Leucine-rich repeat flightless-I-interacting protein 2 (LRRFIP2) is a myeloid differentiation factor 88-interacting protein with a positive regulatory function in toll-like receptor signaling. In this study, seven LRRFIP2 protein variants (LvLRRFIP2A-G) were identified in Litopenaeus vannamei. All the seven LvLRRFIP2 protein variants encode proteins with a DUF2051 domain. LvLRRFIP2s were upregulated in hemocytes after challenged with lipopolysaccharide, poly I:C, CpG-ODN2006, Vibrio parahaemolyticus, Staphylococcus aureus, and white spot syndrome virus (WSSV). Dual-luciferase reporter assays in Drosophila Schneider 2 cells revealed that LvLRRFIP2 activates the promoters of Drosophila and shrimp AMP genes. The knockdown of LvLRRFIP2 by RNA interference resulted in higher cumulative mortality of L. vannamei upon V. parahaemolyticus but not S. aureus and WSSV infections. The expression of L. vannamei AMP genes were reduced by dsLvLRRFIP2 interference. These results indicate that LvLRRFIP2 has an important function in antibacterials via the regulation of AMP gene expression.
Stress contributes to a variety of diseases and disorders such as depression and peptic ulcer. The present study aimed to investigate the correlation between stress ulcer and depression in pathogenesis and treatment by using chronic stress depression (CSD), chronic psychological stress ulcer (CPSU) and water immersion restrain stress models in rats. Our data showed that the ulcer index of the animals after CSD exposure was significantly higher than that of controls. Depression-like behaviors were observed in rat after CPSU exposure. Fluoxetine hydrochloride significantly reduced the ulcer index of rats exposed to CPSU stress, while ranitidine inhibited depression-like behavior of the animals in CSD group. The ulcer index of rats administered with mifepristone after CPSU stress was markedly reduced compared to CPSU group, although there was no significant difference in the depression-like behavior between mifepristone-treated CSD group and naive controls. We also found that the rats exposed to CPSU or CSD stress displayed a lower level of corticosterone than naive controls, however, the acute stress (AS) group showed an opposite result. Additionally, in order to study the relevance of H2 receptors and depression, we treated the CSD group with cimetidine and famotidine respectively. The data showed that cimetidine inhibited depression-like behavior in CSD rats, and famotidine had no impact on depression. Overall our data suggested that the hypothalamic-pituitary-adrenal (HPA) axis dysfunction may be the key role in triggering depression and stress ulcer. Acid-suppressing drugs and antidepressants could be used for treatment of depression and stress ulcer respectively. The occurrence of depression might be inhibited by blocking the central H2 receptors.
Hypoxia/reoxygenation(H/R)-induced apoptosis of cardiomyocytes plays an important role in myocardial injury. Lycopene is a potent antioxidant carotenoid that has been shown to have protective properties on cardiovascular system. The aim of the present study is to investigate the potential for lycopene to protect the cardiomyocytes exposed to H/R. Moreover, the effect on mitochondrial function upon lycopene exposure was assessed.
Methods and Findings
Primary cardiomyocytes were isolated from neonatal mouse and established an in vitro model of H/R which resembles ischemia/reperfusion in vivo. The pretreatment of cardiomyocytes with 5 µM lycopene significantly reduced the extent of apoptosis detected by TUNEL assays. To further study the mechanism underlying the benefits of lycopene, interactions between lycopene and the process of mitochondria-mediated apoptosis were examined. Lycopene pretreatment of cardiomyocytes suppressed the activation of the mitochondrial permeability transition pore (mPTP) by reducing the intracellular reactive oxygen species (ROS) levels and inhibiting the increase of malondialdehyde (MDA) levels caused by H/R. Moreover, the loss of mitochondrial membrane potential, a decline in cellular ATP levels, a reduction in the amount of cytochrome c translocated to the cytoplasm and caspase-3 activation were observed in lycopene-treated cultures.
The present results suggested that lycopene possesses great pharmacological potential in protecting against H/R-induced apoptosis. Importantly, the protective effects of lycopene may be attributed to its roles in improving mitochondrial function in H/R-treated cardiomyocytes.
The nuclear factor-kappa B (NF-κB) pathways play important roles in innate immune responses. IκB is the main cytoplasmic inhibitor of NF-κB. In this study, we identified the LvCactus gene from Litopenaeus vannamei, which is the first cloned IκB homologue in subphylum Crustacea. LvCactus contains six predicted ankyrin repeats, which show similarities to those of Cactus proteins from insects. LvCactus localizes in cytoplasm and interacts with LvDorsal, an L. vannamei homologue to Drosophila melanogaster Dorsal belonging to class II NF-κB family, to prevent its nuclear translocation. Contrary to that of LvDorsal, over-expression of LvCactus down-regulates the activities of shrimp antimicrobial peptides promoters, suggesting LvCactus is an inhibitor of LvDorsal. The promoter of LvCactus was predicted to contain five putative NF-κB binding motifs, among which four were proved to be bound by LvDorsal by chromatin immunoprecipitation assays. Dual-luciferase reporter assays also showed that transcription of LvCactus was promoted by LvDorsal but inhibited by LvCactus itself, indicating a feedback regulatory pathway between LvCactus and LvDorsal. Expression of LvCactus was up-regulated after Lipopolysaccharides, poly (I:C), Vibrio parahaemolyticus, and Staphylococcus aureus injections, suggesting an activation response of LvCactus to bacterial and immune stimulant challenges. Differently, the LvCactus expression levels obviously decreased during white spot syndrome virus (WSSV) infection, indicating the feedback regulatory pathway of LvCactus/LvDorsal could be modified by WSSV.
Myeloid differentiation factor 88 (MyD88) is a universal and essential signaling protein in Toll-like receptor/interleukin-1 receptor-induced activation of nuclear factor-kappa B. In this study, two MyD88 protein variants (LvMyD88 and LvMyD88-1) were identified in Litopenaeus vannamei. The LvMyD88 cDNA is 1,848 bp in length and contains an open reading frame (ORF) of 1,428 bp, whereas the LvMyD88-1 cDNA is 1,719 bp in length and has an ORF of 1,299 bp. Both variants encode proteins with death and Toll/interleukin-1 receptor domains and share 91% sequence identity. In healthy L. vannamei, the LvMyD88 genes were highly expressed in hemocytes but at a low level in the hepatopancreas. The LvMyD88s expression was induced in hemocytes after challenge with lipopolysaccharide, CpG-ODN2006, Vibrio parahaemolyticus, Staphyloccocus aureus, and white spot syndrome virus, but not by poly I∶C. Overexpression of LvMyD88 and LvMyD88-1 in Drosophila Schneider 2 cells led to activation of antimicrobial peptide genes and wsv069 (ie1), wsv303, and wsv371. These results suggested that LvMyD88 may play a role in antibacterial and antiviral response in L. vannamei. To our knowledge, this is the first report on MyD88 in shrimp and a variant of MyD88 gene in invertebrates.
To explore the association of ALOX5AP single nucleotide polymorphisms (SNPs) and haplotype with the occurrence of cerebral infarction in the Han population of northern China.
Blood samples were collected from 236 patients of Han ancestry with a history of cerebral infarction and 219 healthy subjects of Han ancestry with no history of cerebral infarction or cardiovascular disease. Applied Biosystems® TaqMan® SNP Genotyping Assays for SNP genotyping were used to determine the genotypes of 7 ALOX5AP SNP alleles (rs4073259, rs4769874, rs9315050, rs9551963, rs10507391, rs9579646, and rs4147064).
One SNP allele (A) of rs4073259 was significantly associated with development of cerebral infarction (P = 0.049). In comparison to control groups, haplotype rs9315050&rs9551963 AAAC [OR (95% CI) =1.53 (1.02-2.29)], and genotypes rs4147064 CT [OR (95% CI) =1.872 (1.082-3.241)], and rs9551963 AC [OR (95% CI) = 2.015 (1.165-3.484)] increased the risk of cerebral infarction in patients with hypertension. Genotype rs9579646 GG [OR (95% CI) = 2.926 (1.18-7.251)] increased the risk of, while rs4073259 GG [OR (95% CI) = 0.381 (0.157-0.922)] decreased the risk of cerebral infarction in patients with diabetes.
These results suggest the ALOX5AP SNP A allele in rs4073259 and genotype rs9579646 GG, rs9551963 AC, and haplotype rs9315050 & rs9551963 AAAC were associated with an increased risk of ischemic stroke in the Han population, while rs4073259 GG was associated with a decreased risk.
Cerebral infarction; ALOX5AP; FLAP; Han ethnicity; SNP
Platelet aggregation mediated by inflammation played a critical role in the development of coronary heart diseases (CHD). Our previous clinical researches showed that Th17 cells and their characteristic cytokine IL-17A were associated with the plaque destabilization in patients with acute coronary syndrome (ACS). However, the potent effect of IL-17A on platelets-induced atherothrombosis remains unknown.
Methods and Results
In this study, we detected the plasma IL-17A levels and platelet aggregation in patients with stable angina (SA), unstable angina (UA), acute myocardial infarction (AMI) and chest pain syndrome (CPS). In addition, the markers of platelet activation (CD62P/PAC-1) and the mitogen-activated protein kinases (MAPKs) pathway were detected in platelets from ACS patients. We found that plasma IL-17A levels and platelet aggregation in patients with ACS (UA and AMI) were significantly higher than patients with SA and CPS, and the plasma IL-17A levels were positively correlated with the platelet aggregation (R = 0.47, P<0.01). In addition, in patients with ACS, the platelet aggregation, CD62P/PAC-1 and the phosphorylation of ERK2 signaling pathway were obviously elevated in platelets pre-stimulated with IL-17A in vitro. Furthermore, the specific inhibitor of ERK2 could attenuate platelet aggregation and activation triggered by IL-17A.
Our experiment firstly proved that IL-17A could promote platelet function in patients with ACS via activating platelets ERK2 signaling pathway and may provide a novel target for antiplatelet therapies in CHD.
In order to investigate the behavior, distribution, and characteristics of heavy metals including rare earth elements (REEs), thorium (Th), and uranium (U) in sludge, the total and fractional concentrations of these elements in sludge collected from an industry water treatment plant were determined and compared with those in natural soil. In addition, the removal/recovery process of heavy metals (Pb, Cr, and Ni) from the polluted sludge was studied with biosurfactant (saponin and sophorolipid) elution by batch and column experiments to evaluate the efficiency of biosurfactant for the removal of heavy metals. Consequently, the following matters have been largely clarified. (1) Heavy metallic elements in sludge have generally larger concentrations and exist as more unstable fraction than those in natural soil. (2) Nonionic saponin including carboxyl group is more efficient than sophorolipid for the removal of heavy metals in polluted sludge. Saponin has selectivity for the mobilization of heavy metals and mainly reacts with heavy metals in F3 (the fraction bound to carbonates) and F5 (the fraction bound to Fe-Mn oxides). (3) The recovery efficiency of heavy metals (Pb, Ni, and Cr) reached about 90–100% using a precipitation method with alkaline solution.
In the title herbicideh/phytocide, known as imazapic, C14H17N3O3, the pyridine and imidazole rings are almost coplanar [dihedral angle = 3.08 (5)°]. An intramolecular O—H⋯N hydrogen bond occurs. In the crystal, an N—H⋯O hydrogen bond links molecules into a chain parallel to .
Ant-aphid mutualism is known to play a key role in the structure of the arthropod community in the tree canopy, but its possible ecological effects for the forest floor are unknown. We hypothesized that aphids in the canopy can increase the abundance of ants on the forest floor, thus intensifying the impacts of ants on other arthropods on the forest floor. We tested this hypothesis in a deciduous temperate forest in Beijing, China. We excluded the aphid-tending ants Lasius fuliginosus from the canopy using plots of varying sizes, and monitored the change in the abundance of ants and other arthropods on the forest floor in the treated and control plots. We also surveyed the abundance of ants and other arthropods on the forest floor to explore the relationships between ants and other arthropods in the field. Through a three-year experimental study, we found that the exclusion of ants from the canopy significantly decreased the abundance of ants on the forest floor, but increased the abundance of beetles, although the effect was only significant in the large ant-exclusion plot (80*60 m). The field survey showed that the abundance of both beetles and spiders was negatively related to the abundance of ants. These results suggest that aphids located in the tree canopy have indirect negative effects on beetles by enhancing the ant abundance on the forest floor. Considering that most of the beetles in our study are important predators, the ant-aphid mutualism can have further trophic cascading effects on the forest floor food web.
Angiogenesis plays an important role in tumor growth and metastasis, therefore antiangiogenic therapy was widely investigated as a promising approach for cancer therapy. Recently, pigment epithelium-derived factor (PEDF) has been shown to be the most potent inhibitor of angiogenesis. Adeno-associated virus (AAV) vectors have been intensively studied due to their wide tropisms, nonpathogenicity, and long-term transgene expression in vivo. The objective of this work was to evaluate the ability of AAV-mediated human PEDF (hPEDF) as a potent tumor suppressor and a potential candidate for cancer gene therapy.
Recombinant AAV2 encoding hPEDF (rAAV2-hPEDF) was constructed and produced, and then was assigned for in vitro and in vivo experiments. Conditioned medium from cells infected with rAAV2-hPEDF was used for cell proliferation and tube formation tests of human umbilical vein endothelial cells (HUVECs). Subsequently, colorectal peritoneal carcinomatosis (CRPC) mouse model was established and treated with rAAV2-hPEDF. Therapeutic efficacy of rAAV2-hPEDF were investigated, including tumor growth and metastasis, survival time, microvessel density (MVD) and apoptosis index of tumor tissues, and hPEDF levels in serum and ascites.
rAAV2-hPEDF was successfully constructed, and transmission electron microscope (TEM) showed that rAAV2-hPEDF particles were non-enveloped icosahedral shape with a diameter of approximately 20 nm. rAAV2-hPEDF-infected cells expressed hPEDF protein, and the conditioned medium from infected cells inhibited proliferation and tube-formation of HUVECs in vitro. Furthermore, in CRPC mouse model, rAAV2-hPEDF significantly suppressed tumor growth and metastasis, and prolonged survival time of treated mice. Immunofluorescence studies indicated that rAAV2-hPEDF could inhibit angiogenesis and induce apoptosis in tumor tissues. Besides, hPEDF levels in serum and ascites of rAAV2-hPEDF-treated mice were significant higher than those in rAAV2-null or normal saline (NS) groups.
Thus, our results suggest that rAAV2-hPEDF may be a potential candidate as an antiangiogenic therapy agent.
AAV; PEDF; Tumor; Antiangiogesis; Gene therapy
Gene therapy provides a novel method for the prevention and treatment of cancer, but the clinical application of gene therapy is restricted, mainly because of the absence of an efficient and safe gene delivery system. Recently, we developed a novel nonviral gene carrier, ie, heparin-polyethyleneimine (HPEI) nanoparticles for this purpose.
Methods and results
HPEI nanoparticles were used to deliver plasmid-expressing mouse survivin-T34A (ms-T34A) to treat C-26 carcinoma in vitro and in vivo. According to the in vitro studies, HPEI nanoparticles could efficiently transfect the pGFP report gene into C-26 cells, with a transfection efficiency of 30.5% ± 2%. Moreover, HPEI nanoparticle-mediated ms-T34A could efficiently inhibit the proliferation of C-26 cells by induction of apoptosis in vitro. Based on the in vivo studies, HPEI nanoparticles could transfect the Lac-Z report gene into C-26 cells in vivo. Intratumoral injection of HPEI nanoparticle-mediated ms-T34A significantly inhibited growth of subcutaneous C-26 carcinoma in vivo by induction of apoptosis and inhibition of angiogenesis.
This research suggests that HPEI nanoparticle-mediated ms-T34A may have a promising role in C-26 colon carcinoma therapy.
gene therapy; mouse survivin-T34A; colon cancer; polyethyleneimine; nanoparticles; cancer therapy
In the title compound, [Cd(NO3)2(C18H16N2O2)2]n, the six-coordinated CdII ion is located on an inversion center and has a distorted octahedral environment defined by four N atoms from four 1,4-bis(pyridin-3-ylmethoxy)benzene ligands and two O atoms from two nitrate anions. The ligands link the CdII ions into a ribbon-like structure running along . One O atom of the nitrate anion is disordered over two positions with site-occupancy factors of 0.59 (2) and 0.41 (2).
Leptin, a 16 kDa nonglycosylated hormone, is produced by mature adipocytes and functions primarily in the hypothalamus to reduce food intake and body weight. To explore a new approach for high-level expression of human Leptin in Escherichia coli, the human Leptin gene, synthesized according to the published sequence, was cloned into the vector pET32a to construct a fusion expression plasmid: Trx–Leptin/pET32a. Our data showed that more than 40% of the fusion protein Trx–Leptin was expressed in soluble form. After purified by Ni-IDA affinity chromatography, cleaved by enterokinase and applied Ni-IDA affinity chromatography again, purified Leptin with homogeneity over 96% was achieved. The bio-functional experiments of purified Leptin showed a significant reduction in food intake and body weight of female mice treated with Leptin by comparing with control mice, and it indicated that the purified Leptin has full biological activity. In addition, our expression system was a very low-cost and efficient prokaryotic expression system. So taken together, our results demonstrated that our expression system of bio-active Leptin provided a new method for producing Leptin in big scale and would be widely applied in commercial Leptin producing industries.
Human leptin; Trx; Escherichia coli; Fusion expression; Enterokinase; Affinity purification
In the title compound, [CuCl2(C18H16N2O2)], the CuII atom lies on a twofold axis and is six-coordinated in a distorted octahedral environment defined by two N and two O atoms from the ligand and by two Cl atoms. In the crystal, π–π interactions [centroid–centroid distance = 3.838 (1) Å] and C—H⋯Cl hydrogen bonds link adjacent molecules into a chain structure along .
In the title compound, [Cu(CH3COO)2(C18H16N2O2)]·4H2O, the CuII ion is six-coordinated in a Jahn–Teller-distorted octahedral geometry environment defined by four O atoms and two N atoms. A chain structure along  is built up by intermolecular O—H⋯O hydrogen bonds involving the uncoordinated water molecules.
VEGF is a well-validated target for antiangiogenic intervention in cancer. To date, RNAi technology has been proven to be a promising approach for targeted therapy. DDP is frequently used as a first-line drug in chemotherapy for lung cancer but usually causes severe toxicity. In this study, we investigated a novel strategy of administering and combining RNAi mediated VEGF-targeted therapy with DDP for treatment of lung cancer, with the aim of increasing efficacy and decreasing toxicity.
In this study, a plasmid encoding VEGF shRNA was constructed to knockdown VEGF both in vitro and in vivo. In vitro, specificity and potency of the targeting sequence were validated in A549 lung adenocarcinoma cells by RT-PCR and ELISA assays. In vivo, therapy experiments were conducted on nude mice bearing A549 xenograft tumors. The VEGF shRNA expressing plasmids were administered systemically in combination with low-dose DDP on a frequent basis. The tumor volume and weight were measured. MVD, the number of apoptotic cells and proliferation index in tumor tissues were assessed by CD31, TUNEL and PCNA immunostaining.
The VEGF shRNA was highly effective in attenuating VEGF expression both in vitro and in vivo. The treatment with the VEGF shRNA alone reduced the mean tumor weight by 49.40% compared with the blank control (P < 0.05). The treatment with the VEGF shRNA plus DDP yielded maximal benefits by reducing the mean tumor weight by 83.13% compared with the blank control (P < 0.01). The enhanced antitumor efficacy was associated with decreased angiogenesis and increased induction of apoptosis.
Our study demonstrated synergistic antitumor activity of combined VEGF shRNA expressing plasmids and low-dose DDP with no overt toxicity, suggesting potential applications of the combined approach in the treatment of lung cancer.
In the title compound, [Cu(CH3COO)2(C18H16N2O2)]·H2O, the CuII ion is six-coordinated in a typically Jahn–Teller distorted octahedral environment defined by two O and two N atoms from the ligand and two O atoms from acetate anions. A linear chain structure propagating in  is built up by intermolecular O—H⋯O hydrogen bonds involving the uncoordinated water molecules.
PhaR which is a repressor protein for microbial polyhydroxyalkanoates (PHA) biosynthesis, is able to attach to bacterial PHA granules in vivo, was developed as an affinity tag for in vitro protein purification. Fusion of PhaR-tagged self-cleavable Ssp DnaB intein to the N-terminus of a target protein allowed protein purification with a pH and temperature shift. During the process, the target protein was released to the supernatant while PhaR-tagged intein was still immobilized on the PHA nanoparticles which were then separated by centrifugation.
Fusion protein PhaR-intein-target protein was expressed in recombinant Escherichia coli. The cell lysates after sonication and centrifugation were collected and then incubated with PHA nanoparticles to allow sufficient absorption onto the PHA nanoparticles. After several washing processes, self-cleavage of intein was triggered by pH and temperature shift. As a result, the target protein was released from the particles and purified after centrifugation. As target proteins, enhanced green fluorescent protein (EGFP), maltose binding protein (MBP) and β-galactosidase (lacZ), were successfully purified using the PhaR based protein purification method.
The successful purification of EGFP, MBP and LacZ indicated the feasibility of this PhaR based in vitro purification system. Moreover, the elements used in this system can be easily obtained and prepared by users themselves, so they can set up a simple protein purification strategy by themselves according to the PhaR method, which provides another choice instead of expensive commercial protein purification systems.
A specific and sensitive liquid chromatography (LC)-tandem mass spectrometric method for quantitative determination of methylprednisolone (MP) in rat plasma and liver was developed and validated using triamcinolone acetonide as an internal standard. Liquid-liquid extraction using tert-butyl methyl ether was used to extract the drug and the internal standard from plasma and liver. The separation of MP was performed on a C18 column with a mobile phase of acetonitrile:0.5% formic acid aqueous solution (85:15, v/v) over 4 min. The assay was based on the selected reaction monitoring transitions at m/z 375→161 for MP in plasma, 375→357 for MP in liver, and 435→415 for internal standard in both plasma and liver. The lower limit of quantification was 20 ng/mL based on 100 μL of plasma or liver homogenate. Intra- and inter-day assay variations were ≤15%, and the accuracy values were between 85.8 and 118%. The extraction recoveries ranged from 76.8 to 79.2% for plasma and 76.8 to 80.8% for liver across the calibration curve range. The method was successfully applied to measurement of low concentrations of regenerated MP in plasma and liver after intravenous administration of a single dose (5 mg/kg) of a liver-targeted dextran prodrug of MP to rats.
Methylprednisolone; Dextran-methylprednisolone prodrug; Rat plasma; Rat liver; Liquid chromatography-tandem mass spectrometry; Pharmacokinetics
The cation of the salt, C18H18N2O2
−, lies about a twofold rotation axis. The pyridinium ring is almost coplanar with the phenylene ring [dihedral angle between rings = 5.69 (9)°]. The crystal structure shows π–π stacking interactions [centroid–centroid distance = 3.70 (1) Å] between the pyridinium rings and the phenylene rings, generating a linear chain structure. The cation also forms two N—H⋯O hydrogen bonds to two nitrate groups.
The objective of the present research was to stabilize a heat-labile novel prodrug of Δ9-tetrahydrocannabinol (THC), THC-hemiglutarate (THC-HG), in polyethylene oxide (PEO) [PolyOx® WSR N-80 (PEO N-80), MW 200,000 Daltons] polymeric matrix systems produced by hot-melt fabrication for systemic delivery of THC through the oral transmucosal route. For this purpose, the effects of processing conditions (processing temperature and heating duration), plasticizer type and concentration and storage conditions on the stability of the prodrug were investigated. The selected plasticizers studied included vitamin E succinate (VES), acetyltributyl citrate (ATBC), triethyl citrate (TEC), triacetin and polyethylene glycol 8000 (PEG 8000). Furthermore, the influence of plasticizer concentration on drug release was also studied. The stability of THC-HG in PEO matrices was influenced by all of the aforementioned variables. Films processed at 110 °C for 7 min were found to be favorable for hot-melt processing with a post- processing drug content of 95%, while significant degradation of THC-HG (~42%) was observed in those processed at 200 °C for 15 min. The degradation of the prodrug during hot-melt fabrication and also upon storage was considerably reduced in the presence of the plasticizers investigated, VES being the most effective. Modulation of the microenvironmental pH to an acidic range via incorporation of citric acid in PEO-plasticizer matrices significantly improved the stability of the prodrug, with almost 90% of the theoretical drug remaining as opposed to only 15% remaining in PEO-only matrices when stored at 40 °C for up to 3 months. The release of drug from PEO matrices was influenced both by the plasticizer type and concentration. A faster release resulted from water-soluble plasticizers, PEG 8000 and triacetin, and with increasing concentration. However, a slower release was observed with an increase in concentration of water-insoluble plasticizers, VES and ATBC.
THC; Plasticizers; Stability; Hot-melt; Poly (ethylene oxide); Release; Microenvironmental pH; Prodrug
The molecule of the title compound, C18H16N2O2, lies about a center of inversion. The central phenylene ring is aligned at 62.7 (1)° with respect to the pyridyl ring. In the crystal, weak intermolecular C—H⋯N hydrogen bonds link molecules into sheets parallel to (104). C—H⋯O interactions are also present.
In the title compound, C18H16N2O2, the phenylene ring is located on inversion center. The pyridyl ring makes a dihedral angle of 39.9 (1)° with the phenylene ring. In the crystal, adjacent molecules are linked by intermolecular C—H⋯N hydrogen bonds, forming a linear chain along the a axis.
The asymmetric unit of the centrosymmetric title compound, C18H16N2O2, contains one half-molecule. The central benzene ring forms a dihedral angle of 66.8 (1)° with two outer aromatic rings. In the crystal structure, weak intermolecular C—H⋯N hydrogen bonds link molecules into sheets parallel to (104).