Experimental AA-amyloidosis in mice is inhibited by treatment with the anti-rheumatic drug tenidap.
In a mouse model for induction of experimental AA-amyloidosis, treatment with tenidap was shown to inhibit the development of amyloidosis. Studies have shown that the drug inhibits the cytokines interleukin (IL)-6, IL-1 and tumour necrosis factor alpha (TNF-alpha) which are known to stimulate hepatocytes to synthesize acute phase proteins (APPs). The APP serum amyloid protein (SAA) is the precursor for amyloid protein AA and tenidap treatment reduces the serum levels of SAA in mouse and humans. It is suggested that reduction of SAA levels reduces the risk of AA fibril formation and thus the development of amyloidosis.
Husebekk
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Department of Immunology and Transfusion Medicine, University Hospital of Tromsø, Norway.
Stenstad
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T
D000686:Amyloidosis / Q000139:chemically induced* / Q000473:pathology; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects / Q000627:therapeutic use*; D004396:Coloring Agents; D003224:Congo Red; D004801:Eosine Yellowish-(YS); D005260:Female; D006416:Hematoxylin; D007211:Indoles / Q000009:adverse effects / Q000627:therapeutic use*; D051379:Mice; D008808:Mice, Inbred CBA; D000078183:Oxindoles; D000685:Serum Amyloid A Protein / Q000032:analysis / Q000378:metabolism*; D013154:Spleen / Q000473:pathology; D013194:Staining and Labeling
D000894:Anti-Inflammatory Agents, Non-Steroidal; D004396:Coloring Agents; D007211:Indoles; D000078183:Oxindoles; D000685:Serum Amyloid A Protein; D003224:Congo Red; C062866:tenidap; D004801:Eosine Yellowish-(YS); D006416:Hematoxylin