Unraveling the energy storage mechanism in graphene-based nonaqueous electrochemical capacitors by gap-enhanced Raman spectroscopy.

Graphene has been extensively utilized as an electrode material for nonaqueous electrochemical capacitors. However, a comprehensive understanding of the charging mechanism and ion arrangement at the graphene/electrolyte interface remain elusive. Herein, a gap-enhanced Raman spectroscopic strategy is designed to characterize the dynamic interfacial process of graphene with an adjustable number of layers, which is based on synergistic enhancement of localized surface plasmons from shell-isolated nanoparticles and a metal substrate. By employing such a strategy combined with complementary characterization techniques, we study the potential-dependent configuration of adsorbed ions and capacitance curves for graphene based on the number of layers. As the number of layers increases, the properties of graphene transform from a metalloid nature to graphite-like behavior. The charging mechanism shifts from co-ion desorption in single-layer graphene to ion exchange domination in few-layer graphene. The increase in area specific capacitance from 64 to 145 µF cm-2 is attributed to the influence on ion packing, thereby impacting the electrochemical performance. Furthermore, the potential-dependent coordination structure of lithium bis(fluorosulfonyl) imide in tetraglyme ([Li(G4)][FSI]) at graphene/electrolyte interface is revealed. This work adds to the understanding of graphene interfaces with distinct properties, offering insights for optimization of electrochemical capacitors.

Optical power degradation mechanisms in 271†nm AlGaN-based deep ultraviolet light-emitting diodes.

The degradation of AlGaN-based UVC LEDs under constant temperature and constant current stress for up to 500 hrs was analyzed in this work. During each degradation stage, the two-dimensional (2D) thermal distributions, I-V curves, optical powers, combining with focused ion beam and scanning electron microscope (FIB/SEM), were thoroughly tested and analyzed the properties and failure mechanisms of UVC LEDs. The results show that: 1) the opto-electrical characteristics measured before/during stress indicate that the increased leakage current and the generation of stress-induced defects increase the non-radiative recombination in the early stress stage, resulting in a decrease in optical power; 2) the increase of temperature caused by the deterioration of the Cr/Al layer of p-metal after 48 hrs of stress aggravates the optical power in UVC LEDs. The 2D thermal distribution in conjunction with FIB/SEM provide a fast and visual way to precisely locate and analyze the failure mechanisms of UVC LEDs.

Five Tibetan patent medicines orally for ischemic stroke: A systematic review and meta-analysis of randomized controlled trials.

ETHNOPHARMACOLOGICAL RELEVANCE: Tibetan Patent Medicines (TPMs) have unique advantages in the treatment of ischemic stroke (IS) with the features of multi-component, multi-channel, and multi-target. In China, five TPMs mainly consisting of precious medicinal materials such as gold, pearls, and agate are widely utilized to treat IS and have achieved good results according to the current clinical practice. AIM OF THE STUDY: To systematically evaluate the efficacy and safety of the five TPMs orally in treating IS and provide a reference for future clinical application and research. MATERIALS AND METHODS: We searched the following 24 databases up to December 11, 2022: China National Knowledge Infrastructure (CNKI), Wanfang database, China Science and Technology Journal Database, Chinese Biomedical Database (CBM), PubMed, Embase, Web of Science, MEDLINE, Scopus, the Cochrane Library, ScienceDirect, etc. Comprehensive searches for randomized controlled trials (RCTs) of the five TPMs for IS were conducted. Outcome measures included clinical effective rate, neurological impairment score, activities of daily living (ADL), hematologic indices, and adverse events (AEs). The meta-regression, subgroup analyses, and sensitivity analyses were conducted to explore the sources of heterogeneity. We assessed the evidence grade of outcomes via the GRADE system. TSA software was used for trial sequential analyses of the clinical effective rate, neurological impairment score, and ADL. RESULTS: 17 RCTs (1603 patients) met our criteria. Compared with the control groups, the five TPMs showed greater improvement in clinical effective rate (RR = 1.23, 95% CI 1.17 to 1.29, P < 0.00001), neurological impairment score (SMD = -1.71, 95% CI -2.31 to -1.10, P < 0.00001), ADL (SMD = 1.97, 95% CI 1.26 to 2.68, P < 0.00001), hematocrit (MD = -1.56, 95% CI -2.83 to -0.29, P = 0.02), and hypersensitive-c-reactive-protein (MD = -2.96, 95% CI -3.30 to -2.61, P < 0.00001). AEs were reported in four RCTs and there was no statistical difference between groups (RD = -0.00, 95% CI -0.04 to 0.03, P = 0.82). The quality of evidence of the outcomes was rated as low to very low according to the GRADE system. The results of TSA provided firm evidence for the significant effect of the five TPMs on clinical effective rate, neurological impairment score, and ADL. CONCLUSIONS: This review showed that the five TPMs were beneficial in improving clinical effective rate, neurological impairment scores, and ADL. However, no definite conclusions for hematologic indices and AEs were drawn due to insufficient studies. Further high-quality clinical trials are required to confirm these findings.

Acyl-coenzyme A binding protein MoAcb1 regulates conidiation and pathogenicity in Magnaporthe oryzae.

Magnaporthe oryzae is a filamentous fungus that causes rice blast. Rice blast seriously threatens the safety of food production. The normal synthesis and metabolism of fatty acids are extremely important for eukaryotes, and acyl-CoA is involved in fatty acid metabolism. Acyl-CoA binding (ACB) proteins specifically bind both medium-chain and long-chain acyl-CoA esters. However, the role of the Acb protein in plant-pathogenic fungi has not yet been investigated. Here, we identified MoAcb1, a homolog of the Acb protein in Saccharomyces cerevisiae. Disruption of MoACB1 causes delayed hyphal growth, significant reduction in conidial production and delayed appressorium development, glycogen availability, and reduced pathogenicity. Using immunoblotting and chemical drug sensitivity analysis, MoAcb1 was found to be involved in endoplasmic reticulum autophagy (ER-phagy). In conclusion, our results suggested that MoAcb1 is involved in conidia germination, appressorium development, pathogenicity and autophagy processes in M. oryzae.

Effects of Information Technology-Based Two-Way Referral on Diagnosis and Management of Cervical Lesions: A Cluster-Controlled Trial in China.

This study investigates the effectiveness of information technology-based 2-way referral in the diagnosis and management of cervical lesions in Minhang District, Shanghai, China. Women who underwent screening for cervical lesions in 4 community health centers constituted the intervention group, whereas women from the other 9 community health centers were included as controls. The diagnosis rate of cervical lesions was higher in the intervention group (7.61%) than in the control group (0.36%; P = .000). The diagnosis rate of early cervical lesion was 97.11% in the intervention group and 85.71% in the control group, showing no statistically significant differences ( P = .080). However, early diagnosis rate of precancerous lesion was much higher in the intervention group (95.45%) compared with the control group (64.29%; P = .001). In conclusion, higher effectiveness of early diagnosis and management of cervical lesions was observed in the intervention group compared with the control group.

[Effect and mechanism of danshensu on hepatitis B virus reverse transcriptase and antigen expression].

MTT assay was used in this study to investigate the inhibitory effect of danshensu on the activity of 2.2.15 cells among human hepatoma cell line (HepG2); indirect fluorescence labeling method was used to measure the changes of reactive oxygen levels in the cells; ELISA method was used to determine hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) levels in cellular supernatants; HBV DNA level was measured with fluorogenic quantitative PCR method. The inhibitory effect of danshensu on HBV RT(hepatitis B virus reverse transcriptase) was studied by using enzyme inhibition dynamics, and the effect of danshensu on secondary structure of HBV reverse transcriptase was monitored by using circular dichroism. The results showed that danshensu had a good inhibitory effect on the growth of HepG2.2.15 cells, with a half inhibitory concentration (IC50) of (15.35±2.43) µmol•L⁻¹; danshensu could significantly inhibit HBsAg and HBeAg expressions, and showed an inhibitory effect on HBV DNA replication. In addition, danshensu was an effective inhibitor for HBV reverse transcriptase [IC50 (21.32±2.43) µmol•L⁻¹]. The fluorescence labeling results showed that the reactive oxygen levels in the cells were increased with the increase of danshensu concentration. Circular dichroism analysis showed that danshensu could induce partial change of conformation of HBV reverse transcriptase and gradually increased α-helical content. These results indicated that danshensu could make the structure of the enzyme become closer by binding to HBV reverse transcriptase, which was not conducive to the formation of the active center, so it could finally decrease the activity of HBV reverse transcriptase. Such decrease in enzyme activity would directly affect the HBV DNA replication, and combined with the decrease of the antigen levels, the effect of danshensu on HBV was increased.

Ginsenoside Rg1 relieves tert-Butyl hydroperoxide-induced cell impairment in mouse microglial BV2 cells.

Microglial activation plays an important role in neurodegenerative diseases associated with oxidative stress. tert-Butyl hydroperoxide (t-BHP), an analog of hydroperoxide, mimics the oxidative damage to microglial cells. It has been reported that ginsenoside Rg1 (G-Rg1), an active ingredient of Panax ginseng, has anti-stress and anti-inflammatory properties. The present study aims to investigate the ability of G-Rg1 to decrease the t-BHP-mediated cell damage of BV2 microglial cells. We performed flow cytometry assays to facilitate the detection of reactive oxygen species as well as Western blotting analyses and immunofluorescence assays using specific antibodies, such as antibodies against phospho-mitogen-activated protein kinases (p-MAPKs), phospho-nuclear factor-κB (p-NF-κB), B-cell lymphoma 2 (Bcl-2), Bcl-2-associated X (Bax), Caspase-3, autophagy marker light chain 3 (LC3), and Becline-1. We found that treatment with 50 µM G-Rg1 protected microglial cells against oxidative damage induced by 10 µM t-BHP.

mGluR5 Upregulation increases excitability of hypothalamic presympathetic neurons through NMDA receptor trafficking in spontaneously hypertensive rats.

The hypothalamic paraventricular nucleus (PVN) is critically involved in elevated sympathetic output and the development of hypertension. However, changes in group I metabotropic glutamate receptors (mGluR1 and mGluR5) and their relevance to the hyperactivity of PVN presympathetic neurons in hypertension remain unclear. Here, we found that selectively blocking mGluR5 significantly reduced the basal firing activity of spinally projecting PVN neurons in spontaneously hypertensive rats (SHRs), but not in normotensive Wistar-Kyoto (WKY) rats. However, blocking mGluR1 had no effect on the firing activity of PVN neurons in either group. The mRNA and protein levels of mGluR5 in the PVN and rostral ventrolateral medulla were significantly higher in SHRs than in WKY rats. The group I mGluR selective agonist (S)-3,5-dihydroxyphenylglycine (DHPG) similarly increased the firing activity of PVN neurons in WKY rats and SHRs. In addition, blocking NMDA receptors (NMDARs) through bath application or intracellular dialysis not only decreased the basal firing in SHRs, but also eliminated DHPG-induced excitation of spinally projecting PVN neurons. DHPG significantly increased the amplitude of NMDAR currents without changing their decay kinetics. Interestingly, DHPG still increased the amplitude of NMDAR currents and caused reappearance of functional NMDAR channels after initially blocking NMDARs. In addition, protein kinase C (PKC) inhibition or intracellular dialysis with synaptosomal-associated protein of 25 kDa (SNAP-25)-blocking peptide abolished DHPG-induced increases in NMDAR currents of PVN neurons in SHRs. Our findings suggest that mGluR5 in the PVN is upregulated in hypertension and contributes to the hyperactivity of PVN presympathetic neurons through PKC- and SNAP-25-mediated surface expression of NMDARs.

The inhibitory effect of Binens bipinnata L. extract on U14 tumour in mice.

The objective of this paper was to study the in vitro and in vivo inhibitory effect of Bidens bipinnata L. extract on growth of cervical carcinoma U14 cells. MTT method was used to determine the inhibitory effect of Bidens bipinnata L. extract on U14 tumour cells, and the effects of Bidens bipinnata L. extract on inhibition rate of solid tumour and life prolongation rate of ascites tumour were observed through the establishment of two animal models of mouse cervical carcinoma U14 solid tumour and ascites tumour. In the in vitro MTT assay, the inhibition rate gradually increased with the increase of dose of Bidens bipinnata L. and the extension of time. Its inhibition rate was 70.44% at a concentration of 80µg/L. Solid tumour inhibition rates in the high- and low-dose groups and cisplatin group were 49.13%, 2.26% and 75.72% respectively; life prolongation rates in each ascites tumour group were 63.63%, 34.86% and 87.34% respectively. The Bidens bipinnata L. extract has a certain inhibitory effect on growth of mouse cervical carcinoma U14.

[Effects of antagonist and agonist of nicotinic acetylcholine receptors on injury of rat neurons induced by amyloid ß-protein].

OBJECTIVE: To explore the chronic effects of nicotinic antagonist and agonist on rat neurons injury induced by ß-amyloid protein. METHODS: The rat model of neuron injury was established by the exposure to Aß25-35 and the intervention agent was either methyllycaconitine (MLA) or nicotine (Nic). And the experimental groups were control (distilled water), Aß25-35, MLA (MLA and Aß25-35) and Nic (Nic and Aß25-35). Cellular viability was detected by methyl thiazolyl tetrazolium (MTT) chromatometry while apoptosis and necrosis were detected by flow cytometer. RESULTS: Compared with control, cellular viability decreased while the apoptotic and necrotic rates increased in Aß25-35 group(P = 0.00). The values of cellular viability at (0.75 ± 0.02) and (0.75 ± 0.09) in Aß25-35 and MLA groups respectively were significantly lower than that of Nic group (0.81 ± 0.02, P = 0.01) at Day 3 and 7. No significant differences existed in cellular viability between Aß25-35 and MLA groups. At Day 14, the differences of cellular viability were not obvious in all groups. At Day 21, cell viability of MLA group (0.64 ± 0.10) was significantly higher than those of Aß25-35 (0.57 ± 0.04, P = 0.019) and Nic groups (0.56 ± 0.04, P = 0.008). The apoptotic rate was lower than that of Aß25-35 group (3.70% ± 0.20% vs 4.70% ± 0.46%, P = 0.008) while the necrotic rate lower than that of Aß25-35 group (7.73% ± 0.86% vs 16.30% ± 1.05%, P = 0.00) and Nic group (16.03% ± 1.53%, P = 0.00). However, no significant differences existed in cellular viability or apoptotic and necrotic rate between Aß25-35 and Nic groups. CONCLUSION: With chronic treatment, the protective effect of α7 nicotinic antagonist methyllycaconitine increases whereas that of nicotinic agonist nicotine decreases.

[Relevance of erythrocyte parameters on fluid management in critical care].

OBJECTIVE: To manage fluid therapy in severely ill patients through investigating the relationship between erythrocyte parameters and central venous pressure (CVP) and its denoted blood volume. METHODS: The research project was divided into two parts. Part I: CVP and concurrent erythrocyte parameters [red blood count (RBC), hemoglobin (Hb), haematocrit (HCT)] were serially recorded in a severely ill patient every morning for 38 days. The obtained values of CVP were divided into three groups (<8 cm H2O group, 8-10 cm H2O group, >10 cm H2O group), then erythrocyte parameters of each period were compared to obtain the relationship among them. At the same time, "the best" CVP (blood volume was in suitable state) and "the best" erythrocyte parameters (accordingly the blood was not be diluted or concentrated) were obtained. Part II: "the best" CVP and corresponding "the best" erythrocyte parameters were determined in another patient. When the patient's blood volume was in doubt, detected her erythrocyte parameters right away. If the variance between the "practical" and "the best" values was notable, blood volume replenishment or diureses were performed. Then the resulting CVP of fluid expansion or diuresis before and after the treatment were compared, or else other influencing factors should be seeked. RESULTS: Part I: the values of RBC, Hb and HCT in group CVP>10 cm H2O were lower than those of group CVP<8 cm H2O and CVP 8-10 cm H2O (RBC: 3.05±0.32×10(9)/L vs. 3.59±0.25×10(9)/L, 3.42±0.24×10(9)/L; Hb: 85.3±6.8 g/L vs. 104.2±3.6 g/L, 97.5±4.9 g/L; HCT: 0.271±0.023 vs. 0.321±0.015, 0.309±0.019, all P<0.01), and Hb in group CVP 8-10 cm H2O was lower than group CVP<8 cm H2O (97.5±4.9 g/L vs. 104.2±3.6 g/L, P<0.01). CVP was negatively correlated with RBC, Hb and HCT, and coefficients of correlation (r value) were -0.735, -0.903 and -0.822, respectively (all P<0.01), and positive correlations were found among RBC, Hb and HCT, with r value 0.804, 0.931 and 0.863, respectively (all P<0.01). The patient's vital signs were stable when CVP was 8 to 10 cm H2O, therefore it was assigned as "the best" CVP, and the corresponding "the best" erythrocyte parameters were determined (RBC was 3.43×10(9)/L, Hb was 97.4 g/L, HCT was 0.310). Part II: "the best" CVP of the this patient was 8 to 10 cm H2O too, accordingly "the best" erythrocyte parameter in term of Hb was 105 g/L. The CVP was obviously elevated in the group in which Hb was higher than "the best" Hb subsequent to fluid expansion (8.29±1.80 cm H2O vs. 5.86±1.57 cm H2O, P<0.05), and the CVP was obvious lowered in the group which Hb was lower than "the best" Hb through diuresis (8.80±2.39 cm H2O vs. 12.20±1.92 cm H2O, P<0.05). CONCLUSION: CVP was negatively correlated with erythrocyte parameters, "the best" erythrocyte parameters accompanying "the best" CVP would probably guide fluid therapy best in severely ill patients.

Inhibition of signal transducer and activator of transcription 3 and cyclooxygenase-2 is involved in radiosensitization of cepharanthine in HeLa cells.

OBJECTIVES: To investigate the radiosensitizing effects of cepharanthine (CEP) in the human cervical adenocarcinoma HeLa cell line and to examine the underlying mechanisms. MATERIALS/METHODS: Survival of HeLa cells after treatment with or without ionizing radiation (IR) and CEP administration was investigated. MTT assays and apoptosis analysis were used to assess cytotoxicity. Nude mouse xenografts were established to evaluate the antitumor effects of CEP and IR in vivo. Expression of signal transducer and activator of transcription 3 (STAT3) and its downstream signaling molecules as well as cyclooxygenase-2 (COX-2) were examined by Western blot analysis. RESULTS: Clonogenic assays showed that treatment with CEP and IR resulted in significant radiosensitization. Cepharanthine and IR treatment achieved maximum cytotoxic effects on HeLa cells with regard to apoptosis induction. Cepharanthine efficiently decreased IR-induced STAT3 and COX-2 activation. The STAT3 target genes, including the antiapoptotic Bcl-2 and the cell cycle regulator c-Myc, were decreased concomitantly. In vivo administration of CEP (20 mg/kg every 2 days) combined with radiation in HeLa xenografts enhanced tumor growth delay and apoptosis (indicated by activated caspase-3 Western blot analysis), with reduced expression of STAT3, Bcl-2, c-Myc, and COX-2. CONCLUSIONS: Cepharanthine was shown to induce radiation sensitization in HeLa cells in vitro and in vivo. The inhibitory effects of CEP on STAT3 signaling pathway and COX-2 help us to better understand the radiosensitization of CEP.

N,N-Dimethyl-N,N-diphenyl-pyrimidine-4,5,6-triamine.

In the title compound, C(18)H(19)N(5), the pyrimidine ring makes dihedral angles of 56.49 (9) and 70.88 (9)° with the phenyl rings. The dihedral angle between the two phenyl rings is 72.45 (9)°. No significant inter-molecular inter-actions are observed in the crystal structure.

N,N-Dimethyl-5-nitro-N,N-diphenyl-pyrimidine-4,6-diamine.

In the title compound, C(18)H(17)N(5)O(2), the pyrimidine ring makes dihedral angles of 66.09 (12), 71.39 (13) and 56.7 (3)° with two phenyl rings and the nitro group, respectively. The dihedral angle between the two phenyl rings is 44.05 (14)°.

6-Chloro-N-methyl-N-phenyl-pyrimidine-4,5-diamine.

In the title compound, C(11)H(11)ClN(4), the dihedral angle between the aromatic rings is 66.47 (8)°. In the crystal, mol-ecules are linked by N-H⋯N hydrogen bonds, generating C(5) chains propagating in [010]. Slipped aromatic π-π stacking between centrosymmetrically related pairs of pyrim-idine rings also occurs [centroid-centroid separation = 3.7634 (12)Å and slippage = 1.715 Å].

Luteolin reduces primary hippocampal neurons death induced by neuroinflammation.

OBJECTIVES: This study examined whether luteolin may exert an anti-inflammatory effect in microglia and may be neuroprotective by regulating microglia activation. METHODS: We treated BV2 microglia with 1.0 µg/ml lipopolysaccharide (LPS) after incubation with luteolin for 1 hour, the nitric oxide (NO) levels were determined by a Griess reaction, the inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor-alpha (TNF-alpha), and interleukin 1beta (IL-1beta) mRNA expression were determined by real-time PCR analysis, the iNOS and COX-2 protein induction were determined by Western blot analysis, and the levels of prostaglandin E(2) (PGE(2)), TNF-alpha, and IL-1beta were determined by enzyme-linked immunosorbent assay (ELISA) kits. Rat primary hippocampal neurons were co-cultured with LPS-activated BV2 microglia with 20 µM luteolin for 24 hours, the hippocampal neurons viability was determined by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, and the number of apoptotic hippocampal neurons was determined by immunofluorescence detection. RESULTS: Luteolin significantly inhibited the expression of iNOS and COX-2 in LPS-induced BV2 microglia. Moreover, the compound down-regulated the proinflammatory cytokines (TNF-alpha and IL-1beta) as well as the production of NO and PGE(2) in these cells. When hippocampal neurons were co-cultured with LPS-stimulated BV2 microglia, the administration of 20 µM luteolin increased the neurons viability and reduced the number of apoptotic neurons. CONCLUSION: These data demonstrate that anti-inflammatory activity of luteolin in microglia contributes to its neuroprotective effect and suggest that it may have a potential therapeutic application in the treatment of neurodegenerative diseases.

6-Chloro-N-methyl-5-nitro-N-phenyl-pyrimidin-4-amine.

In the title compound, C(11)H(9)ClN(4)O(2), the dihedral angle between the aromatic rings is 79.67 (8)°. π-π stacking between centrosymmetrically related pairs of pyrimidine rings occurs along [100] [centroid-centroid separations = 3.4572 (8) and 3.5433 (7) Å].

Induction of apoptosis by evodiamine involves both activation of mitotic arrest and mitotic slippage.

Evodiamine (Evo) is an indole quinazoline alkaloid isolated from the fruit of Evodia rutaecarpa Bentham. Previous studies have shown that Evo exhibits anti-proliferative anti-tumor activities in several cancer types, but its target(s) and underlying mechanism(s) of action remain unclear. In the present study, we sought to establish a cell synchronization model in order to examine the anti-proliferative and apoptotic mechanisms of Evo in the human gastric cancer cell line SGC-7901. In addition, we transfected these cells with full-length or non-degradable (ND) cyclinB1 to evaluate the relationship between the induction of apoptosis and activation of mitotic arrest and mitotic slippage by Evo. Our results demonstrated that Evo markedly inhibited cell growth and was cytotoxic to SGC-7901 cells. Furthermore, transient Evo treatment (<16 h) caused reversible mitotic arrest, but sustained mitotic arrest was required to initiate apoptosis. The time required to reverse the apoptotic effects of Evo was between 16 and 20 h. We also demonstrated that promotion of mitotic slippage by a CDK1 inhibitor enhanced apoptosis. Furthermore, we evaluated the effect of delaying mitotic slippage by overexpressing ND cyclinB1, which delayed apoptosis. In conclusion, these results indicate that Evo-induced apoptosis is associated with mitotic arrest and subsequent mitotic slippage, which may underlie the actions of Evo in the treatment and prevention of cancer.

Luteolin inhibits microglial inflammation and improves neuron survival against inflammation.

Microglia activation is one of the causative factors for neuroinflammation, which results in brain damage during neurodegenerative disease. Accumulating evidence has shown that the flavonoid luteolin (Lut) possesses potent anti-inflammatory properties; however, its effect on microglia inhibition is currently unknown. Moreover, it is not clear whether Lut also has indirect neuroprotective effects by reducing inflammatory mediators and suppressing microglia activation. In this study, we examined the effects of Lut on lipopolysaccharide (LPS)-induced proinflammatory mediator production and signaling pathways in murine BV2 microglia. In addition, we cocultured microglia and neurons to observe the indirect neuroprotective effects of Lut. Lut inhibited the LPS-stimulated expression of inducible NO synthase (iNOS), cyclooxygenase-2 (COX-2), tumor necrosis factor alpha (TNF-α), and interleukin-1ß (IL-1ß) as well as the production of nitric oxide (NO) and prostaglandin E(2) (PGE(2)). Moreover, Lut blocked LPS-induced nuclear factor kappa B (NF-κB) activation. Preincubation of microglia with Lut diminished the neurotoxic effects, owing to the direct anti-inflammatory effects of the compound. Taken together, our findings suggest that Lut may have a potential therapeutic application in the treatment of neuroinflammatory disorders.