Effects of prostaglandin E1 analogue, misoprostol, on the development of adjuvant arthritis in rats

Rainsford, K. D.; Whitehouse, M. W.; Vernon‐Roberts, B.

doi:10.1007/bf02659110

Cited by 4 publications

(1 citation statement)

References 20 publications

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“…Another interesting class are prostanoid‐mimetics, such as misoprostol, inhibiting TNF ‐ α production 18,19 and effective co‐drugs for controlling acute inflammation 20 or experimental arthritis 21 . It is unfortunate that so much NSAID therapy also targets the beneficial cytokine‐regulant 22,23 and repair‐promoting 24 activities of the natural prostaglandins.…”

Section: Synthetic Drugs: Some Justifiably Rejected On Grounds Of Toxmentioning

confidence: 99%

Beyond conventional DMARDs: extending TNF‐regulant therapies to the vast majority/less privileged who do need them

Butters¹,

Whitehouse

2009

Int J of Rheum Dis

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This article is a plea to find (better) ways to extend the benefits of anti-cytokine therapies to ensure they will become available as widely as possible. Pessimistically, this will probably involve substituting more affordable, although somewhat less specific, non-biological agents for present target-specific bio-DMARDs (disease-modifying antirheumatic drugs) to ensure far wider distribution of benefits. Optimistically, new developments in technology and bio-engineering might dramatically reduce costs of present 'biological' therapies. (The antibiotics we now take for granted were once also horrendously expensive.). Pragmatically, one goal for this mission should include seriously pursuing more research and pilot clinical trials of non-protein combination therapies able to control: (i) TNF or other pro-inflammatory cytokines; and also (ii) other mediators sustaining chronic inflammation (-->pain, effusion, fibrosis, porosis, etc.). This can be immediately facilitated by drawing upon the immense resources of non-prescription Asia-Pacific traditional therapies--particularly when these have already been shown to either reduce TNF synthesis or control TNF-induced responses in preclinical studies. Could this be a major goal for the next decade, helping rectify some of the omissions of the current Bone & Joint Decade 2000-2010?

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Section: Synthetic Drugs: Some Justifiably Rejected On Grounds Of Toxmentioning

confidence: 99%

Beyond conventional DMARDs: extending TNF‐regulant therapies to the vast majority/less privileged who do need them

Butters¹,

Whitehouse

2009

Int J of Rheum Dis

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Professor Barrie Vernon-Roberts, AO, MD, BSc, PhD, FRCPath, FRCPA, FAOrthA (Hon), FRS.SA

Rainsford

Haynes

2013

Inflammopharmacol

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Prostanoids as friends, not foes: Further evidence from the interference by cycloxygenase-inhibitory drugs when inducing tolerance to experimental arthritigens in rats

Whitehouse

2005

Inflammopharmacol

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Pharmacologists have generally been prejudiced against prostanoids, uncritically accepting their suppression as desirable therapy, especially for 'quick-fix' analgesia. This myopic perception for a long time ignored (a) the essentiality of prostanoid precursors in nutrition, (b) the physiological protective functions of natural prostaglandins (PGs) (vasculature, stomach, kidney), (c) resolution of inflammation after the expression of COX-2 and (d) increasing therapeutic use of either synthetic PGs (for erectile dysfunction, ophthalmic disorders, inducing parturition, etc) or their natural precursors, e.g., omega3-rich polyunsaturated oils, to treat arthritis. Experimental studies in rats have indicated that prostaglandins (E series) are (i) useful, perhaps auto-regulators of established immunoreactivity and (ii) able to amplify (or even induce) anti-inflammatory activity with other agents. Furthermore, anti-prostanoid therapy (APT) can be arthritigenic!!, interfering with the acquisition of tolerance to some arthritigens. For patients with rheumatoid arthritis this additional side-effect of APT, barely recognised to date, may actually perpetuate their arthritis by impairing prostanoid-mediated remission processes. Hopefully, recent adverse publicity about COX-2 inhibitory drugs might stimulate serious re-assessment of some traditional anti-inflammatory therapies with low APT activity for the management of both acute pain (non-addictive cannabinoids, celery seed, etc.) and chronic inflammation, e.g., Lyprinol (a mussel lipid extract).

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Effects of prostaglandin E1 analogue, misoprostol, on the development of adjuvant arthritis in rats

Cited by 4 publications

References 20 publications

Beyond conventional DMARDs: extending TNF‐regulant therapies to the vast majority/less privileged who do need them

Beyond conventional DMARDs: extending TNF‐regulant therapies to the vast majority/less privileged who do need them

Professor Barrie Vernon-Roberts, AO, MD, BSc, PhD, FRCPath, FRCPA, FAOrthA (Hon), FRS.SA

Prostanoids as friends, not foes: Further evidence from the interference by cycloxygenase-inhibitory drugs when inducing tolerance to experimental arthritigens in rats

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