Interaction of phenothiazine sulphonate and chlorophenothiazine sulphonate with the B-determinant of the third component of complement (C3)

Asghar, Syed S.; Kammeijer, A.

doi:10.1016/0161-5890(79)90054-3

Cited by 3 publications

(2 citation statements)

References 13 publications

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“…Suramin was obtained from Bayer Pharmaceuti cals (Leverkusen, FRG), chlorpromazine hydrochlo ride from Nogepha BV (Alkmaar, The Netherlands), 2-hydroxystilbamidine isethionate from May and Baker (Dagenham, UK) and chlorophenothiazine sul phonate was synthesized as described [16], Human serum albumin (HSA) was purchased from Sigma Chemicals Co. (St. Louis, Mo., USA). Fluorescein iso thiocyanate (FTC)-labelled goat anti-rabbit C3 (ß 1A + P1C) (batch No.…”

Section: Chemicals and Antiseramentioning

confidence: 99%

“…More recently, suppression of development of EAE and suppression of hu man vasculitis by the complement inhibitors suramin [6] and chlorpromazine [7], respec tively, has been shown. Here we show that certain low molecular weight complement in hibitors, namely suramin [8][9][10][11][12], 2-hydroxystilbamidine [13,14], chlorpromazine [15] and chlorophenothiazine sulphonate [ 16] can strongly suppress complement-mediated vas cular injury seen in the Arthus reaction. of saline and incomplete Freund's adjuvant was given.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Suppression of Complement-Mediated Vascular Injury at Arthus Reaction Sites by Complement Inhibitors

Ss¹,

Kp²,

Kammeijer³

et al. 1986

Complement

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Certain complement inhibitors, namely chlorpromazine, suramin, 2-hydroxystilbamidine and chlorophenothiazine sulphonate were tested for their ability to suppress complement deposition and vascular injury at the site of an Arthus reaction. Deposition of complement was suppressed in the order 2-hydroxystilbamidine > suramin > chlorpromazine. All the above mentioned four compounds strongly protected vascular injury as observed by electron microscopic studies. At Arthus reaction sites prepared without drug treatment venules ranged from normal to severely altered and damaged. Discontinuities in endothelial linings varied from small to longer stretches. In the latter situation remaining endothelial cells were degenerated and endothelial remnants did not have an intact basal lamina. After treatment with the above complement inhibitors, at arthus reaction sites some venules appeared normal, whereas others were altered but in all cases the endothelium and its basal lamina remained intact.

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Section: Chemicals and Antiseramentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Suppression of Complement-Mediated Vascular Injury at Arthus Reaction Sites by Complement Inhibitors

Ss¹,

Kp²,

Kammeijer³

et al. 1986

Complement

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In vitro inhibition of the classical pathway of human complement by a natural microbial product, colistin sulphate

Asghar

Koster²,

Helm

1986

Biochemical Pharmacology

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Artificial inhibition of the complement system

et al. 2007

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A great number of natural substances affect the complement system in addition to its natural regulators. Among the complement effectors, the most important are inhibitors of the activation cascade. The necessity of searching for preparations capable of a purposeful effect on complement by inhibition of single stages of the activation cascade and without influence on its other functions is connected with the current importance of use in medicine of novel therapeutic regulators of the complement system. Important directions are the search for complement inhibitors that (a) interfere with the rejection of transplants; (b) can replace C1 inhibitor in hereditary angioedema, and (c) have a high anti-inflammatory activity in the therapy of rheumatic diseases, diabetes, and other autoimmune disorders. It is expedient to use the available techniques for the directed detection of the action of medicinal substances on complement, which allow the determination of their action on the complement system at various stages of the cascade of its activation.

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Interaction of phenothiazine sulphonate and chlorophenothiazine sulphonate with the B-determinant of the third component of complement (C3)

Cited by 3 publications

References 13 publications

Suppression of Complement-Mediated Vascular Injury at Arthus Reaction Sites by Complement Inhibitors

Suppression of Complement-Mediated Vascular Injury at Arthus Reaction Sites by Complement Inhibitors

In vitro inhibition of the classical pathway of human complement by a natural microbial product, colistin sulphate

Artificial inhibition of the complement system

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