scholarly journals Skrining Virtual dan Elusidasi Moda Ikatan Senyawa dalam Bawang Putih (Allium Sativum L.) sebagai Penghambat Reseptor Advanced Glycation end Products

2019 ◽  
Vol 17 (2) ◽  
pp. 210
Author(s):  
Esti Mulatsari ◽  
Esti Mumpuni ◽  
Ikhsan Ramadhan
Keyword(s):  
Molecular Docking ◽  
Advanced Glycation End Products ◽  
Allium Sativum ◽  
Advanced Glycation ◽  
Advanced Glycation Endproduct ◽  
Glycation End Products ◽  
End Products

Diabetes memiliki dampak jangka panjang seperti aterosklerosis, nefropati, dan retinopati yang disebabkan oleh pembentukan Advanced Glycation End Products (AGEs). Penelitian secara in vitro pada ekstrak bawang putih (Allium sativum L.) terhadap aktivitas penghambatan pembentukan AGEs telah banyak dilakukan, namun belum diketahui mekanisme penghambatan dan senyawa apa yang berperan aktif dalam aktivitas penghambatan tersebut. Penelitian ini bertujuan untuk melakukan skrining virtual senyawa – senyawa dalam bawang putih (Allium sativum L.) yang aktif menghambat reseptor Advanced Glycation Endproduct sehingga senyawa aktif bisa dipertimbangkan sebagai kandidat senyawa obat. Metode yang digunakan adalah molecular docking dengan software PLANTS, YASARA, MarvinSketch, dan visualisasi ikatan senyawa uji pada asam amino reseptor menggunakan PyMOL, piridoksamin dan aminoguanidin digunakan sebagai kontrol positif inhibitor AGEs. Hasil docking 24 senyawa uji diperoleh tujuh senyawa yang aktif menghambat reseptor 3B75.pdb dan lima senyawa aktif menghambat reseptor 3O3U.pdb. Kandidat senyawa obat terdiri dari senyawa organosulfur, fenol dan flavonoid. Senyawa Ɣ-glutamil-sistein, E-ajoene, Nα-(1-Deoksi-Dfructosa-1-YL)-L-Arginin, Kaempferol-3-o-β-D-glukopiranosa, Iso-rhamnetin-3-o-β-D-glukopiranosa merupakan senyawa – senyawa dalam bawang putih yang memiliki kemampuan menghambat baik reseptor 3B75 maupun 3O3U dengan aktivitas yang lebih baik dari piridoksamin dan aminoguanidin.

scholarly journals CHARACTERISATION, IN SILICO AND IN VITRO DETERMINATION OF ANTIDIABETIC AND ANTI INFLAMMATORY POTENTIAL OF ETHANOLIC EXTRACT OF SARGASSUM WIGHTII.

2017 ◽  
Vol 10 (4) ◽  
pp. 297 ◽  
Author(s):  
Hemalatha S ◽  
Fazeela Mahaboob Begum
Keyword(s):  
Ascorbic Acid ◽  
Molecular Docking ◽  
Advanced Glycation End Products ◽  
Ethanolic Extract ◽  
Advanced Glycation ◽  
Sargassum Wightii ◽  
Glycation End Products ◽  
End Products ◽  
Anti Inflammatory

 Objective: The current study was intended to investigate and characterize the phytoconstituents of  Sargassum wightii ,evaluate its anti diabetic  and anti inflammatory potential under in silico and in vitro conditions.Methods: The marine algae S.wightii was extracted with ethanol. The ethanolic extract was screened for various phytoconstituents, quantified for total flavonoid and polyphenol content. FTIR and Mass spectrometry was used for characterizing the ethanolic extract. Antidiabetic potential of the phytoconstituents was analysed by molecular docking and enzyme inhibition assays. The anti inflammatory potential was evaluated by albumin denaturation assay.Results: The phytochemical screening revealed the presence of flavonoids, polyphenols, alkaloids, tannins, carbohydrates, proteins, oils and fat present in the ethanol extract. The FTIR analysis showed the presence of α,b unsaturated ketone, alcohol and ether groups in the extract.  MS analysis identified l - (+) - Ascorbic acid 2, 6 dihexadeconoate and Dotriacontyl isopropyl ether in the ethanolic extract. The molecular docking studies revealed that l - (+) - Ascorbic acid 2, 6 dihexadeconoate interacted with both α amylase and α glucosidase with a consensus score of 5.The results of  in vitro analysis showed that the ethanolic extract exhibited strong inhibitory activity on α amylase (IC 50 8mg/ml) and α glucosidase (IC 50 6mg/ml) respectively. The ethanolic extract also inhibited the formation of advanced glycation end products (IC 50 10mg/ml).Further the ethanolic extract inhibited the denaturation of albumin (IC 50 2.5 mg/ml) there by revealing the anti inflammatory potential of S.wightii.Conclusion: Hence it can be concluded that S.wightii possess anti diabetic and anti inflammatory potential which may be due to the presence of l - (+) - Ascorbic acid 2, 6 dihexadeconoate and flavonoids, polyphenols, alkaloids, tannins, carbohydrates, proteins, oils and fat present in the extract.Key words: Sargassum wightii, α amylase, α glucosidase, advanced glycation end products, molecular docking.

Sulforaphane inhibits formation of advanced glycation end products in vitro

2014 ◽  
Vol 1 (e1) ◽  
pp. 001-001 ◽  
Author(s):  
Kei Fukami ◽  
Takanori Matsui ◽  
Sho-ichi Yamagishi
Keyword(s):  
Advanced Glycation End Products ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products

scholarly journals Influence of Dopamine on Fluorescent Advanced Glycation End Products Formation Using Drosophila melanogaster

Biomolecules ◽  
2021 ◽  
Vol 11 (3) ◽  
pp. 453
Author(s):  
Ana Filošević Vujnović ◽  
Katarina Jović ◽  
Emanuel Pištan ◽  
Rozi Andretić Waldowski
Keyword(s):  
Drosophila Melanogaster ◽  
Advanced Glycation End Products ◽  
Model Organism ◽  
Covalent Modification ◽  
Advanced Glycation ◽  
Biomarkers Of Aging ◽  
Glycation End Products ◽  
End Products

Non-enzymatic glycation and covalent modification of proteins leads to Advanced Glycation End products (AGEs). AGEs are biomarkers of aging and neurodegenerative disease, and can be induced by impaired neuronal signaling. The objective of this study was to investigate if manipulation of dopamine (DA) in vitro using the model protein, bovine serum albumin (BSA), and in vivo using the model organism Drosophila melanogaster, influences fluorescent AGEs (fAGEs) formation as an indicator of dopamine-induced oxidation events. DA inhibited fAGEs-BSA synthesis in vitro, suggesting an anti-oxidative effect, which was not observed when flies were fed DA. Feeding flies cocaine and methamphetamine led to increased fAGEs formation. Mutants lacking the dopaminergic transporter or the D1-type showed further elevation of fAGEs accumulation, indicating that the long-term perturbation in DA function leads to higher production of fAGEs. To confirm that DA has oxidative properties in vivo, we fed flies antioxidant quercetin (QUE) together with methamphetamine. QUE significantly decreased methamphetamine-induced fAGEs formation suggesting that the perturbation of DA function in vivo leads to increased oxidation. These findings present arguments for the use of fAGEs as a biomarker of DA-associated neurodegenerative changes and for assessment of antioxidant interventions such as QUE treatment.

scholarly journals Advanced glycation end products induce a prothrombotic phenotype in mice via interaction with platelet CD36

Blood ◽  
2012 ◽  
Vol 119 (25) ◽  
pp. 6136-6144 ◽  
Author(s):  
Weifei Zhu ◽  
Wei Li ◽  
Roy L. Silverstein
Keyword(s):  
Diabetes Mellitus ◽  
Mouse Models ◽  
Advanced Glycation End Products ◽  
Vascular Complications ◽  
Dependent Manner ◽  
Advanced Glycation ◽  
Drug Induced ◽  
Glycation End Products ◽  
End Products

Abstract Diabetes mellitus has been associated with platelet hyperreactivity, which plays a central role in the hyperglycemia-related prothrombotic phenotype. The mechanisms responsible for this phenomenon are not established. In the present study, we investigated the role of CD36, a class-B scavenger receptor, in this process. Using both in vitro and in vivo mouse models, we demonstrated direct and specific interactions of platelet CD36 with advanced glycation end products (AGEs) generated under hyperglycemic conditions. AGEs bound to platelet CD36 in a specific and dose-dependent manner, and binding was inhibited by the high-affinity CD36 ligand NO2LDL. Cd36-null platelets did not bind AGE. Using diet- and drug-induced mouse models of diabetes, we have shown that cd36-null mice had a delayed time to the formation of occlusive thrombi compared with wild-type (WT) in a FeCl3-induced carotid artery injury model. Cd36-null mice had a similar level of hyperglycemia and a similar level of plasma AGEs compared with WT mice under this condition, but WT mice had more AGEs incorporated into thrombi. Mechanistic studies revealed that CD36-dependent JNK2 activation is involved in this prothrombotic pathway. Therefore, the results of the present study couple vascular complications in diabetes mellitus with AGE-CD36–mediated platelet signaling and hyperreactivity.

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