Chapter 19. Modulation of Arachidonic Acid Metabolism in the Treatment of Rheumatoid Arthritis

Carty, Thomas J.; Marfat, Anthony; Masamune, Hiroko

doi:10.1016/s0065-7743(08)60847-7

Cited by 18 publications

(30 citation statements)

References 83 publications

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“…Many of these pathways have been demonstrated to be involved in rheumatoid arthritis. For example, modulation of arachidonic acid metabolism and linoleic acid metabolism is believed as two possible ways to treat arthritis 27 , 28 . To help visualize the mechanism of Fuzi, a compound-target-pathway network was constructed (Fig.…”

Section: Resultsmentioning

confidence: 99%

Revealing the efficacy-toxicity relationship of Fuzi in treating rheumatoid arthritis by systems pharmacology

Feng

Liu

Zhang

et al. 2021

Sci Rep

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In recent decades, herbal medicines have played more and more important roles in the healthcare system in the world because of the good efficacy. However, with the increasing use of herbal medicines, the toxicity induced by herbal medicines has become a global issue. Therefore, it is needed to investigate the mechanism behind the efficacy and toxicity of herbal medicines. In this study, using Aconiti Lateralis Radix Praeparata (Fuzi) as an example, we adopted a systems pharmacology approach to investigate the mechanism of Fuzi in treating rheumatoid arthritis and in inducing cardiac toxicity and neurotoxicity. The results showed that Fuzi has 25 bioactive compounds that act holistically on 61 targets and 27 pathways to treat rheumatoid arthritis, and modulation of inflammation state is one of the main mechanisms of Fuzi. In addition, the toxicity of Fuzi is linked to 32 compounds that act on 187 targets and 4 pathways, and the targets and pathways can directly modulate the flow of Na+, Ca2+, and K+. We also found out that non-toxic compounds such as myristic acid can act on targets of toxic compounds and therefore may influence the toxicity. The results not only reveal the efficacy and toxicity mechanism of Fuzi, but also add new concept for understanding the toxicity of herbal medicines, i.e., the compounds that are not directly toxic may influence the toxicity as well.

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Section: Resultsmentioning

confidence: 99%

Revealing the efficacy-toxicity relationship of Fuzi in treating rheumatoid arthritis by systems pharmacology

Feng

Liu

Zhang

et al. 2021

Sci Rep

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“…COX is recognized to be the rate determining enzyme for PG formation and, as such, is critically important for determining PG levels at the inflammatory site. NSAIDs, which reduce pain and swelling associated with inflammation, share the property of suppressing prostaglandin production via inhibition of the COX enzyme [23,24,49]. Tenidap exhibited nanomolar potency in inhibiting prostaglandin D2 formation by cultured rat basophilic leukemia cells (ICs0, 20nM, Table 1), as well as PGE 2 production by human neutrophils [50].…”

Section: Discussionmentioning

confidence: 99%

Tenidap, a structurally novel drug for the treatment of arthritis: Antiinflammatory and analgesic properties

et al. 1996

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Tenidap is a new anti-rheumatic agent which has clinical properties characteristic of a disease modifying drug combined with acute antiinflammatory and analgesic activity. This paper details tenidap's cyclooxygenase (COX) inhibitory activity and the resulting pharmacological properties in experimental animals. Tenidap inhibited calcium ionophore-stimulated prostaglandin D2 synthesis by rat basophilic leukemia cells (COX-1) with an IC50 of 20 nM. In two different in vitro human test systems, tenidap inhibited COX-1 activity more potently than COX-2, although the relative potency ratio (COX-1/COX-2) differed markedly between the two systems. Tenidap inhibited the COX pathway when added to human blood in vitro (IC50, 7.8 mu M) and when administered orally to monkeys, rats and dogs (at 5, 2.5 and 10 mg/kg p.o., respectively) and COX activity measured ex vivo in blood collected 2 to 4 hours post dose. After oral administration to rats, tenidap inhibited carrageenan-induced paw edema with an ED50 of 14 mg/kg and inhibited the glucocorticoid-resistant UV erythema in guinea pigs with an ED50 of 1.4 mg/kg. It retained antiinflammatory activity in adrenalectomized rats indicating that this property is independent of adrenal stimulation. Oral administration of tenidap inhibited the development of adjuvant-induced polyarthritis in the rat and exhibited antinociceptive activity in the murine phenylbenzoquinone and rat acetic acid abdominal constriction tests. These data indicate that tenidap is an effective antiinflammatory and analgesic agent in animal models. These cyclooxygenase-dependent pharmacologic activities do not explain tenidap's disease modifying anti-arthritic properties but add a useful symptom modifying component to its clinical profile.

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“…Second, myricetin-3-O-b-D-glucuronide inhibits both COX and 5-LOX, a mechanism which is also considered to yield GI-safer drugs [25]. One hypothesis for NSAIDinduced GI-toxicity is the so called shunt to the leukotrienes.…”

Section: Discussionmentioning

confidence: 99%

Anti-inflammatory activity of myricetin-3-O-β-D-glucuronide and related compounds

Hiermann¹,

Schramm

Laufer

1998

Inflamm. res.

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Chapter 19. Modulation of Arachidonic Acid Metabolism in the Treatment of Rheumatoid Arthritis

Cited by 18 publications

References 83 publications

Revealing the efficacy-toxicity relationship of Fuzi in treating rheumatoid arthritis by systems pharmacology

Revealing the efficacy-toxicity relationship of Fuzi in treating rheumatoid arthritis by systems pharmacology

Tenidap, a structurally novel drug for the treatment of arthritis: Antiinflammatory and analgesic properties

Anti-inflammatory activity of myricetin-3-O-β-D-glucuronide and related compounds

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