• Korean Journal of Pharmacognosy
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• v.17 no.2
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• pp.161-167
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• 1986

The smear method developed by Velaskar and Chitre was modified to allow the screening of plant extracts and/or fractions for platelet anti-aggregating activity. The modified smear method was also found suitable for massive screening of pure compounds. Sample fractions prepared from various plant extracts were examined for their effects against ADP, arachidonic acid (AA) or collagen induced platelet aggregations. Several solvent fractions of plant extracts including water fraction prepared from the methanol extract of Acanthopanax sp. was inhibitory against rat platelet aggregations. The activity guided treatments and fractionations of the water fraction from A. senticosus Max yielded two anti-platelet aggregatory substances, 3, 4-dihydroxybenzoic acid (I) and its artefact ethyl 3, 4-dihydroxybenzoate(II). The inhibitory activities of I and II against rat platelet aggregation were compared with that of aspirin, a known inhibitor of platelet aggregation. Discussions also included the results of the investigations on the structural activity relationships among the various dihydroxybenzoic acid derivatives against platelet aggregations induced by either one of ADP, AA or collagen.

• Food Science and Biotechnology
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• v.16 no.2
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• pp.218-222
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• 2007

The anticoagulant properties of Cinnamomum cassia bark-derived materials were evaluated against platelet aggregation induced by arachidonic acid (AA), collagen, platelet activating factor (PAF), or thrombin, and these effects were then compared to those of three commercially available compounds (cinnamic acid, cinnamyl alcohol, and aspirin). The active constituent obtained from C. cassia barks was isolated by silica gel column chromatography and high pressure liquid chromatography (HPLC), and was characterized as trans-cinnamaldehyde by MS, $^1H-NMR$, $^{13}C-NMR$, and IR spectroscopy. With regard to 50% inhibitory concentration ($IC_{50}$) values, cinnamaldehyde was found to effectively inhibit platelet aggregation induced by AA ($IC_{50},\;43.2\;{\mu}M$) and collagen ($IC_{50},\;3.1\;{\mu}M$). By way of comparison, cinnamaldehyde proved to be a significantly more potent platelet inhibitor against platelet aggregation induced by collagen than aspirin. The effect exerted by cinnamaldehyde against platelet aggregation induced by AA was 1.2 times less than that of aspirin. These results indicate that cinnamaldehyde may prove useful as a lead compound for the inhibition of platelet aggregation induced by AA and collagen.

• Journal of Periodontal and Implant Science
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• v.44 no.4
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• pp.169-177
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• 2014

Purpose: We aimed to investigate the impact of nonsurgical periodontal treatment combined with one-year dietary supplementation with omega (${\omega}$)-3 on the serum levels of eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), docosapentaenoic acid (DPA), and arachidonic acid (AA). Methods: Fifteen patients with chronic generalized periodontitis were treated with scaling and root planing. The test group consisted of seven patients ($43.1{\pm}6.0$ years) supplemented with ${\omega}$-3, consisting of EPA plus DHA, three capsules, each of 300 mg of ${\omega}$-3 (180-mg EPA/120-mg DHA), for 12 months. The control group was composed of eight patients ($46.1{\pm}11.6$ years) that took a placebo capsule for 12 months. The periodontal examination and the serum levels of DPA, EPA, DHA, and AA were performed at baseline (T0), and 4 (T1), and 12 (T2) months after therapy. Results: In the test group, AA and DPA levels had been reduced significantly at T1 (P<0.05). AA and EPA levels had been increased significantly at T2 (P<0.05). The ${\Delta}EPA$ was significantly higher in the test compared to the placebo group at T2-T0 (P=0.02). The AA/EPA had decreased significantly at T1 and T2 relative to baseline (P<0.05). Conclusions: Nonsurgical periodontal treatment combined with ${\omega}$-3 supplementation significantly increased the EPA levels and decreased the AA/EPA ratio in serum after one year follow-up. However, no effect on the clinical outcome of periodontal therapy was observed.

• Journal of the Korean Applied Science and Technology
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• v.7 no.2
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• pp.55-61
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• 1990

To investigate the influence of saturated fats, ${\alpha}-linolenic$ acid, EPA and DHA on the lipid hydroperoxide concentration and fatty acid composition in liver microsomes and in plasma lipid of rabbits, the animals were fed on the perilla oil rich ${\alpha}-linolenic$ acid or sardine oil rich EPA and DHA diet for four weeks Were examined. The fatty acid composition of plasma lipid and liver microsomes of rabbits fed on the perilla oil diet was an accumulation of arachidonic acid(AA) 20:4 n-6, eicosapentaenoic acid(EPA) 20:5 n-3, and docosahexaenoic acid(DHA) 22:6 n-3, The fatty acid composition of plasma lipid and liver microsomes of rabbits fed on the sardine oil was an accumulation of ${\alpha}-linolenic$ acid(LNA) 18:3 n-3, and arachidonic acid(AA) 20:4. The p/s ratio of rabbits fed on the perilla oil diet changed from 7.4 to 2.27 for plasma lipid and 2.47 for liver microsomes. The concentration of lipid hydroperoxide was 3.48 nmol MDA/ml and 4.35 nmol MDA/ml for plasma lipid and liver microsomes, respectively, in perilla oil diet. The lipid hydroperoxide liver was 4.22 nmol MDA/ml and 67 nmol MDA/ml for plasma lipid and liver microsornes in sardine oil diet.

• Korean Journal of Food Science and Technology
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• v.47 no.3
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• pp.281-285
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• 2015

An oleaginous fungus was isolated from soil and identified as Mortierella sp. (M-12) for producing arachidonic acid (AA). Cell disruption methods, extraction methods, and particle sizes of freeze-dried biomass were tested to achieve maximum extraction of total lipids and AA. M-12 grown in glucose yeast media at $25^{\circ}C$ for 7 days contained 35.5% total lipid, and 47% of the total lipid was AA. Lipid extraction yield from wet biomass was shown to be similar to that in a dry state. Maximum lipid extraction was achieved using a mixture of chloroform and methanol (2:1) as an extraction solvent. Different mechanical cell disruption methods did not affect lipid extraction yields. The smaller the particle size of the biomass, the better the lipid extraction yield was observed. Particle size of biomass was shown to more strongly affect lipid extraction than extraction time. The highest AA content was observed in the class of neutral lipids.

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.242.2-243
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• 2002

We have previously reported that activation of $K^{+}$-$Cl^{-}$-cotransport (KCC) by N-ethylmaleimide (NEM) induces apoptosis through generation of reactive oxygen species (ROS) in HepG2 human hepatoblastoma cells. In this study we investigated the possible role of phospholipase $A_2$($PLA_2$)-arachidonic acid (AA) signals in the mechanism of the NEM actions. (omitted)

• Journal of Ginseng Research
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• v.43 no.2
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• pp.236-241
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• 2019

Background: Thromboxane A2 ($TXA_2$) induces platelet aggregation and promotes thrombus formation. Although ginsenoside Ro (G-Ro) from Panax ginseng is known to exhibit a $Ca^{2+}-antagonistic$ antiplatelet effect, whether it inhibits $Ca^{2+}-dependent$ cytosolic phospholipase $A_2$ ($cPLA_{2{\alpha}}$) activity to prevent the release of arachidonic acid (AA), a $TXA_2$ precursor, is unknown. In this study, we attempted to identify the mechanism underlying G-Ro-mediated $TXA_2$ inhibition. Methods: We investigated whether G-Ro attenuates $TXA_2$ production and its associated molecules, such as cyclooxygenase-1 (COX-1), $TXA_2$ synthase (TXAS), $cPLA_{2{\alpha}}$, mitogen-activated protein kinases, and AA. To assay COX-1 and TXAS, we used microsomal fraction of platelets. Results: G-Ro reduced $TXA_2$ production by inhibiting AA release. It acted by decreasing the phosphorylation of $cPLA_{2{\alpha}}$, p38-mitogen-activated protein kinase, and c-Jun N-terminal kinase1, rather than by inhibiting COX-1 and TXAS in thrombin-activated human platelets. Conclusion: G-Ro inhibits AA release to attenuate $TXA_2$ production, which may counteract $TXA_2-associated$ thrombosis.

• Herbal Formula Science
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• v.30 no.3
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• pp.155-163
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• 2022

Objectives : Lonicera japonica is known for anti-inflammation and antibiotic effect in Korean medicine. This study aimed for investigating the cytoprotective effect of Lonicera japonica extract (LJE) for HepG2 cells against arachidonic acid (AA)+iron-induced oxidative stress. Methods : The effect of LJE on cell viability was assessed by MTT assay. ROS assay was selected to assess antioxidant effect of LJE. To assess LJE's effect on mitochondrial function, flow cytometric analysis was operated. And immunoblot analysis was used to establish the underlying mechanism of LJE. Results : LJE protected HepG2 cells against AA+iron-induced oxidative stress by phosphorylation of liver kinase B1 and blocked the decline of procaspase 3. Also, LJE preserved the mitochondrial membrane permeability induced by AA+iron. Conclusion : LJE protected the hepatocyte from AA+iron-induced oxidative stress by activation of LKB1 by the preservation of mitochondrial functions.

• Korean Journal of Pharmacognosy
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• v.21 no.2
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• pp.126-129
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• 1990

Platelet anti-aggregating activities were evaluated with three combined crude drug preparations which have been used for 'eahyul'-one of the pathological concept in oriental medicine presumably concerning blood stasis or stagnant syndrome. The water extract of each combined preparation and each component plant was tested for their effects against ADP, arachidonic acid (AA) or collagen induced rat platelet aggregations. Mild inhibitory activities were observed with all the three tested preparations, Kaechibokryung-Hwan, Dangkqijakyak-San and Ohnkyung-Tang, and the component plants which are included in at least two of the above preparations.

• The Korean Journal of Zoology
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• v.38 no.4
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• pp.457-464
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• 1995

Hela cells, a transformed human epithelial cell line, attach to various substrata but subsequent spreading is specific to collagen or gelatin. The spreading is initiated by the activation of phospholipase $A_2$ (PLA$_2$) which produces arachidonic acid (AA) as a consequence of cell surface collagen receptor clustering. This study examines the mechanism of PLA$_2$activation and which phospholipids are hydrolyzed by PIA$_2$ to release AA in response to Hela cell adhesion to a gelatin substratum. The levels of phosphatidyicholine decreases, among various phospholipids, during attachment and spreading of Hela cells. Lysophosphatidyicholine Is the only lysophospholipids formed during ileLa cell adhesion indicating that clustered collagen receptors activate PLA$_2$to hydrolyze posphatidylcholine to AA and lysophosphatidylcholine. Among various molecular entitles which are known to regulate PLA$_2$ activation, we have previously shown that PLA2 activation is not mediated by either changes in $Ca_2$+ levels, alkalinization of cytoplasmic p11, or activation of protein hinase C. It is also likely that PIA2 activation is not mediated by either pertussis or cholera toxinsensitive G proteins as those toxins do not affect both AA release and cell spreading.