INT131816

Context Info Confidence 0.19 First Reported 2006 Last Reported 2006 Negated 0 Speculated 0 Reported most in Abstract Documents 1 Total Number 2 Disease Relevance 1.05 Pain Relevance 1.31

mitochondrion (Pars2) translation (Pars2) ligase activity (Pars2) cytoplasm (Pars2)

Pars2 (Mus musculus)

Pain Link Frequency Relevance Heat COX-2 inhibitor 8 99.88 Analgesic 2 99.42 Hyperalgesia 8 97.80 Inflammation 12 97.54

Disease Link Frequency Relevance Heat Hyperalgesia 8 97.80 INFLAMMATION 6 97.54

Sentences Mentioned In

Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

In conclusion, NO reverses endotoxin-induced inflammatory hyperalgesia via inhibition of prostacyclin production, and also contributes to the analgesic effect of NF-kappaB, COX or PARS inhibitors.

Negative_regulation (inhibitors) of PARS associated with hyperalgesia, inflammation and analgesic

1) Confidence 0.19 Published 2006 Journal Pharmacol. Res. Section Abstract Doc Link 16310374 Disease Relevance 0.52 Pain Relevance 0.66

Injection of endotoxin (10 mg kg(-1), i.p.) to mice elicited hyperalgesia, determined by hot plate test, which is prevented by NO precursor (L-arginine), cNOS/iNOS inhibitor (N(G)-nitro-L-arginine methyl ester; L-NAME), NF-kappaB inhibitor (N-acetylserotonin), COX inhibitor (indomethacin), COX-2 inhibitor (DFU) and PARS inhibitor (3-aminobenzamide).

Negative_regulation (inhibitor) of PARS associated with hyperalgesia and cox-2 inhibitor

2) Confidence 0.14 Published 2006 Journal Pharmacol. Res. Section Abstract Doc Link 16310374 Disease Relevance 0.53 Pain Relevance 0.65

General Comments

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