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Q235 steel is widely used in the infrastructure industry due to its high performance and low price, but it is prone to corrode in both terrestrial atmospheric environment and high salt fog environment at the seaside. In the marine field, inorganic zinc - rich coatings are the most commonly used anticorrosive conductive coatings, and the modification research on such coatings is promising. In this paper, the coatings were added with 2% graphene + 2% calcium carbonate for the purpose of improving corrosion resistance. Subsequently, the corrosion behaviors of the as - prepared coatings were investigated through simulated seawater immersion experiments and simulated sea salt aerosol experiments with the help of electrochemical impedance (EIS), scanning electron microscopy (SEM) and X - ray diffraction (XRD) analysis. Results showed that in the comparison of the original formula coating, the coating added with 2% graphene and 2% calcium carbonate possessed higher impedance value and lower corrosion current density. In addition, the generated corrosion products prevented the intrusion of corrosive medium and slowed down the corrosion. In general, the inorganic zinc - rich coating added with 2% graphene + 2% calcium carbonate had better corrosion resistance compared with the original formula coating.

The quality of construction projects is related to the safety of people's lives and property, and also has a greater impact on the stability of the entire society; factory structure is one of the most common productive buildings, and some factory buildings have been partially lost its using function due to a long service history; in order to ensure the safety, applicability and durability of these factory buildings and continue to utilize or strengthen these factory structures, it is necessary to perform safety testing and identification for factory buildings at the first time. Structural safety assessment is the process of inspecting, measuring, analyzing and evaluating the structural effects, structural resistance and their interrelationships and finally obtaining structural safety grade of buildings that have been built or in service for many years. On the basis of summarizing and analyzing previous research works, this article expounded the research background, current status and future challenges of building safety grade identification, elaborated material testing methods, specifications, frameworks and processes of security grade identification for factory structure buildings, analyzed the concrete strength and steel corrosion detection, structural seismic identification and bearing capacity calculation of factory building, and proposed corresponding reinforcement measures and discussed its reinforcement effect. The final identification results of an engineering case are in good agreement with its actual construction conditions and on-site inspections and basically satisfactory the results of the factory building structure. The study results of this paper provide a reference for the further researches on the safety grade identification and reinforcement effect of the factory structure building. [ABSTRACT FROM AUTHOR]

Our previous study has revealed that EphA7 was upregulated in patient-derived esophageal squamous cell carcinoma (ESCC) xenografts with hyper-activated STAT3, but its mechanism was still unclear. To assess the association between EphA7 and STAT3, western blotting, immunofluorescence, ChIP assay, and qRT-PCR were conducted. Truncated mutation and luciferase assay were performed to examine the promoter activity of EphA7. CCK-8 assay and colony formation were performed to assess the proliferation of ESCC. Cell-derived xenograft models were established to evaluate the effects of EphA7 on ESCC tumor growth. RNA-seq analyses were used to assess the effects of EphA7 on related signals. In this study, EphA7 was found upregulated in ESCC cell lines with high STAT3 activation, and immunofluorescence also showed that EphA7 was co-localized with phospho-STAT3 in ESCC cells. Interestingly, suppressing STAT3 activation by the STAT3 inhibitor Stattic markedly inhibited the protein expression of EphA7 in ESCC cells, in contrast, activation of STAT3 by IL-6 obviously upregulated the protein expression of EphA7. Moreover, the transcription of EphA7 was also mediated by the activation of STAT3 in ESCC cells, and the −2000∼−1500 region was identified as the key promoter of EphA7. Our results also indicated that EphA7 enhanced the cell proliferation of ESCC, and silence of EphA7 significantly suppressed ESCC tumor growth. Moreover, EphA7 silence markedly abolished STAT3 activation-derived cell proliferation of ESCC. Additionally, RNA-seq analyses indicated that several tumor-related signaling pathways were significantly changed after EphA7 downregulation in ESCC cells. Our results showed that the transcriptional expression of EphA7 was increased by activated STAT3, and the STAT3 signaling may act through EphA7 to promote the development of ESCC. [ABSTRACT FROM AUTHOR]

The complete chloroplast genome of Lonicera similis Hemsl. has been characterized by reference-based assembly using Illumina paired-end data. The circular complete cp genome is 155,463 bp in length, containing a large single copy (LSC) region of 89,282 bp, a small single copy (SSC) region of 18,661 bp, which are separated by a pair of inverted repeat (IR) regions of 23,760 bp. A total of 129 genes were predicted from the cp genome, including 83 protein-coding genes, 37 tRNA genes, and eight rRNA genes. Phylogenetic analysis reveals that L. similis is more closely related to Lonicera japonica Thunb. and Lonicera dasystyla Rehd. Our result will provide a reference for the phylogenetic relationship, plant identification and resource development and utilization of Lonicera species. [ABSTRACT FROM AUTHOR]

Background: Sedum sarmentosum, which is recorded in Chinese Pharmacopoeia, has been applied clinically to treat liver and gallbladder diseases.Purpose: This study aimed to explore the hepatoprotective effect of S. sarmentosum less polar extract (SSE) against ANIT-induced liver injury in rats, and the protective activity and mechanism of one major constituent isolated from this extract on D-GalN-induced human hepatic QSG7701 cell damage.Methods: Rats were divided into groups and then administrated intragastrically with SSE at doses of 100, 200 and 400 mg/kg for 7 days. They were modeled in the experiments with ANIT (70 mg/kg) to induce liver injury after the sixth day administration. The levels of serum biochemical markers ALT, AST, ALP, GGT/γ-GT, DBiL, TBiL, ALB, TP, and bile flow rate, as well as the histopathology of the liver tissue were used as indices of liver damage and measured. The inflammatory response and oxidative stress were thought to be key contributors to ANIT-induced liver injury in rats. Therefore, the inflammatory mediators (TNF-α, IFN-γ, IL-4) and oxidative stress (ROS, SOD, GSH-PX) were measured in the serum and liver homogenates, respectively. Next, phytochemical research was performed to produce the main component, and the isolated compound was evaluated for its hepatoprotective activity against QSG7701 cell injured by D-GalN through the measurement of cell viabilities, ALT, AST, IL-1β, TNF-α, IL-6, ROS, GSH-PX and SOD productions. Furthermore, the protein expression of the Nrf2 and NF-κB pathways were analyzed by western blotting.Results: SSE had an obvious effect on the decreases of ALT, AST, ALP, GGT/γ-GT, DBiL and TBiL levels, the increases of ALB and TP levels in serum, and the ANIT-induced deceleration in bile flow for liver injury. Meanwhile, SSE pretreatment alleviated ANIT-induced liver pathological injuries exhibited by HE stain of the liver. Moreover, SSE significantly suppressed levels of pro-inflammatory cytokines TNF-α and IFN-γ, and elevated level of anti-inflammatory cytokine IL-4 in serum. SSE also attenuated oxidative stress by reducing ROS level and by enhancing antioxidative enzymes (SOD and GSH-PX) activities after ANIT administration in liver tissue. Further, the major compound shown in HPLC was isolated from SSE. Its structure was identified by the spectroscopic data analysis and comparison with literature values. The principal constituent had potent protective effect on D-GalN-induced QSG7701 cells damage in a dose dependent manner with survival rates of 58.2% and 69.5% at 10 μM and 20 μM, respectively. Its cytoprotective effect was associated with the reduction of ALT, AST, IL-1β, TNF-α, IL-6 and ROS levels, and the elevation of GSH-PX and SOD productions in QSG7701 cells induced by D-GalN. Western blotting showed that this compound enhanced the expression of Nrf2, HO1, NQO1 and GCLC, and inhibited D-GalN-induced IκBα and NF-κB p65 phosphorylation.Conclusions: Current study showed that SSE treatment exerted a protective effect on ANIT-induced liver injury. The main compound δ-amyrone isolated from the extract was characterized as the effective component with hepatoprotective activity by promoting Nrf2 antioxidant defense and suppressing NF-κB inflammatory response. [ABSTRACT FROM AUTHOR]

Renal fibrosis is thought to be the final common pathway leading to chronic kidney disease (CKD) and end-stage renal failure. Except for renal replacement therapy, no adequate treatment regimen is available; therefore studies on the treatment of renal fibrosis have attracted significant interest. In recent years, studies have shown that traditional Chinese medicine (TCM) may represent an attractive source to produce drugs with antifibrosis effects. The aim of this study was to establish a robust cell-based high-content screening (HCS) approach to identify TCM compounds with antifibrosis effects in NRK49F cells following TGF-β1 exposure. When designing the model, one of the most important steps involved the stability and reproducibility of this cell-based model. Therefore, we initially optimized the experimental parameters. Then, our HCS model was validated using SB525334, an inhibitor of the TGF-β1 receptor, and curcumin and emodin, two TCM compounds with well-documented anti-renal fibrosis activity. Subsequently, the proven reliable HCS model was used to screen a standard TCM compound library, which included 344 TCM molecules. Based on our HCS algorithm, a total of 16 compounds were identified to have prospective inhibitory activity. These compounds were further validated by verification experiments. Strikingly, eight compounds have been shown to inhibit renal fibrosis; six of them had rarely been described in the literature, namely, Ligustrazine, Glycyrrhizic acid, Astragaloside iv, Hydroxysafflor Yellow A, Crocin, and Gypenosides. To the best of our knowledge, this is the first study in which a HCS assay was performed to identify TCM compounds with anti-renal fibrosis effects. The HCS approach was successfully applied to screen active compounds and will be propitious to further anti-renal fibrosis drugs discovery research. Meanwhile, it may offer possibilities for identifying lead compounds for treating other diseases from registered Chinese herbal medicines. [ABSTRACT FROM AUTHOR]

Background: This study was aimed at investigating whether metformin can reverse the resistance of ovarian cancer cells to cisplatin and exploring the underlying mechanism.Methods: Ovarian cancer cell proliferation in vitro was evaluated using a CCK-8 assay. The resistance index of platinum-resistant ovarian cancer cells was determined and cell cycle and apoptosis rate determined by annexin V/propidium iodide double-staining in CP70 cells. Western blotting was used to determine IGF1, IGF1R, AKT, p-IGF1, p-IGF1R, p-AKT, and MRP2 levels in cells treated with different concentrations of metformin and LY29400, an inhibitor of the insulin-like growth factor pathway. Changes in gene expression levels of MRP2, IGF1, IGF1R, and AKT were determined by fluorescence real-time quantitative PCR assay of CP70 cells treated with metformin. Tumors of human ovarian cancer cell lines CP70 and A2780 were established by subcutaneous transplantation of cells in nude mice and the effect of metformin on MRP2 expression and tumor inhibition assessed.Results: The IC50 value of cisplatin in CP70 cells decreased significantly as metformin concentration increased (P < 0.05). The cell cycle distribution in CP70 cells changed with metformin treatment; the percentage of cells in the G0/G1 phase, as well as the natural apoptosis rate was significantly increased with metformin treatment (P < 0.05). IGF1, IGF1R, AKT p-IGF1, p-IGF1R, and p-Akt protein expression was enhanced dose-dependently with metformin, and was also significantly changed by treatment of CP70 cells with 0 mM metformin +10 mM LY294002. Moreover, changes in the expression of MRP2, IGF1, IGF1R, and AKT was metformin-concentration dependent, and was significantly different from that in the untreated control group (P < 0.05). In nude mice, the tumor volumes of the cisplatin-treated groups were significantly less than in the control group, and was further suppressed by co-treatment with cisplatin and metformin (P < 0.05), indicating that these 2 drugs had a synergistic effect on tumor inhibition.Conclusion: Metformin can improve the sensitivity of ovarian cancer CP70 cells to cisplatin in a concentration-dependent manner by activating the AKT signaling pathway, inhibiting the IGF1R signaling pathway, and reducing MRP2 expression. [ABSTRACT FROM AUTHOR]

Arbuscular mycorrhizal fungi (AMF) as a biostimulant enhance salt tolerance in plants, while the informations regarding AMF-induced changes in soil structure are only available to a limited degree. In this study, trifoliate orange (Poncirus trifoliata) seedlings were inoculated withDiversispora versiformisunder 100 mM NaCl for 85 days. The salt stress considerably inhibited mycorrhizal colonization by 26%, compared with non-salt stress. Mycorrhizal inoculation significantly increased plant height, stem diameter, leaf number, shoot biomass, and root biomass, length, surface area, and volume in comparison to non-mycorrhizal inoculation under salt stress or non-salt stress. Mycorrhization induced significantly higher production of easily extractable glomalin-related soil protein (EE-GRSP), and total glomalin-related soil protein (T-GRSP), higher percentage of water-stable aggregates (WSAs) in 0.25–0.50, 0.50–1.00, and 1.00–2.00 mm size, and lower in 2.00–4.00 mm size, regardless of non-salt stress or salt stress. Mycorrhizal soils represented higher aggregate stability (in terms of mean weight diameter) under salt and non-salt stress, which was related with root colonization, root surface area, root volume, EE-GRSP, and T-GRSP. The better soil structure by mycorrhization provided higher leaf water potential under salt stress. It suggests that mycorrhizas had a positive contribution to improve plant growth and soil structure, thereby enhancing salt tolerance. [ABSTRACT FROM AUTHOR]

A cuprous bromide-catalyzed heteroannulation reaction of [60]fullerene with ketoxime acetates has been exploited to prepare novel 1-fulleropyrrolines through the cleavage of N–O and C–H bonds and formation of C–C and C–N bonds under thermal conditions. A plausible mechanism for the formation of 1-fulleropyrrolines is proposed on the basis of the experimental results. The electrochemistry of the obtained products has also been investigated. [ABSTRACT FROM AUTHOR]

Trichothecenes are a large family of structurally related toxins mainly produced by Fusarium genus. Among the trichothecenes, T-2 toxin and deoxynivalenol (DON) cause the most concern due to their wide distribution and highly toxic nature. Trichothecenes are known for their inhibitory effect on eukaryotic protein synthesis, and oxidative stress is one of their most important underlying toxic mechanisms. They are able to generate free radicals, including reactive oxygen species, which induce lipid peroxidation leading to changes in membrane integrity, cellular redox signaling, and in the antioxidant status of the cells. The mitogen-activated protein kinases signaling pathway is induced by oxidative stress, which also induces caspase-mediated cellular apoptosis pathways. Several new metabolites and novel metabolic pathways of T-2 toxin have been discovered very recently. In human cell lines, HT-2 and neosolaniol (NEO) are the major metabolites of T-2 toxin. Hydroxylation on C-7 and C-9 are two novel metabolic pathways of T-2 toxin in rats. The metabolizing enzymes CYP3A22, CYP3A29, and CYP3A46 in pigs, as well as the enzymes CYP1A5 and CYP3A37 in chickens, are able to catalyze T-2 toxin and HT-2 toxin to form the C-3′-OH metabolites. Similarly to carboxylesterase, CYP3A29 possesses the hydrolytic ability in pigs to convert T-2 toxin to NEO. T-2 toxin is able to down- or upregulate cytochrome P-450 enzymes in different species. The metabolism of DON in humans is region-dependent. Free DON and DON-glucuronide are considered to be the biomarkers for humans. The masked mycotoxin DON-3-β- d-glucoside can be hydrolyzed to free DON in the body. This review will provide useful information on the progress of oxidative stress as well as on the metabolism and the metabolizing enzymes of T-2 toxin and DON. Moreover, the literature will throw light on the blind spots of metabolism and toxicological studies in trichothecenes that have to be explored in the future. [ABSTRACT FROM AUTHOR]

A new fluorescent probe, N-(4-(1,5-diphenyl-4,5-dihydro-1H-pyrazol-3-yl)phenyl)-2,4-dinitrobenzenesulfonamide (probe 3), was designed and synthesized as a highly sensitive and selective fluorescent probe for recognizing and detecting glutathione among biological thiols in aqueous media. Probe 3 is a nonfluorescent compound. On being mixed with biothiols under neutral aqueous conditions, the 2,4-dinitrobenzenesulfoyl moiety can be cleaved off by glutathione, and the blue emission of the pyrazoline at 464 nm is switched on, with a fluorescence enhancement of 488-fold for glutathione. Furthermore, probe 3 was highly selective for glutathione without interference from some biologically relevant analytes. The detection limit of glutathione was 4.11 × 10−7 M. The emission of the probe is pH independent in the physiological pH range. Moreover, the probe can be used for fluorescent imaging of cellular glutathione and can be used for detecting glutathione in calf serum. [ABSTRACT FROM AUTHOR]

Seven layered C5N configurations constructed from hexagonal BN and graphite structures are studied using an ab initio pseudopotential density functional method. The structural and electronic properties, and pressure-induced phase transition are investigated by calculating the total energy, structural parameter, formation energy, elastic constant, band structure and electron density of state. The results show that the three C5N configurations constructed from the h-BN structure are more stable energetically than those four configurations from graphite structure. The C5N-I configuration with the highest symmetry and the AA stacking sequence along the c-axis is the most stable. This structure is stable mechanically and its phase separation is difficult. The C5N phase is expected to have a metallic character. A critical pressure of about 20GPa is predicted for the synthesis of a monoclinic C5N phase from the layered C5N phase. [ABSTRACT FROM AUTHOR]

Study Objective: To compare the incidence of postoperative cognitive dysfunction (POCD) in elderly surgical patients (>60years) receiving different anesthetics (propofol, sevoflurane, or isoflurane) and to identify potential biomarkers of POCD in this patient population.Design: Prospective, randomized, double-blind clinical trial.Setting: University-affiliated teaching hospital.Patients: One hundred and fifty elderly patients scheduled for laparoscopic cholecystectomy.Interventions: Elderly patients undergoing laparoscopic cholecystectomy were randomly assigned to receive propofol, sevoflurane, or isoflurane anesthesia.Measurements: Cognitive function was assessed using neuropsychological tests at baseline (1day before surgery [D0]), and on postoperative day 1 (D1) and day 3 (D3). Plasma S-100β and Aβ1-40 protein, IL-1β, IL-6 and TNF-α concentrations were assessed before induction of anesthesia (T0), after extubation (T1), and 1h (T2) and 24h (T3) postoperatively.Main Results: The incidence of POCD was significantly lower in the propofol group compared to the isoflurane group and the sevoflurane group at D1 and D3 (propofol vs. isoflurane: D1 and D3, P<0.001; propofol vs. sevoflurane: D1, P=0.012; D3, P=0.013). The incidence of POCD was significantly lower in the sevoflurane group compared to the isoflurane group at D1 (P=0.041), but not at D3. Postoperatively, plasma S-100β and Aβ1-40 protein, IL-1β, IL-6, and TNF-α concentrations were significantly decreased in the propofol group compared to the isoflurane group.Conclusions: Propofol anesthesia may be an option for elderly surgical patients. [ABSTRACT FROM AUTHOR]

Max-cut is one of the most classic NP-hard combinatorial optimization problems. The symmetry nature of it leads to special difficulty in extracting meaningful configuration information for learning; none of the state-of-the-art algorithms has employed any learning operators. This paper proposes an original learning method for max-cut, namely post-flip edge-state learning (PF-ESL). Different from previous algorithms, PF-ESL regards edge-states (cut or not cut) rather than vertex-positions as the critical information of a configuration, and extracts their statistics over a population for learning. It is based on following observations. 1) Edges are the only factors considered by the objective function. 2) Edge-states keep invariant when rotating a local configuration to its symmetry position, but vertex-positions do not. These suggest that edge-states contain more meaningful information about a configuration than vertex-positions do. It is impossible to set the state of an edge without influencing some other edges' states due to their dependencies. Therefore, instead of setting edge-states directly, PF-ESL samples the flips on vertices. Flips on vertices are sampled according to their capacities in increasing the similarity on edge-states between the given solution and a population. PF-ESL is employed in an EDA (Estimation of Distribution Algorithm) perturbation operator and a path-relinking operator. Experimental results show that our algorithm is competitive, and show that edge-state learning is value-added for both the two operators. The main contributions of this paper are as follows. Firstly, previous state-of-the-art evolutionary algorithms for max-cut focus on vertex positions in their evolutionary operation, this paper proposes a new and more reasonable perspective suggesting that edge-states are the critical information of divided graphs rather than vertex positions, and introduces a novel method to measure and utilize their similarities based on it. Such a perspective is fundamental to learning based algorithms design for max-cut and other graph partitioning problems, and can shed lights on future researches. Furthermore, since max-cut is one of the most classic and fundamental NP hard problems, many real-world problems involve dividing graph data into different parts to optimize certain functions, this new perspective may inspire related or similar problems. Secondly, besides the original edge-states based perspective, and the post-flip edge-states learning (PFESL) operator based on it, our memetic algorithm also incorporates a novel evolutionary framework which alternates between EDA based Iterated Tabu search (ITS) and path relinking based genetic algorithm. Finally, the proposed algorithm provides competitive results on two mostly used benchmark sets and improves the best-known results of 6 most challenging instances. • An original edge-state perspective for design learning operators for max-cut. • A novel learning operator to learn edge states. • A new evolutionary framework for max-cut. • It provides competitive results on two mostly used benchmark sets. [ABSTRACT FROM AUTHOR]

Stresses, such as neurohumoral activation, induced pathological cardiac hypertrophy is the main risk factor for heart failure. The ubiquitin-proteasome system (UPS) plays a key role in maintaining protein homeostasis and cardiac function. However, research on the role and mechanism of deubiquitinating enzymes (DUBs) in cardiac hypertrophy is limited. Here, we observe that the deubiquitinating enzyme ubiquitin-specific protease 12(USP12) is upregulated in Ang II-induced hypertrophic hearts and primary neonatal rat cardiomyocytes (NRCMs). Inhibition of USP12 ameliorate Ang II-induced myocardial hypertrophy, while overexpression of USP12 have the opposite effect. USP12 deficiency also significantly attenuate the phenotype of Ang II-induced cardiac hypertrophy in vivo. Moreover, we demonstrate that USP12 aggravate Ang II-induced cardiac hypertrophy by enhancing METTL3, a methyltransferase which catalyze N6-methyladenosine (m6A) modification on messenger RNA and acts as a harmful factor in pathological cardiac hypertrophy. Upregulation of METTL3 reverse the reduction of myocardial hypertrophy induced by USP12 silencing in NRCMs. In contrast, knockdown of METTL3 attenuate the aggravation of myocardial hypertrophy in USP12-overexpressing NRCMs. Furthermore, we discover that USP12 promote the expression of METTL3 via upregulating p300. Mechanistically, USP12 binds and stabilizes p300, thereby activating the transcription of its downstream gene METTL3. Finally, our data show that USP12 is partially dependent on the stabilization of p300 to activate METTL3 expression and promote myocardial hypertrophy. Taken together, our results demonstrate that USP12 acts as a pro-hypertrophic deubiquitinating enzyme via enhancing p300/METTL3 axis, indicating that targeting USP12 could be a potential treatment strategy for pathological cardiac hypertrophy. Proposed model of Deubiquitination of p3 00 by USP12 Critically Enhances METTL3 Expression and Ang II-induced Cardiac Hypertrophy. In this study, we demonstrated that Ang II treatment induced the expression of USP12, thereby increasing the interaction between USP12 and histone acetyltransferase p300. USP12 deubiquitinated the ubiquitination modification of p300 to block its degradation and increase p300 expression, thus promoting the transcription of METTL3 to aggravate Ang II-induced cardiomyocyte hypertrophy. [Display omitted] • The expression of USP12 is increased in Ang II-induced cardiac hypertrophy in vitro and in vivo. • USP12 aggravates Ang II-induced cardiomyocyte hypertrophy via upregulating METTL3. • USP12 promoted METTL3 expression via modulating p300. • USP12 suppresses the ubiquitination of p300 to block its degradation. [ABSTRACT FROM AUTHOR]

Phytochemical investigation of the stems and leaves of Lonicera hypoglauca Miq. led to the isolation of one novel methoxylated flavone, acunminatin (7,2′,4′-trihydroxyl-5,5′- methoxyflavone) (1), and fourteen known compounds (2 – 15), including six flavonoids (mearnsetin 2 , kaempferol 3 , acacetin 4 , 5,7,3′,4′-tetramethoxyflavone 5 , tricin 6 , and 5,7,3′,4′,5′-pentamethoxyflavone 7), two coumarins (umbelliferone 8 and scopoletin 9), two phenylpropanoids (trans-ferulic acid 10 and chlorogenic acid 11), two iridoid glycosides (loganin 12 and sweroside 13), and two triterpenoids (uvaol 14 and ursolic acid 15). The structures of the compounds were identified by spectroscopic analysis and by comparing their spectral data with those reported in the literature. Five of these compounds (1 , 2 , 4 , 5 , and 7) were isolated from the L. genus for the first time, and compounds 6 – 8 and 14 – 15 were isolated for the first time from L. hypoglauca. The chemotaxonomic significance of the isolated compounds in the L. genus and the Caprifoliaceae family are discussed herein. [Display omitted] • One new methoxylated flavone named as acunminatin (1) and fourteen known compounds were obtained from Lonicera hypoglauca. • Nine compounds (1 - 2 , 4 - 8 , and 14 - 15) were isolated from the species for the first time. • Five compounds (1 - 2 , 4 - 5 , and 7) were firstly isolated from the genus Lonicera. • Three compounds (1 , 2 and 5) were first time reported from family Caprifoliaceae. [ABSTRACT FROM AUTHOR]