group (experimental group; n = 5). EPCs were pre-treated with Tß4 24 hours before transplantation in experimental group. Cardiac function was evaluated using echocardiography and emission computed tomography, as well as the 6-min walking test before and 6 months after the intervention. RESULTS: After 6 months of follow-up, the average 6-min walking distance was increased by 38.2 m (from 263 ± 42 m to 302 ± 34 m) in the control group and 75.7 m (from 264 ± 42 m to 340 ± 44 m) in the experimental group; the average difference of the 6-min walking distance was 37.5 m (95% confidence interval [CI], 28.7-56.3 m; P < 0.01). In addition, the cardiac function in the experimental group was more significantly improved than that of the control group. There were no severe complications related to the procedure in either group during the follow-up. DISCUSSION: Our pilot study suggested that Tß4-optimized EPC transplantation appeared to be feasible and safe, and might have beneficial effects on exercise capacity and left ventricular function in patients with STEMI.

Anti-inflammatory effect of methanolic extract of Conyzacanadensis in lipopolysaccharide (LPS)-stimulated RAW264.7 murine macrophage cells.

The aim of this study was to investigate the potential anti-inflammatory effect of Conyzacanadeusis methanol extract (CME) using a cell model of RAW264.7 murine macrophage cell stimulated with lipopolysaccharide (LPS)(1µg/ml). Co-treatment with different concentrations (10, 50 and 100µg/ml) of CME was concentration-dependently reduced the LPS-induced generation of prostaglandin E2 (PGE2), nitric oxide (NO) tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-6. In addition, CME also reduced the mRNA expressions of cyclooxygenase-2 (COX-2), inducible nitric oxide (iNOS), TNF-α, IL-1ß and IL-6 in LPS-stimulated RAW264.7 cells. These results suggested that CME showed an anti-inflammatory activity through reduced the mRNA expression of COX-2, iNOS, TNF-α IL-1ß and IL-6 and also decreased the productions of PGE2, NO, TNF-α IL-1ß and IL-6in LPS-stimulated RAW264.7 cells.