Figure 7 - uploaded by Yan Zhang
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PGE2 Biosynthetic pathway. PLA2 = cytosolic phospholipase A2; COX = cyclooxygenases; NSAIDS = nonsteroidal anti-inflammatory drugs; PGH2 = prostaglandin H2; PGES = prostaglandin E synthase, PGD2 = prostaglandin D2; PGE2 = prostaglandin E2; PGI2 = prostaglandin I2; PGF2α = prostaglandin F2α; TxA2 = Thromboxane A2. Revised from (Chizzolini and Brembilla, 2009)

PGE2 Biosynthetic pathway. PLA2 = cytosolic phospholipase A2; COX = cyclooxygenases; NSAIDS = nonsteroidal anti-inflammatory drugs; PGH2 = prostaglandin H2; PGES = prostaglandin E synthase, PGD2 = prostaglandin D2; PGE2 = prostaglandin E2; PGI2 = prostaglandin I2; PGF2α = prostaglandin F2α; TxA2 = Thromboxane A2. Revised from (Chizzolini and Brembilla, 2009)

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A common mechanism by which redox stress may activate inflammatory responses to potentially initiate, propagate and maintain many diseases has not been characterized. Accumulating evidence suggests that pattern recognition receptors of the innate immune system such as the toll-like receptors (TLRs) are involved. In the present study, we tested the...

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... is not stored but synthesized de novo from membrane-released arachidonic acid (AA) when cells are activated by stimuli such as mechanical trauma, cytokines, and growth factors. As Fig. 7 shows, PGE2 synthesis is initiated by a family member of phospholipase A (PLA), a family of enzymes that catalyze the hydrolysis of membrane phospholipids at the sn- 2 position, liberating A (a 20-carbon unsaturated fatty acid). Both cytosolic PLA2 (cPLA2) and secretory group V PLA2 (sPLA2-V) are shown to be involved in regulating AA ...
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... shown in RAW-Blue cells (Chapters 2 and 3), we have also examined two treatment paradigms for primary pM: induced cytotoxicity in a concentration-dependent manner ( Fig. 27 A and 27 B). With PPC at 5 μM and SIN-1 at 1 mM, 86% and 90% of the control cells derived from both TLR4-WT and TLR4-KO mice were viable, respectively (Fig. 27 A). Consistently, long-term treatment with PPC at 5 μM or SIN-1 at 1 mM for 16 h incubation caused ≤ 10% cytotoxicity (Fig. 27 ...
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... shown in RAW-Blue cells (Chapters 2 and 3), we have also examined two treatment paradigms for primary pM: induced cytotoxicity in a concentration-dependent manner ( Fig. 27 A and 27 B). With PPC at 5 μM and SIN-1 at 1 mM, 86% and 90% of the control cells derived from both TLR4-WT and TLR4-KO mice were viable, respectively (Fig. 27 A). Consistently, long-term treatment with PPC at 5 μM or SIN-1 at 1 mM for 16 h incubation caused ≤ 10% cytotoxicity (Fig. 27 ...
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... pM: induced cytotoxicity in a concentration-dependent manner ( Fig. 27 A and 27 B). With PPC at 5 μM and SIN-1 at 1 mM, 86% and 90% of the control cells derived from both TLR4-WT and TLR4-KO mice were viable, respectively (Fig. 27 A). Consistently, long-term treatment with PPC at 5 μM or SIN-1 at 1 mM for 16 h incubation caused ≤ 10% cytotoxicity (Fig. 27 ...
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... pM derived from TLR4-KO mice showed no response to either oxidant treatment alone or LPS-EK sensitization with respect to protein expression of cPLA2, COX-1, COX-2, or mPGES-1 (Fig. 47). Due to the limited number of wells in SDS-PAGE mini gel, we run samples of TLR4-WT and TLR4-KO in separate gels. However, all the other procedures such as the amount of total protein loaded, running gel, transferring, blocking, primary antibody incubation were done under the same conditions in parallel procedures. The histogram ...