1981
DOI: 10.1016/0006-2952(81)90236-7
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Effects of various anti-inflammatory and anti-rheumatic agents on the synthesis, secretion, and activity of a cartilage proteoglycan-degrading enzyme and other macrophage enzymes

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Cited by 14 publications
(4 citation statements)
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“…Lysosomal stabilisation by CQ and other anti-malarials Therapy and pharmacological properties of hydroxychloroquine and chloroquine could conceivably be a major site of action of these drugs in controlling degradation of connective tissues in arthritic conditions (Whitehouse and Cowley 1966). Several studies have shown that CQ inhibits degradation of proteoglycans in vitro and has direct effects on elastase and other enzymes released from macrophages (Whitehouse and Boström 1965;Cowey and Whitehouse 1966;Fulkerson et al 1979;Famaey and Fontaine 1980;Ackerman et al 1981;Tauber et al 1985;Bartholomew and Lowther 1987;Adeyemi et al 1990;Kamal and Bassiouni 1992;Schug and Kalbhen 1995;Lullmann-Rauch et al 1996). The central role of the destruction of cartilage (and bone) by pro-inflammatory cytokines (IL-1, TNFa) in arthritic conditions has been well recognised for several decades (Etherington et al 1981;Cox and Duff 1996).…”
Section: Cartilage Metabolism and Degradationmentioning
confidence: 96%
“…Lysosomal stabilisation by CQ and other anti-malarials Therapy and pharmacological properties of hydroxychloroquine and chloroquine could conceivably be a major site of action of these drugs in controlling degradation of connective tissues in arthritic conditions (Whitehouse and Cowley 1966). Several studies have shown that CQ inhibits degradation of proteoglycans in vitro and has direct effects on elastase and other enzymes released from macrophages (Whitehouse and Boström 1965;Cowey and Whitehouse 1966;Fulkerson et al 1979;Famaey and Fontaine 1980;Ackerman et al 1981;Tauber et al 1985;Bartholomew and Lowther 1987;Adeyemi et al 1990;Kamal and Bassiouni 1992;Schug and Kalbhen 1995;Lullmann-Rauch et al 1996). The central role of the destruction of cartilage (and bone) by pro-inflammatory cytokines (IL-1, TNFa) in arthritic conditions has been well recognised for several decades (Etherington et al 1981;Cox and Duff 1996).…”
Section: Cartilage Metabolism and Degradationmentioning
confidence: 96%
“…Cartilage degradation is mostly caused by pro-inflammatory cytokines, such as IL-1, IL-17 and TNFa, and their production can be repressed by HCQ treatment (Picot et al, 1991;Sperber et al, 1993;Van Den Borne et al, 1997;Jang et al, 2006;McInnes & Schett, 2007;da Silva et al, 2013). In vitro experiments have also established that CQ inhibits proteoglycan turnover (Fulkerson et al, 1979;Ackerman et al, 1981;Schug & Kalbhen, 1995;Rainsford et al, 2015), and early autoradiographic studies following tritium-labelled HCQ have revealed that this drug accumulates in the cartilage of mice (Cecchi & Porzio, 1964). These findings and its water-soluble properties led to the proposition that HCQ accumulates in the cartilage by binding acidic proteoglycans and protecting them from degradation by proteolytic enzymes (Rainsford et al, 2015).…”
Section: Clinical Impact Of Hcq On Radsmentioning
confidence: 99%
“…При некоторых РЗ ГХ способен снижать уровень провоспалительных цитокинов: ФНОα, ИЛ1β, ИЛ6, ИЛ17, ИЛ18, ИЛ22. Накапливаясь в тканях сустава, ГХ может оказывать протективное влияние на хрящевую ткань, уменьшая разрушение протеогликанов и синтез провоспалительных цитокинов и протеолитических ферментов [37][38][39][40].…”
Section: гидроксихлорохин (гх)unclassified