scholarly journals Anti-Platelet Aggregation and Anti-Cyclooxygenase Activities for a Range of Coffee Extracts (Coffea arabica)

2020 ◽  
Author(s):  
Nuntouchporn Hutachok ◽  
Pongsak Angkasith ◽  
Chaiwat Chumpun ◽  
Suthat Fucharoen ◽  
Ian Mackie ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Biological Activities ◽  
Total Phenolic ◽  
Inhibitory Effects ◽  
Phenolic Contents ◽  
Inhibition Of Platelet Aggregation ◽  
Dependent Inhibition ◽  
Cox 2 ◽  
Activation Pathways ◽  
Cox 1

Coffee is rich in caffeine (CF), chlorogenic acid (CGA) and phenolics. Differing types of coffee beverages and brewing procedures may result in differences in total phenolic contents (TPC) and biological activities. Inflammation and increases of platelet activation and aggregation can lead to thrombosis. We focused on determining the chemical composition, antioxidant activity and inhibitory effects on agonist-induced platelet aggregation and cyclooxygenase (COX) of coffee beverages in relation to their preparation method. We prepared instant coffee and brewed coffee beverages using drip, espresso and boiling techniques. Coffee extracts were assayed for their CF and CGA contents using HPLC, TPC using colourimetry, platelet aggregation with an aggregometer and COX activity using ELISA. The findings have shown all coffee extracts, except the decaffeinated types, contained nearly equal amounts of CF, CGA and TPC. Inhibitory effects of coffee extracts on platelet aggregation differed depending on the activation pathways induced by different agonists. All espresso, drip and boiled coffee extracts caused dose dependent inhibition of platelet aggregation induced by ADP, collagen, epinephrine, and arachidonic acid (ARA). The most marked inhibition was seen at low doses of collagen or ARA. Espresso and drip extracts inhibited collagen-induced platelet aggregation more than purified caffeine or CGA. Espresso, boiled and drip coffee extracts were also a more potent inhibitors of COX-1 and COX-2 than purified caffeine or CGA. We conclude that inhibition of platelet aggregation and COX-1 and COX-2 may contribute to anti-platelet and anti-inflammatory effects of espresso and drip coffee extracts.

scholarly journals Anti-Platelet Aggregation and Anti-Cyclooxygenase Activities for a Range of Coffee Extracts (Coffea arabica)

Molecules ◽  
2020 ◽  
Vol 26 (1) ◽  
pp. 10
Author(s):  
Nuntouchaporn Hutachok ◽  
Pongsak Angkasith ◽  
Chaiwat Chumpun ◽  
Suthat Fucharoen ◽  
Ian J. Mackie ◽  
...  
Keyword(s):  
Platelet Aggregation ◽  
Biological Activities ◽  
Total Phenolic ◽  
Inhibitory Effects ◽  
Phenolic Contents ◽  
Inhibition Of Platelet Aggregation ◽  
Dependent Inhibition ◽  
Cox 2 ◽  
Activation Pathways ◽  
Cox 1

Coffee is rich in caffeine (CF), chlorogenic acid (CGA) and phenolics. Differing types of coffee beverages and brewing procedures may result in differences in total phenolic contents (TPC) and biological activities. Inflammation and increases of platelet activation and aggregation can lead to thrombosis. We focused on determining the chemical composition, antioxidant activity and inhibitory effects on agonist-induced platelet aggregation and cyclooxygenase (COX) of coffee beverages in relation to their preparation method. We prepared instant coffee and brewed coffee beverages using drip, espresso, and boiling techniques. Coffee extracts were assayed for their CF and CGA contents using HPLC, TPC using colorimetry, platelet aggregation with an aggregometer, and COX activity using ELISA. The findings have shown all coffee extracts, except the decaffeinated types, contained nearly equal amounts of CF, CGA, and TPC. Inhibitory effects of coffee extracts on platelet aggregation differed depending on the activation pathways induced by different agonists. All espresso, drip and boiled coffee extracts caused dose dependent inhibition of platelet aggregation induced by ADP, collagen, epinephrine, and arachidonic acid (ARA). The most marked inhibition was seen at low doses of collagen or ARA. Espresso and drip extracts inhibited collagen-induced platelet aggregation more than purified caffeine or CGA. Espresso, boiled and drip coffee extracts were also a more potent inhibitors of COX-1 and COX-2 than purified caffeine or CGA. We conclude that inhibition of platelet aggregation and COX-1 and COX-2 may contribute to anti-platelet and anti-inflammatory effects of espresso and drip coffee extracts.

scholarly journals Inhibitory Mechanisms of Lusianthridin on Human Platelet Aggregation

2021 ◽  
Vol 22 (13) ◽  
pp. 6846
Author(s):  
Hla Nu Swe ◽  
Boonchoo Sritularak ◽  
Ponlapat Rojnuckarin ◽  
Rataya Luechapudiporn
Keyword(s):  
Arachidonic Acid ◽  
Platelet Aggregation ◽  
Adenosine Diphosphate ◽  
Docking Studies ◽  
Secondary Wave ◽  
Inhibitory Effects ◽  
Antiplatelet Aggregation ◽  
Cyclooxygenase 1 ◽  
Cox 2 ◽  
Cox 1

Lusianthridin is a phenanthrene derivative isolated from Dendrobium venustum. Some phenanthrene compounds have antiplatelet aggregation activities via undefined pathways. This study aims to determine the inhibitory effects and potential mechanisms of lusianthridin on platelet aggregation. The results indicated that lusianthridin inhibited arachidonic acid, collagen, and adenosine diphosphate (ADP)-stimulated platelet aggregation (IC50 of 0.02 ± 0.001 mM, 0.14 ± 0.018 mM, and 0.22 ± 0.046 mM, respectively). Lusianthridin also increased the delaying time of arachidonic acid-stimulated and the lag time of collagen-stimulated and showed a more selective effect on the secondary wave of ADP-stimulated aggregations. Molecular docking studies revealed that lusianthridin bound to the entrance site of the cyclooxygenase-1 (COX-1) enzyme and probably the active region of the cyclooxygenase-2 (COX-2) enzyme. In addition, lusianthridin showed inhibitory effects on both COX-1 and COX-2 enzymatic activities (IC50 value of 10.81 ± 1.12 µM and 0.17 ± 1.62 µM, respectively). Furthermore, lusianthridin significantly inhibited ADP-induced suppression of cAMP formation in platelets at 0.4 mM concentration (p < 0.05). These findings suggested that possible mechanisms of lusianthridin on the antiplatelet effects might act via arachidonic acid-thromboxane and adenylate cyclase pathways.

Design, Synthesis, Characterization and in silico molecular docking studies and in vivo anti-inflammatory Activity of Pyrazoline clubbed Thiazolinone Derivatives

2020 ◽  
Vol 17 ◽  
Author(s):  
Deepak Kumar Singh ◽  
Mayank Kulshreshtha ◽  
Yogesh Kumar ◽  
Pooja A Chawla ◽  
Akash Ved ◽  
...  
Keyword(s):  
Molecular Docking ◽  
Biological Activities ◽  
Inflammatory Activity ◽  
Standard Drug ◽  
Docking Score ◽  
Chemical Structures ◽  
Cox 2 ◽  
Anti Inflammatory ◽  
Cox 1

Background: The pyrazolines give the reactions of aliphatic derivatives, resembling unsaturated compounds in their behavior towards permanganate and nascent hydrogen. This nucleus has been associated with various biological activities including inflammatory. Thiazolinone is a heterocyclic compound that contains both sulfur and nitrogen atom with a carbonyl group in their structure.Thiazolinone and their derivatives have attracted continuing interest because of their various biological activities, such as anti-inflammatory, antimicrobial, anti-proliferative, antiviral, anticonvulsant etc. The aim of the research was to club pyrazoline nucleus with thiazolinone in order to have significantanti-inflammatory activity. The synthesized compounds were chemically characterized for the establishment of their chemical structures and to evaluate as anti-inflammatory agent. Method: In the present work, eight derivatives of substituted pyrazoline (PT1-PT8) were synthesized by a three step reaction.The compounds were subjected to spectral analysis by Infrared, Mass and Nuclear magnetic resonance spectroscopy and elemental analysis data. All the synthesized were evaluated for their in vivo anti-inflammatory activity. The synthesized derivatives were evaluated for their affinity towards target COX-1 and COX-2, using indomethacin as the reference compound molecular docking visualization through AutoDock Vina. Results: Compounds PT-1, PT-3, PT-4 and PT-8 exhibited significant anti-inflammatory activity at 3rd hour being 50.7%, 54.3%, 52.3% and 57% respectively closer to that of the standard drug indomethacin (61.9%).From selected anti-inflammatory targets, the synthesized derivatives exhibited better interaction with COX-1 and COX-2 receptor, where indomethacin showed docking score of -6.5 kJ/mol, compound PT-1 exhibited highest docking score of -9.1 kJ/mol for COX-1 and compound PT-8 having docking score of 9.4 kJ/mol for COX-2. Conclusion: It was concluded that synthesized derivatives have more interaction with COX-2 receptors in comparison to the COX-1 receptors because the docking score with COX-2 receptors were very good. It is concluded that the synthesized derivatives (PT-1 to PT-8) are potent COX-2 inhibitors.

scholarly journals Total phenolic and flavonoid contents and biological activities of Cachrys cristata DC. extracts

2014 ◽  
Vol 66 (3) ◽  
pp. 1117-1123
Author(s):  
Jelena Matejic ◽  
Ana Dzamic ◽  
Tatjana Mihajilov-Krstev ◽  
Vladimir Randjelovic ◽  
Ksenija Mileski ◽  
...  
Keyword(s):  
Salmonella Enteritidis ◽  
Antimicrobial Agents ◽  
Biological Activities ◽  
Total Phenolic ◽  
Bacterial Strains ◽  
Phenolic Contents ◽  
Aerial Parts ◽  
Potential Source ◽  
Dilution Assay ◽  
Phenolic And Flavonoid

The total phenolic/flavonoid contents and antioxidant potential of the methanol, ethyl-acetate, acetone and water extracts obtained from the aerial parts and fruits of Cachrys cristata DC.(Apiaceae) were compared. The total phenolic contents of the tested extracts were determined using Folin-Ciocalteu?s reagent. The amounts per g of dry plant extract of gallic acid (GA) and quercetin (Qu) ranged between 22.60-166.97 mg, and 8.91-46.02 mg, respectively. The antioxidant activity, expressed as IC50, ranged from 1.784-17.621 mg/mL and from 1.01-3.42 mg L(+)-ascorbic acid (Vitamin C)/g when tested with 2,2-diphenyl-1-picrylhydrazyl (DPPH) and ABTS, respectively. The antimicrobial activity of the extracts was investigated by the microwell dilution assay, for the most common human gastrointestinal pathogenic bacterial strains: Escherichia coli ATCC 25922, Pseudomonas aeruginosa ATCC 9027, Salmonella enteritidis ATCC 13076, Bacillus cereus ATCC 10876, Listeria monocytogenes ATCC15313, Staphylococcus aureus ATCC 25923 and yeast Candida albicans ATCC 10231. The results indicate that C. cristata can be regarded as a potential source of antioxidant and antimicrobial agents.

scholarly journals The Induction of Cyclooxygenase-2 in IL-1β-Treated Endothelial Cells is Inhibited by Prostaglandin E2 through cAMP

1999 ◽  
Vol 8 (6) ◽  
pp. 287-294 ◽  
Author(s):  
Pravit Akarasereenont ◽  
Kitirat Techatrisak ◽  
Sirikul Chotewuttakorn ◽  
Athiwat Thaworn
Keyword(s):  
Endothelial Cells ◽  
Biological Activities ◽  
Umbilical Vein ◽  
The Body ◽  
Prostaglandin E ◽  
Dependent Manner ◽  
Negative Feedback Regulation ◽  
Cox 2 ◽  
Arachidonic Acids ◽  
Cox 1

Prostaglandins (PGS) have numerous cardiovascular and inflammatory effects. Cyclooxygenase (COX), which exists as COX-1 and COX-2 isoforms, is the first enzyme in the pathway in which arachidonic acid is converted to PGs. Prostaglandin E2 (PGE2) exerts a variety of biological activities for the maintenance of local homeostasis in the body. Elucidation of PGE2 involvement in the signalling molecules such as COX could lead to potential therapeutic interventions. Here, we have investigated the effects of PGE2 on the induction of COX-2 in human umbilical vein endothelial cells (HUVEC) treated with interleukin-1β (IL-1β 1 ng/ml). COX activity was measured by the production of 6-keto-PGF1α, PGE2, PGF2α and thromboxane B2 (TXB2) in the presence of exogenous arachidonic acids (10 μM for 10 min) using enzyme immunoassay (EIA). COX-1 and COX-2 protein was measured by immunoblotting using specific antibody. Untreated HUVEC contained only COX-1 protein while IL-1β treated HUVEC contained COX-1 and COX-2 protein. PGE2 (3 μM for 24 h) did not affect on COX activity and protein in untreated HUVEC. Interestingly, PGE2 (3 μM for 24 h) can inhibit COX-2 protein, but not COX-1 protein, expressed in HUVEC treated with IL1 β. This inhibition was reversed by coincubation with forskolin (100 μM). The increased COX activity in HUVEC treated with IL-1β was also inhibited by PGE2 (0.03, 0.3 and 3 μM for 24 h) in a dose-dependent manner. Similarly, forskolin (10, 50 or 100 μM) can also reverse the inhibition of PGE2 on increased COX activity in IL-1β treated HUVEC. The results suggested that (i) PGE2 can initiate negative feedback regulation in the induction of COX-2 elicited by IL-1β in endothelial cells, (ii) the inhibition of PGE2 on COX-2 protein and activity in IL-1β treated HUVEC is mediated by cAMP and (iii) the therapeutic use of PGE2 in the condition which COX-2 has been involved may have different roles.

scholarly journals Endothelium-dependent inhibition of platelet aggregation

1986 ◽  
Vol 88 (2) ◽  
pp. 411-415 ◽  
Author(s):  
Hiroshi Azuma ◽  
Masayuki Ishikawa ◽  
Satomi Sekizaki
Keyword(s):  
Platelet Aggregation ◽  
Inhibition Of Platelet Aggregation ◽  
Dependent Inhibition

Endothelin-B-Receptors-Dependent-Inhibition of Platelet Aggregation in the CD-1 Mouse

2000 ◽  
Vol 36 (Supplement 1) ◽  
pp. S184-S186 ◽  
Author(s):  
Julie Labonté ◽  
Ghassan Bkaily ◽  
Pedro DʼOrléans-Juste
Keyword(s):  
Platelet Aggregation ◽  
Inhibition Of Platelet Aggregation ◽  
Dependent Inhibition ◽  
Endothelin B

Inhibition of Human and Rat Platelet Aggregation by Extracts of Mo-er (Auricularia auricula)

1982 ◽  
Vol 48 (02) ◽  
pp. 162-165 ◽  
Author(s):  
K C Agarwal ◽  
F X Russo ◽  
R E Parks
Keyword(s):  
Platelet Aggregation ◽  
Cyclic Amp ◽  
Human Platelet ◽  
Rapid Onset ◽  
Hot Water ◽  
Inhibitory Effects ◽  
Inhibition Of Platelet Aggregation ◽  
Auricularia Auricula ◽  
Human Platelet Aggregation ◽  
Induced Aggregation

SummaryHot water extracts of Mo-er (1 gm by 15 ml of water), an oriental food (Auricularia auricula), inhibit strongly both human and rat platelet ADP-induced aggregation. HPLC analysis of two varieties of Mo-er, A.auricula and A.polytricha (a black tree fungus), shows that they contain adenosine (Ado), 133 and 154 micrograms per gram of dry fungus, respectively. The inhibition of ADP-induced platelet aggregation by Mo-er extracts and by Ado was compared. Mo-er extracts caused a more rapid onset and a longer duration of inhibition than produced by equivalent amounts of Ado. Furthermore, Mo-er extract treated with adenosine deaminase to degrade the Ado retained the capacity to inhibit platelet aggregation. The inhibitory effects of Mo-er extracts on ADP-induced human platelet aggregation are greatly potentiated by the inhibitors of cyclic AMP phosphodiesterase such as oxagrelate (phthalazinol) and papaverine. The inhibition of platelet aggregation is only partially blocked by 2’,5’-dideoxy-adenosine (DDA), an inhibitor of platelet adenylate cyclase and 5’-deoxy, 5’-methylthioadenosine (MTA), an antagonist of Ado receptors. ADP-induced rat platelet aggregation is strongly inhibited by Mo-er extracts, but not by Ado. This inhibition is not reversed by either DDA or MTA. These findings indicate that Mo-er extracts contain an agent (or agents) in addition to Ado, that blocks platelet aggregation by a mechanism that does not involve the platelet cyclic AMP system.

Verapamil Inhibits Platelet Aggregation by a Calcium-Independent Mechanism

1986 ◽  
Vol 56 (03) ◽  
pp. 308-310 ◽  
Author(s):  
Giovanni Bonadonna ◽  
Clara Lechi ◽  
Paola Corradini ◽  
Daniela Sinigaglia ◽  
Piero De Togni ◽  
...  
Keyword(s):  
Protein Kinase C ◽  
Platelet Aggregation ◽  
Channel Blocker ◽  
Inhibitory Effects ◽  
Myristate Acetate ◽  
Fluorescent Indicator ◽  
Inhibition Of Platelet Aggregation ◽  
Kinase C ◽  
Aggregation Response ◽  
Independent Mechanism

SummaryWe studied the inhibitory effects of the calcium channel blocker verapamil both on platelet aggregation and intracellular calcium [Ca2+]i in platelets loaded with a fluorescent indicator (quin 2).The inhibitory effects of verapamil on the platelet aggregation response to both thrombin and ionomycin were seen to be clearly dissociated from the verapamil-induced inhibition of the [Ca2+]i increase produced by these agonists. Verapamil-induced inhibition of platelet aggregation was also obtained when using the “calcium-independent” agonist phorbol-myristate acetate (PMA). It may be deduced that a calcium-independent mechanism plays a role in verapamil-induced inhibition of platelet aggregation. We postulate that this mechanism may operate via a protein-kinase C pathway.

Sign in / Sign up

Export Citation Format

Share Document