Harpulliasides A and B: Two new benzeneacetic acid derivatives from Harpullia pendula

2016 ◽  
Vol 15 ◽  
pp. 131-135 ◽  
Author(s):  
Mohamed Salaheldin A. Abdelkader ◽  
Mostafa E. Rateb ◽  
Gamal A. Mohamed ◽  
Marcel Jaspars
Keyword(s):  
Pharmacology ◽  
2018 ◽  
Vol 103 (1-2) ◽  
pp. 10-16 ◽  
Author(s):  
Alessia Cenani ◽  
Robert J. Brosnan ◽  
Heather K. Knych

Background: Propanidid is a γ-aminobutyric acid type A (GABAA) receptor agonist general anesthetic and its primary metabolite is 4-(2-[diethylamino]-2-oxoethoxy)-3-methoxy-benzeneacetic acid (DOMBA). Despite having a high water solubility at physiologic pH that might predict low-affinity GABAA receptor interactions, DOMBA is reported to have no effect on GABAA receptor currents, possibly because the DOMBA concentrations studied were simply insufficient to modulate GABAA receptors. Our objectives were to measure the propanidid and DOMBA concentration responses on ­GABAA receptors and to measure the behavioral responses of DOMBA in mice at concentrations that affect GABAA receptor currents in vitro. Methods: GABAA receptors were expressed in oocytes using clones for the human GABAA α1, β2 and γ2s subunits. The effects of DOMBA (0.2–10 mmol/L) and propanidid (0.001–1 mmol/L) on oocyte GABAA currents were studied using standard 2-electrode voltage clamp techniques. Based on in vitro results, 6 mice received ­DOMBA 32 mg intraperitoneal and were observed for occurrence of neurologic effects and DOMBA plasma concentration was measured by liquid chromatography tandem mass spectrometry. Results: DOMBA both directly activates GABAA receptors and antagonizes its GABA-mediated opening in a concentration-dependent manner at concentrations between 5–10 and 0.5–10 mmol/L respectively. In vivo, DOMBA produced rapid onset sedation at plasma concentrations that correlate with direct GABAA receptor activation. Conclusion: DOMBA modulation of GABAA receptors is associated with sedation in mice. Metabolites of propanidid analogues currently in development may similarly modulate GABAA, and impaired elimination of these metabolites could produce clinically relevant neurophysiologic effects.


2001 ◽  
Vol 17 (12) ◽  
pp. 1465-1466 ◽  
Author(s):  
Nongnuj JAIBOON ◽  
Kijtisak YOS-IN ◽  
Songtham RUANGCHAITHAWEESUK ◽  
Narongsak CHAICHIT ◽  
Rudkloa THUTIVORANATH ◽  
...  
Keyword(s):  

2016 ◽  
Vol 61 (7) ◽  
pp. 2335-2345 ◽  
Author(s):  
Kanti Kumar Athankar ◽  
Kailas L. Wasewar ◽  
Mahesh N. Varma ◽  
Diwakar Z. Shende

2005 ◽  
Vol 61 (6) ◽  
pp. o1528-o1529 ◽  
Author(s):  
Kaushik Banerjee ◽  
Axel Patrick Ligon ◽  
Markus Schürmann ◽  
Hans Preut ◽  
Michael Spiteller
Keyword(s):  

Molbank ◽  
10.3390/m294 ◽  
2003 ◽  
Vol 2002 (1) ◽  
pp. M294
Author(s):  
Matthias Treu ◽  
Ulrich Jordis
Keyword(s):  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Zhao Ju ◽  
Jianlin Shao ◽  
Meiling Zhou ◽  
Jing Jin ◽  
Huiji Pan ◽  
...  

Abstract Background Silica exposure underlies the development of silicosis, one of the most serious occupational hazards worldwide. We aimed to explore the interaction of the silica-induced epithelial–mesenchymal transition (EMT)-related transcripts with the cellular metabolism regulated by p53. Methods We knocked out p53 using CRISPR/Cas9 in the human bronchial epithelial (HBE) cell line. The transcriptomic and metabolomic analyses and integrative omics were conducted using microarrays, GC–MS, and MetaboAnalyst, respectively. Results Fifty-two mRNAs showed significantly altered expression in the HBE p53-KO cells post-silica exposure. A total of 42 metabolites were putatively involved in p53-dependent silica-mediated HBE cell dysfunction. Through integrated data analysis, we obtained five significant p53-dependent metabolic pathways including phenylalanine, glyoxylate, dicarboxylate, and linoleic acid metabolism, and the citrate cycle. Through metabolite screening, we further identified that benzeneacetic acid, a key regulation metabolite in the phenylalanine metabolic pathway, attenuated the silica-induced EMT in HBE cells in a p53-dependent manner. Interestingly, despite the extensive p53-related published literature, the clinical translation of these studies remains unsubstantial. Conclusions Our study offers new insights into the molecular mechanisms by which epithelial cells respond to silica exposure and provide fresh perspective and direction for future clinical biomarker research and potential clinically sustainable and translatable role of p53.


2020 ◽  
Author(s):  
Meiling Zhou ◽  
Zhao Ju ◽  
Jing Jin ◽  
Huiji Pan ◽  
Ping Ding ◽  
...  

Abstract Background: Silica exposure underlies the development of silicosis, one of the most serious occupational hazards worldwide. We aimed to explore the interaction of the silica-induced epithelial–mesenchymal transition (EMT)-related transcripts with the cellular metabolism regulated by p53.Methods: We knocked out p53 using CRISPR/Cas9 in the human bronchial epithelial (HBE) cell line. The transcriptomic and metabolomic analyses and integrative omics were conducted using microarrays, GC-MS, and MetaboAnalyst, respectively. Results: Fifty-two mRNAs showed significantly altered expression in the HBE p53-KO cells post-silica exposure. A total of 42 metabolites were putatively involved in p53-dependent silica-mediated HBE cell dysfunction. Through integrated data analysis, we obtained five significant p53-dependent metabolic pathways including phenylalanine, glyoxylate, dicarboxylate, and linoleic acid metabolism, and the citrate cycle. Through metabolite screening, we further identified that benzeneacetic acid, a key regulation metabolite in the phenylalanine metabolic pathway, attenuated the silica-induced EMT in HBE cells ina p53-dependent manner. Interestingly, despite the extensive p53-related published literature, the clinical translation of these studies remains unsubstantial. Conclusions: Our study offers new insights into the molecular mechanisms by which epithelial cells respond to silica exposure and provide fresh perspective and direction for future clinical biomarker research and potential clinically sustainable and translatable role of p53.


2019 ◽  
Vol 3 (1) ◽  
pp. 42
Author(s):  
Choiroel Anam

 Nata adalah selulosa ekstraseluler yang dihasilkan dari aktiivitas bakteri Acetobacter xylinum dalam proses fermentasi, dan  merupakan salah satu makanan kesehatan yang kaya akan serat. Nata yang paling umum ditemukan adalah nata de coco dengan media fermentasi air kelapa. Faktor-faktor dominan dalam pembuatan nata adalah ketersediaan nutrisi (karbon dan nitrogen), derajat keasaman dan media fermentasi yang digunakan. Penentuan kualitas terbaik media air kelapa yang digunakan, penentuan konsentrasi nitrogen dan sukrosa yang ditambahkan serta kondisi pH optimum  akan menghasilkan nata yang maksimal.Penelitian ini bertujuan untuk mencari kualitas terbaik pada fermentasi dalam proses pembuatan nata de coco, dan mengetahui senyawa fungsional yang terdapat pada nata de coco sebagai pangan fungsional. Hasil pengujian analisa sampel nata de coco menggunakan Gas chromatography–mass spectrometry (GC-MS) menunjukkan senyawa yang sangat bermaaf bagi kesehatan tubuh manusia. Sepuluh besar senyawa fungsional yag terdapat pada nata de coco yaitu:  Benzeneacetic Acid sebagai anti fungal dan scavenger. Hexadecanoid Acid memiliki efek anti-inflamasi, anti bakteri dan anti fungi. 22-Hydroxyhopane, Tetradecanoic Acid yang mempunyai aktivitas antimikroba dan antifungal. 9-Octadecanoid Acid, ρ-Cresol  memiliki aktivitas antioksidan. 9-Octadecenamide berfungsi untuk mencegah Alzheimer, menurunkan kolesterol dan menurunkan tekanan darah, Senyawa fungsional yang lain diantaranya (Z), Phenol, 4-(2-aminoethyl), Pentadecanoic Acid, 1-Heptadecanecarboxylic acid. Komposisi kimia nata  de coco dihasilkan kadar air 95%.  abu 0,35% dan protein 0,45%. Penelitian menunjukkan peningkatkan produksi nata dengan kualitas  yang baik sesuai persyaratan standar yang telah ditetapkan dan mempunyai senyawa senyawa  yang bermanfaat sebagai pangan fungsional yang bermanfaat bagi kesehatan.


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