• Proceedings of the PSK Conference
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• 2002.10a
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• pp.258.1-258.1
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• 2002

Piperine (piperinoyl-piperidine) is a nitrogenous pungent substance contained in black pepper. the well know spice obtained from Piper nigrum L. (Piperaceae). Pharmacological studies have shown that piperine reduces inflammation and pain. possesses anticonvulsant and antiulcer activity. protects the liver and has deleterious effects on testis function. Prostaglandins(PGs) are a family of intercellular and intracellular messengers derived from arachidonic acid(AA) by phospholipase(PL) and cyclooxygenase(COX). (omitted)

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.151.2-152
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• 2003

Bee venom (BV) has been utilized to relieve pain and to treat inflammatory diseases such as rheumatoid arthritis (RA). BV contains a variety of different peptides including melittin, apamin, adolapin and mast cell degranulating (MCD) peptide. In addition, it also contains enzyme (i.e. phospholipase A2), biologically active amines and non-peptide components. (omitted)

• Proceedings of the Korean Society of Applied Pharmacology
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• 2002.07a
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• pp.248-248
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• 2002

• Kidney Research and Clinical Practice
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• v.37 no.4
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• pp.426-426
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• 2018

• Proceedings of the PSK Conference
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• 2003.04a
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• pp.192.1-192.1
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• 2003

Histamine is found in most tissues of the body and activates polymodal nociceptors via unmyelinated afferent C-fibres. We have demonstrated that bradykinin. acting at B2 bradykinin receptors. excites sensory nerve endings by activating capsaicin receptors via production of 12-lipoxygenase metabolites of arachidonic acid in dorsal root ganglion. Histamine is known to the activator of phospholipase A2- arachidonic acid pathway via a G-protein- coupled H1 receptor. (omitted)

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.65.3-66
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• 2003

Bacillariolide III was isolated from the culture medium of the marine diatom, Pseudonitzschia multi series, a causative organism of amnesic shellfish poisoning by Shimizu et al. This extracellular metabolite features bicyclic system of hydroxycyclopentane and (Z)-pentenoic acid-bearing lactone ring. Bacillariolide I is known to possess significant inhibitory activity against phospholipase A$_2$, but the biological function of bacillariolide III is still under investigation. The unique structural feature as well as the promising biological activity led us to the total synthesis of bacillariolide III. (omitted)

• Proceedings of the PSK Conference
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• 2002.10a
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• pp.260.1-260.1
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• 2002

Green tea contains several antioxidants including polyphenols of the catechin. which have been shown to act in vitro and in vivo as anti-inflammatory. anti-viral and anti-tumor drugs. Prostaglandins (PGs) are a family of intercellular and intracellular messengers derived from arachidonic acid(AA) by phospholipase(PL) and cyclooxygenase(COX). These mediators exert a wide range of effects on processes such as smooth muscle tone. vascular permeability, cellular proliferation. and inflammatory/immune function. (omitted)

• Asian Pacific Journal of Cancer Prevention
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• v.15 no.4
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• pp.1797-1802
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• 2014

Background: The prostaglandin-endoperoxide synthase 2 (PTGS2) and phospholipase A2 group IIA (PLA2G2A) genes encode enzymes that are involved in arachidonic acid and prostaglandin biosynthesis. Dysregulation of both genes is associated with inflammation and carcinogenesis, including esophageal squamous cell carcinoma (ESCC). We therefore hypothesized that there is an association between single nucleotide polymorphisms (SNPs) in these genes and susceptibility to ESCC. Methods: We performed a gene-wide tag SNP-based association study to examine the association of SNPs in PTGS2 and PLA2G2A with ESCC in 269 patients and 269 healthy controls from Taihangshan Mountain, Henan and Hebei Provinces, the rural area of China which has the highest incidence of esophageal cancer in the world. Thirteen tag SNPs in PLA2G2A and 4 functional SNPs in PTGS2 were selected and genotyped using a high-throughput Mass Array genotyping platform. Results: We found a modest increased risk of ESCC in subjects with the PTGS2 rs12042763 AA genotype (OR=1.23; 95% CI, 1.00-3.04) compared with genotype GG. For PLA2G2A, a decreased risk of ESCC was observed in subjects with the rs11677 CT (OR=0.51, 95%CI, 0.29-0.85) or TT genotype (OR=0.51, 95%CI, 0.17-0.96) or the T carriers (CT+TT) (OR=0.52, 95%CI, 0.31-0.85) when compared with the CC genotype. Also for PLA2G2A, rs2236771 C allele carriers were more frequent in the control group (P=0.02). Subjects with the GC (OR=0.55, 95%CI, 0.33-0.93) or CC genotype (OR=0.38, 95% CI, 0.16-0.94) or the C carriers (GC+CC) (OR=0.52, 95%CI, 0.32-0.85) showed a negative association with ESCC susceptibility. Conclusions: Our results suggest that PTGS2 and PLA2G2A gene polymorphisms may modify the risk of ESCC development.

• Archives of Pharmacal Research
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• v.24 no.2
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• pp.126-135
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• 2001

Quinacrine (QU), a phospholipase-A2 (PLA-2) inhibitor has been used clinically as a chemotherapeutic adjuvant. To understand the mechanisms leading to its chemotherapeutic effect, we have investigated QU-induced apoptotic signaling pathways in human cervical squamous carcinoma HeLa cells. In this study, we found that QU induced cytochrome c-dependent apoptotic signaling. The release of pro-apoptotic cytochrome c was QU concentration- and time-dependent, and preceded activation of caspase-9 and -3. Flow cytometric FACScan analysis using fluorescence intensities of $DiOC_6$/ demonstrated that QU-induced cytochrome c release was independent of mitochondrial permeability transition (MPT), since the concentrations of QU that induced cytochrome c release did not alter mitochondrial membrane potential (${\blacktriangle}{\Psi}_m$). Moreover, kinetic analysis of caspase activities showed that cytochrome c release led to the activation of caspase-9 and downstream death effector caspase-3, Caspase-3 inhibitor (Ac-DEVD-CHO) partially blocked QU-induced apoptosis, suggesting the importance of caspase-3 in this apoptotic signaling mechanism. Supplementation with arachidonic acid (AA) sustained caspase-3 activation induced by QU. Using inhibitors against cellular arachidonate metabolism of lipooxygenase (Nordihydroxyguaiaretic Acid, NDGA) and cyclooxygenase (5,8,11,14-Eicosatetraynoic Acid, ETYA) demonstrated that QU-induced apoptotic signaling may be dependent on its role as a PLA-2 inhibitor. Interestingly, NDCA attenuated QU-induced cytochrome c release, caspase activity as well as apoptotic cell death. The blockade of cytochrome c release by NDCA was much more effective than that attained with cyclosporin A (CsA), a MPT inhibitor. ETYA was not effective in blocking cytochrome c release, except under very high concentrations. Caspase inhibitor z-VAD blocked the release of cytochrome c suggesting that this signaling event is caspase dependent, and caspase-8 activation may be upstream of the mitochondrial events. In summary, we report that QU induced cytochrome c-dependent apoptotic signaling cascade, which may be dependent on its role as a PLA-2 inhibitor. This apoptotic mechanism induced by QU may contribute to its known chemotherapeutic effects.

• Korean journal of applied entomology
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• v.51 no.4
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• pp.349-356
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• 2012

Eicosanoid mediates various cellular immune responses in insects. This study aimed to discover its novel action on the modulation of hemocyte populations in response to an immune challenge. Upon bacterial challenge, the last instar larvae of the beet armyworm, Spodoptera exigua, increased their total hemocyte density in 2 h, and then decreased it to a basal hemocyte density level. This rapid increase in total hemocyte density was explained by an increase of plasmatocyte and spherulocyte densities. When larvae were treated with dexamethasone (a specific phospholipase $A_2$ ($PLA_2$) inhibitor), they did not show any increase in hemocyte density in response to bacterial challenge. However, the addition of arachidonic acid (a catalytic product of $PLA_2$) to larvae treated with dexamethasone recovered the up-regulation of hemocyte density in response to bacterial infection. Among eicosanoid, cyclooxygenase (COX), but not lipoxygenase (LOX), products seemed to mediate the increase of hemocyte density in response to bacterial infection because naproxene (a COX inhibitor) inhibited the hemocyte density increase, though esculetin (a LOX inhibitor) did not. Prostaglandin $E_2$, a COX product, significantly increased the hemocyte density even without bacterial infection. These results suggest that eicosaniod mediates a rapid increase in total hemocyte density in response to immune challenge.