The effect of reactive oxygen species on the synthesis of prostanoids from arachidonic acid.

作者: I Baranowska-Bosiacka , I Gutowska , J Korbecki , D Chlubek

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摘要: Reactive oxygen species (ROS), such as hydrogen peroxide, superoxide anion radical or hydroxyl radical, play an important role in inflammation processes well transduction of signals from receptors to interleukin -1β (IL-1β), tumor necrosis factor α (TNF-α) lipopolysaccharides (LPS). NADPH oxidase increases the ROS levels, leading inactivation protein phosphatase 1 (PP1), 2A (PP2A) and tyrosine (PTP): MAPK (MKP-1). Inactivation phosphatases results activation mitogen-activated kinase (MAPK) cascades: c-Jun N-terminal (JNK), p38 extracellular signal-regulated (Erk), which, turn, activate cytosolic phospholipase A₂ (cPLA₂). cause cytoplasmic calcium influx by C (PLC) phosphorylation IP₃-sensitive channels. nuclear κB (NF-κB) via IκB (IKK) through phosphoinositide 3-kinase (PI3K), suppressor tensin homolog (PTEN) B (Akt/PKB) NF-κB-inducing (NIK). IKK phosphorylates NF-κB subunit (IκBα) at Ser³². Oxidative stress inactivates NIK γ subunit/NF-κB essential modulator (IKKγ/NEMO), which might that is independent on inhibitor IκBα degradation, including Tyr⁴² c-Src spleen (Syk), domain rich proline, glutamic acid, serine threonine (PEST) sequence casein II 1B (PTP1B). cascades-activated transcription activator (AP-1) CREB-binding (CBP/p300) lead expression (cPLA₂), cyclooxygenase-2 (COX-2) membrane-bound prostaglandin E synthase (mPGES-1), thus increased release arachidonic acid production prostaglandins, particularly E₂ (PGE₂). increase activity hematopoietic-type PGD (H-PGDS), and, a result, D₂ (PGD₂). However, reacts with nitric oxide forming peroxynitrite I (PGIS), suppressing I₂ (PGI₂). do not affect thromboxane synthesis direct manner; this achieved cPLA₂ COX-2 expression. The aim review was summarize knowledge influence prostanoids acid.

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