Sauchinone, a lignan from Saururus chinensis, attenuates neutrophil pro-inflammatory activity and acute lung injury

( Hui Jing Han ),( Mei Li ),( Jong Keun Son ),( Chang Seob Seo ),( Seung Won Song ),( Sang Hyun Kwak ),( Hong Beom Bae ) 영남대학교 약품개발연구소 2014 영남대학교 약품개발연구소 연구업적집 Vol.24 No.0

Previous studies have shown that sauchinone modulates the expression of inflammatory mediators through mitogen-activated protein kinase (MAPK) pathways in various cell types. However, little information exists about the effect of sauchinone on neutrophils, which play a crucial role in inflammatory process such as acute lung injury (ALI). We found that sauchinone decreased the phosphorylation of p38 MAPK in lipopolysaccharide (LPS)-stimulated murine bone marrow neutrophils, but not ERK1/2 and JNK. Exposure of LPS-stimulated neutrophils to sauchinone or SB203580, a p38 inhibitor, diminished production of tumor necrosis factor (TNF)-α and macrophage inflammatory protein (MIP)-2 compared to neutrophils cultured with LPS. Treatment with sauchinone decreased the level of phosphorylated ribosomal protein S6 (rpS6) in LPS-stimulated neutrophils. Systemic administration of sauchinone to mice led to reduced levels of phosphorylation of p38 and rpS6 in mice lungs given LPS, decreased TNF-α and MIP-2 production in bronchoalveolar lavage fluid, and also diminished the severity of LPS-induced lung injury, as determined by reduced neutrophil accumulation in the lungs, wet/dry weight ratio, and histological analysis. These results suggest that sauchinone diminishes LPS-induced neutrophil activation and ALI.

Sauchinone, a lignan from Saururus chinensis, attenuates neutrophil pro-inflammatory activity and acute lung injury

( Hui Jing Han ),( Mei Li ),( Jong Keun Son ),( Chang Seob Seo ),( Seung Won Song ),( Sang Hyun Kwak ),( Hong Beom Bae ) 영남대학교 약품개발연구소 2013 영남대학교 약품개발연구소 연구업적집 Vol.23 No.0

Previous studies have shown that sauchinone modulates the expression of inflammatory mediators through mitogen-activated protein kinase (MAPK) pathways in various cell types. However, little information exists about the effect of sauchinone on neutrophils, which play a crucial role in inflammatory process such as acute lung injury (ALI). We found that sauchinone decreased the phosphorylation of p38 MAPK in lipopolysaccharide (LPS)-stimulated murine bone marrow neutrophils, but not ERK1/2 and JNK. Exposure of LPS-stimulated neutrophils to sauchinone or SB203580, a p38 inhibitor, diminished production of tumor necrosis factor (TNF)-α and macrophage inflammatory protein (MIP)-2 compared to neutrophils cultured with LPS. Treatment with sauchinone decreased the level of phosphorylated ribosomal protein S6 (rpS6) in LPS-stimulated neutrophils. Systemic administration ofsauchinone to mice led to reduced levels of phosphorylation of p38 and rpS6 in mice lungs given LPS, decreased TNF-α and MIP-2 production in bronchoalveolar lavage fluid, and also diminished the severity of LPS-induced lung injury, as determined by reduced neutrophil accumulation in the lungs, wet/dry weight ratio, and histological analysis. These results suggest that sauchinone diminishes LPS-induced neutrophil activation and ALI. ⓒ2013 Elsevier B.B.All rights reserved.

MUTYH Association with Esophageal Adenocarcinoma in a Han Chinese Population

Kong, Feng,Han, Xue-Ying,Luan, Yun,Qi, Tong-Gang,Sun, Chao,Wang, Jue,Hou, Hua-Ying,Jiang, Yu-Hua,Zhao, Jing-Jie,Cheng, Guang-Hui Asian Pacific Journal of Cancer Prevention 2013 Asian Pacific journal of cancer prevention Vol.14 No.11

Adenocarcinoma of esophagus (AE) is a complex disease, affected by a variety of genetic and environmental factors. Much evidence has shown that the MutY glycosylase homologue (MUTYH) plays a key role in the pathogenesis of many cancers. However, there have been no reports on influence on AE in the Han Chinese population. The objective of this study was to investigate this issue. A gene-based association study was conducted using three single nucleotide polymorphisms(SNPs) reported in previous studies. The three SNPs (rs3219463, rs3219472, rs3219489) were genotyped in 207 unrelated AE patients and 249 healthy controls in a case-control study using polymerase chain reaction and restriction fragment length polymorphism (PCR-RFLP). The results revealed that the genotype distribution of rs3219472 differed between the case and control groups (OR=1.66,95%CI=1.11-2.48, P=0.012), indicating that an association may exist between MUTYH and AE. These findings support a signifcant role for MUTYH in AE pathogenesis in the Han Chinese population.

Effects of Triterpenoid Glycosides from Fresh Ginseng Berry on SW480 Human Colorectal Cancer Cell Line

Jing-Tian Xie,Guang-Jian Du,Eryn McEntee,Han H. Aung,Hui He,Sangeeta R. Mehendale,Chong-Zhi Wang,Chun-Su Yuan 대한암학회 2011 Cancer Research and Treatment Vol.43 No.1

Purpose The pharmacological activities, notably the anticancer properties, of bioactive constituents from fresh American ginseng berry have not yet been well studied. In this study, we investigated the antiproliferative effects of fresh American ginseng berry extract (AGBE) and its representative triterpenoid glycosides using the human colorectal cancer cell line SW480. Materials and Methods Using high performance liquid chromatography (HPLC), the contents of 8 ginsenosides in AGBE were determined. The cell growth inhibitory effects of AGBE and three triterpenoid glycosides (ginsenosides Rb3, Re, and Rg3) were evaluated by proliferation assay and 3H-thymidine incorporation assay. Cell cycle and apoptotic effects were analyzed by using flow cytometry after staining with propidium iodide and annexin V. Results HPLC analysis data showed that AGBE has a distinct ginsenoside profile. AGBE inhibited SW480 cell growth significantly in a time-dependent (24-96 hours) and concentration-dependent (0.1-1.0 mg/mL) manner. Ginsenosides Rb3, Re, and Rg3 also possess significant antiproliferative activities on SW480 cells. 3H-thymidine incorporation assay indicated that AGBE and ginsenosides Rb3, Re, and Rg3 might inhibit the transferring and duplication of DNA in SW480 cells. Flow cytometric assay data suggested that AGBE arrested SW480 cells in S and G2/M phases, and significantly induced cell apoptosis. Conclusion AGBE and ginsenosides Rb3, Re, and Rg3 possessed significant antiproliferative effects and induced changes of morphological appearance on SW480 cells. The mechanisms of the antiproliferation of AGBE and tested ginsenosides involved could be cell cycle arrest and induction of apoptosis.

Influence of Rashba Spin-orbit Coupling on Fano-Kondo Effect in a Parallel Double-quantum-dot Structure

Jing Shan,Yun-Gang Wang,Yu Wang,Hui-Min Wang,Yu Han 한국물리학회 2014 THE JOURNAL OF THE KOREAN PHYSICAL SOCIETY Vol.64 No.3

Electron transport through a parallel double-quantum-dot structure is theoretically studied withone dot in the Kondo region and the other one in the region of local Rashba interaction. Thecoupling between the Kondo dot and the electron reservoirs is found to offer a reference channel forelectron travels, and the connection of the Rashba dot and the leads is found to afford a resonantchannel. The interplay of these two mechanisms gives rise to the Fano effect, which also depends onthe adjustment of the Rashba field. We then conclude that in this structure, the Fano interferenceis more robust because it causes a quenching of the Kondo resonance. In the presence of a localmagnetic flux, the quenched Kondo resonance becomes determined by the electron spin, which ishelpful for spin manipulation.

Research on Competitive Swimming Sports based on Optimal Control Theory

Jing meng Sun,Yueqiu Han,Hui Li 보안공학연구지원센터 2014 International Journal of Multimedia and Ubiquitous Vol.9 No.9

Isolation, Structural Characterization, and Lymphopoiesis Stimulant Activity of a Polysaccharide from the Abalone Gonad

Jing-Feng Yang,Yue-hui Li,Jun Zhao,Peng-fei Li,Ce Zhu,Ye-han Song,Lan-yi Zhang,Bei-Wei Zhu 한국식품과학회 2015 Food Science and Biotechnology Vol.24 No.1

A novel polysaccharide (AGP-32) from the gonad of Haliotis discus hannai Ino was isolated using a protease-assisted process and successive ion-exchange and gel-filtration chromatography. The backbone of AGP-32 was determined using hydrolysis with trifluoroacetic acid. FTIR, NMR, and methylation analysis, and periodate oxidation and Smith degradation analysis revealed that the AGP-32 backbone mainly consisted of (1→6)-linked mannose, (1→3)-linked galactose, and (1→3)-linked glucose in a proportion of 2:3:1. An in vitro cell assay indicated that AGP-32 promoted mice splenic lymphocyte proliferation by 26% at a concentration of 50 μg/mL. AGP-32 had an effect on immune protection and is a candidate for consideration as a functional food.

Preparation and Thermal Performance of Fullerene-Based Lead Salt

Hui-Juan Guan,Rufang Peng,Bo Jin,Hua Liang,Fengqi Zhao,Xing-Bing Bu,Wen-Jing Han,Shijin Chu 대한화학회 2014 Bulletin of the Korean Chemical Society Vol.35 No.8

C60 is widely investigated because of its unique structure. But its applications in solid propellant seem to be relatively neglected. C60 has more outstanding features than carbon black which is widely used as a catalyst ingredient of solid propellant. To combine the advantages of fullerene and lead salts, another good composite in propellant catalysts, we synthesized a kind of fullerene phenylalanine lead salt (FPL) and explored its thermal performances by differential thermal analysis (DTA) and thermogravimetry analysis (TGA). The results show it undergoes four exothermic processes started from 408 K. Combined TGA and X-ray diffractometer (XRD), the decomposition mechanism of FPL was derived by TG-IR and comparing IR spectra of FPL and its residues after burned to 327 °C, 376 °C and 424 °C, respectively. Effect of FPL on the decomposition characteristic of hexogen (RDX), a type of explosive in propellant, has been investigated using DTA at different heating rate, which shows the decomposition temperatures of the explosive are all reduced by more than 20 K. The corresponding activation energy (Ea) is decreased by 30 kJ·mol−1. So FPL has potential application as a combustion catalyst in solid propellant.

The pivotal role of the NLRC4 inflammasome in neuroinflammation after intracerebral hemorrhage in rats

Gan Hui,Zhang Li,Chen Hui,Xiao Han,Wang Lu,Zhai Xuan,Jiang Ning,Liang Ping,Zheng Shuyue,Zhao Jing 생화학분자생물학회 2021 Experimental and molecular medicine Vol.53 No.-

The NLRC4 inflammasome, a member of the nucleotide-binding and oligomerization domain-like receptor (NLR) family, amplifies inflammation by facilitating the processing of caspase-1, interleukin (IL)–1β, and IL-18. We explored whether NLRC4 knockdown alleviated inflammatory injury following intracerebral hemorrhage (ICH). Furthermore, we investigated whether NLRC4 inflammasome activation can be adjusted by the regulator of G protein signaling 2/leucine-rich repeat kinase-2 pathway. Fifty microliters of arterial blood was drawn and injected into the basal ganglion to simulate the ICH model. NLRC4 small interfering RNAs (siRNAs) were utilized to knockdown NLRC4. An LRRK2 inhibitor (GNE7915) was injected into the abdominal cavity. Short hairpin (sh) RNA lentiviruses and lentiviruses containing RGS2 were designed and applied to knockdown and promote RGS2 expression. Neurological functions, brain edema, Western blot, enzyme-linked immunosorbent, hematoxylin and eosin staining, Nissl staining, immunoprecipitation, immunofluorescence assay and Evans blue dye extravasation and autofluorescence assay were evaluated. It was shown that the NLRC4 inflammasome was activated following ICH injury. NLRC4 knockdown extenuated neuronal death, damage to the blood-brain barrier, brain edema and neurological deficiency 3 days after ICH. NLRC4 knockdown reduced myeloperoxidase (MPO) cells as well as tumor necrosis factor (TNF)-α, interleukin (IL)-6, IL-1β and IL-18 following ICH. GNE7915 reduced pNLRC4 and NLRC4 inflammasome activation. RGS2 suppressed the interaction of LRRK2 and NLRC4 and NLRC4 inflammasome activation by regulating pLRRK2. Our study demonstrated that the NLRC4 inflammasome may aggravate the inflammatory injury induced by ICH and that RGS2/LRRK2 may relieve inflammatory injury by restraining NLRC4 inflammasome activation.

The Effect of Caffeic Acid Phenethyl Ester (CAPE) on Phagocytic activity of septic Neutrophil in vitro

장은아,Hui-Jing Han,tran duc tin,조은예,이성헌,곽상현 대한의생명과학회 2023 Biomedical Science Letters Vol.29 No.4

Caffeic acid phenethyl ester (CAPE) is an active component of propolis obtained from honeybee hives. CAPE possesses anti-mitogenic, anti-carcinogenic, anti-inflammatory, and immunomodulatory activities in diverse systems, which know as displays antioxidant activity and inhibits lipoxygenase activities, protein tyrosine kinase, and nuclear factor kappa B (NF-κB) activation. This study aimed to investigate the effect of CAPE on lipopolysaccharide (LPS)-induced human neutrophil phagocytosis. Human neutrophils were cultured with various concentrations of CAPE (1, 10, and 100 μM) with or without LPS. The pro-inflammatory proteins (tumor necrosis factor-alpha [TNF-α], interleukin [IL]-6 and IL-8) levels were measured after 4 h incubation. To investigate the intracellular signaling pathway, we measured the levels of mitogen-activated protein kinases (MAPK), including phosphorylation of p38, extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and c-Jun N-terminal kinase (JNK). Next, to evaluate the potential phagocytosis, neutrophils were labeled with iron particles of superparamagnetic iron oxide nanoparticles (SPIONs, 40 nm) for 1 h in culture medium containing 5 mg/mL of iron. The labeling efficiency was determined by Prussian blue staining for intracellular iron and 3T-wighted magnetic resonance imaging. CAPE decreased the activation of intracellular signaling pathways, including ERK1/2 and c-Jun, and expression of pro-inflammatory cytokines, including TNF-α and IL-6, but had no effect on the signaling pathways of p38 and cytokine IL-8. Furthermore, images obtained after mannan-coated SPION treatment suggested that CAPE induced significantly higher signal intensities than the control or LPS group. Together, these results suggest that CAPE regulates LPS-mediated activation of human neutrophils to reduce phagocytosis.