Effect of
sodium copper chlorophyllin (SCC) on experimental
allergic reaction was investigated.
IgE antibody mediated reactions, homologous passive cutaneous anaphylaxis (PCA) in rats and the release of anaphylactic mediators (
histamine and/or
slow reacting substance of anaphylaxis (
SRS-A] from sensitized guinea pig lung tissues or rat peritoneal mast cells classified as a Type I reaction were clearly inhibited by SCC at a similar potency as N-(3',4'-dimethoxy cinnamoyl)
anthranilic acid (N-5'). The increase of vascular permeability in rat skin caused by
autacoids or
enzymes that participate in the Type I reaction was also inhibited by SCC. Type II or III,
complement dependent, reactions including reversed cutaneous
anaphylaxis (RCA) in rats and Forssman
cutaneous vasculitis (FCV) in guinea pigs were inhibited by SCC.
Prednisolone inhibited RCA in rats, but did not inhibit FCV in guinea pigs. Two experimental types of
glomerulonephritis, nephrotoxic serum (NTS)
nephritis in rats and
immune complex nephritis in (NZW X NZB) F1 mice, in which Type II and III reactions might participate in the onset and the development of the disease, were slightly inhibited by SCC in terms of the biochemical changes of blood and urine parameters and histopathological scores. A moderate remission of the onset and development of these two experimental types of
nephritis was recognized by the administration of
prednisolone.
Delayed hypersensitivity reaction as a Type IV reaction caused by sheep red blood cells (SRBC) in sensitized mouse footpad was not affected by SCC.
Prednisolone clearly inhibited the SRBC induced footpad reaction in mice.
IgM antibody production in mice and
IgE antibody production in rats were not influenced by daily injection of SCC.