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Technique Review : Optical Tools to Investigate Cellular Activity in the Intestinal Wall
( Werend Boesmans ),( Marlene M Hao ),( Pieter Vanden Berghe ) 대한소화기기능성질환·운동학회(구 대한소화관운동학회) 2015 Journal of Neurogastroenterology and Motility (JNM Vol.21 No.3
Live imaging has become an essential tool to investigate the coordinated activity and output of cellular networks. Within the last decade, 2 Nobel prizes have been awarded to recognize innovations in the field of imaging: one for the discovery, use, and optimization of the green fluorescent protein (2008) and the second for the development of super-resolved fluorescence microscopy (2014). New advances in both optogenetics and microscopy now enable researchers to record and manipulate activity from specific populations of cells with better contrast and resolution, at higher speeds, and deeper into live tissues. In this review, we will discuss some of the recent developments in microscope technology and in the synthesis of fluorescent probes, both synthetic and genetically encoded. We focus on how live imaging of cellular physiology has progressed our understanding of the control of gastrointestinal motility, and we discuss the hurdles to overcome in order to apply the novel tools in the field of neurogastroenterology and motility. (J Neurogastroenterol Motil 2015;21:337-351)
Aloui Sarra,Ghazouani Tesnime,Raboudi Faten,Talbi Wafa,Vanden Broeck Jozef,Salghi Rachid,Fattouch Sami 한국곤충학회 2022 Entomological Research Vol.52 No.4
The enzyme phenoloxidase (PO) plays an essential role in insect immune defense. Phenolic compounds sharing structural homology with PO substrates could act as substrate analogues, and may interfere with insect physiological process, thus, leading to their control. Herein, the bioinformatic molecular docking was used to predict the interaction of the crystal 3D structure of the insect Manduca sexta PO (PDB: 3HHS) with the antiseptic 4 hexylresorcinol (4-Hr). The method was firstly validated using phenylthiourea (PTU) as reference ligand. Data demonstrated the ability of the 4-Hr to bind to M. sexta PO with binding energy score ΔG=372,285 Kcal/mol indicative of a plausible affinity to active site of the enzyme, nevertheless, the affinity of PTU was stronger with a binding energy of ΔG=462.173 Kcal/mol. Furthermore, biochemical in vitro assays confirmed the behavior of 4-Hr as substrate-analog when binding to the active site of the insect PO leading to its competitive inhibition. This is the first report demonstrating the molecular bases of the usefulness of hexylresorcinol as a promising insecticide. Further investigations could emphasize synergistic effects of 4-Hr with other insecticides in integrated pest management (IPM) programs.
Validation of Octanoate Breath Test for Measuring Gastric Emptying in Rats
( Ingrid Demedts ),( Christophe Vanormelingen ),( Hubert Van Billoen ),( Tim Vanuytsel ),( Ricard Farre ),( Tatsuhiro Masaoka ),( Alfons Verbruggen ),( Kristien Verbeke ),( Pieter Vanden Berghe ),( Ja 대한소화기기능성질환·운동학회 2013 Journal of Neurogastroenterology and Motility (JNM Vol.19 No.2
Background/Aims Lack of simple and repeatable tests hampers gastric emptying studies in rats. The aim of this study was to adapt the 14C octanoate solid gastric emptying breath test for application in rats, and to validate it against radioscintigraphic method. Methods After ingestion of a meal containing 3 mCi 99mTc and 2 μCi 14C-octanoate, 23 male Wistar rats were placed on a gamma cam-era in a airflow container. Scintigraphic images were taken at regular intervals. The amount of 14CO2 in a regularly replaced hyamine hydroxide solution, capturing CO2 in the outflow air, was counted using liquid scintillation spectrometry. 99mTc gastric retention curves and 14CO2-excretion curves were fitted to their respective data. Three rats underwent the same procedures after administration of atropine. Results Overall Tr10% (time at which 10% of the original amount of 99mTc remained in the stomach) was 355 ± 64 minutes; Te90% (time at which 90% of total amount of 14CO2 was excreted) was 325 ± 106 minutes. Their correlation coefficient was 0.71, R-square 0.50 and P < 0.005. Tr1/2 (50% of original amount of 99mTc remained) was 124 ± 28 minutes; Te1/2 (50% of total amount of 14CO2 excreted) 114 ± 32 minutes. Their correlation coefficient was 0.83 with R-square of 0.69 and P < 0.00005. In 12 immobilized animals correlation was even better: correlation coefficient 0.84; R-square 0.71 and P < 0.001 (Tr10% was 388 ± 117 minutes; Te90% 532 ± 219 minutes; Tr1/2 of 165 ± 54 minutes; Te1/2 of 175 ± 67 minutes). Atropine significantly lengthened all emptying times: 904 ± 307 and 1461 ± 684 minutes for Tr10% and Te90%, respectively; and 432 ± 117 minutes for Tr1/2 and 473 ± 190 minutes for Te1/2. Conclusions We adapted and validated the 14C-octanoate gastric emptying breath test for application in rats.
De Bosscher, Karolien,Beck, Ilse M.,Dejager, Lien,Bougarne, Nadia,Gaigneaux, Anthoula,Chateauvieux, Sé,bastien,Ratman, Dariusz,Bracke, Marc,Tavernier, Jan,Vanden Berghe, Wim,Libert, Claude,Diede Springer Basel 2014 Cellular and molecular life sciences Vol.71 No.1
<P>Glucocorticoids (GCs) block inflammation via interference of the liganded glucocorticoid receptor (GR) with the activity of pro-inflammatory transcription factors NF-κB and AP-1, a mechanism known as transrepression. This mechanism is believed to involve the activity of GR monomers. Here, we explored how the GR monomer-favoring Compound A (CpdA) affects AP-1 activation and activity. Our results demonstrate that non-steroidal CpdA, unlike classic steroidal GCs, blocks NF-κB- but not AP-1-driven gene expression. CpdA rather sustains AP-1-driven gene expression, a result which could mechanistically be explained by the failure of CpdA to block upstream JNK kinase activation and concomitantly also phosphorylation of c-Jun. In concordance and in contrast to DEX, CpdA maintained the expression of the activated AP-1 target gene <I>c</I>-<I>jun</I>, as well as the production of the c-Jun protein. As for the underlying mechanism, GR is a necessary intermediate in the CpdA-mediated gene expression of AP-1-regulated genes, but seems to be superfluous to CpdA-mediated JNK phosphorylation prolongation. The latter phenomenon concurs with the inability of CpdA to stimulate DUSP1 gene expression. ChIP analysis demonstrates that DEX-activated GR, but not CpdA-activated GR, is recruited to AP-1-driven promoters. Furthermore, in mice we observed that CpdA instigates a strong enhancement of TNF-induced AP-1-driven gene expression. Finally, we demonstrate that this phenomenon coincides with an increased sensitivity towards TNF lethality, and implicate again a role for JNK2. In conclusion, our data support the hypothesis that a ligand-induced differential conformation of GR yields a different transcription factor cross-talk profile.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1007/s00018-013-1367-4) contains supplementary material, which is available to authorized users.</P>
The Effects of Ginsenoside Rb1 on JNK in Oxidative Injury in Cardiomyocytes
Chun-Su Yuan,Jing Li,Zuo-Hui Shao,Jing-Tian Xie,Chong-Zhi Wang,Srinivasan Ramachandran,Jun-Jie Yin,Han Aung,Chang-Qing Li,Gina Qin,Terry Vanden Hoek 대한약학회 2012 Archives of Pharmacal Research Vol.35 No.7
Reactive oxygen species (ROS) can induce oxidative injury via iron interactions (i.e. Fenton chemistry and hydroxyl radical formation). Our prior work suggested that American ginseng berry extract and ginsenoside Re were highly cardioprotective against oxidant stress. To extend this study, we evaluated the protective effect of protopanaxadiol-type ginsenoside Rb1 (gRb1)on H2O2-induced oxidative injury in cardiomyocytes and explored the ROS-mediated intracellular signaling mechanism. Cultured embryonic chick cardiomyocytes (4-5 day) were used. Cell death was assessed by propidium iodide and lactate dehydrogenase release. Pretreatment with gRb1 (0.01, 0.1, or 1 μM) for 2 h and concurrent treatment with H2O2 (0.5 mM) for 2 h resulted in a dose-dependent reduction of cell death, 36.6 ± 2.9% (n = 12, p < 0.05), 30.5 ± 5.1% (n = 12, p < 0.05) and 28.6 ± 3.1% (n = 12, p < 0.01) respectively, compared to H2O2-exposed cells (48.2 ± 3.3%, n = 12). This cardioprotective effect of gRb1 was associated with attenuated intracellular ROS generation as measured by 6-carboxy-2’, 7’-dichlorodihydrofluorescein diacetate, preserved the mitochondrial membrane potential as determined using JC-1. In the ESR study, gRb1 exhibited the scavenging DPPH and hydroxyl radical activities. Furthermore, our data showed the increased JNK phosphorylation (p-JNK) in H2O2-exposed cells was suppressed by the pretreatment with gRb 1 (1 μM) (p < 0.01). Co-treatment of gRb1 with a specific inhibitor of JNK SP600125 (10 μM) further reduced the p-JNK and enhanced the cell survival after H2O2exposure. Collectively, our results suggest that gRb1 conferred cardioprotection that was mediated via attenuating ROS and suppressing ROS-induced JNK activation.