Abstract:
:A significant decrease in tissue pH or acidosis is a common feature of numerous diseases, including RA (rheumatoid arthritis). Cartilage homoeostasis is profoundly affected by local acidosis in the joints. The diuretic, amiloride, is neuroprotective in models of cerebral ischaemia, a property attributable to the inhibition of ASICs (acid-sensing ion channels) by the drug. However, little is known about the effect of amiloride on apoptosis induced by extracellular acid in articular chondrocytes. We have found that amiloride could restrain the acid-induced apoptosis of rat articular chondrocytes in vitro. Primary rat articular chondrocytes were isolated, cultured and induced to apoptose by exposure to extracellular solution (pH 6.0), while simultaneously treated with 50-200 μM amiloride. Apoptotic rate, mitochondrial function, levels of apoptosis-related gene Bcl-2 family mRNA and activity of caspase 3/9 in chondrocytes were examined. Amiloride inhibited chondrocyte apoptosis in a dose-dependent manner. Furthermore, amiloride partly restored the levels of mitochondrial membrane potential by regulation of Bcl-2 family gene mRNA expression, and activity of caspase 3/9 in chondrocytes induced by extracellular acid. Our results indicated that amiloride protected against acid-induced apoptosis in rat articular chondrocytes by increasing anti-apoptotic ability and down-regulation of pro-apoptotic factors, thus protecting mitochondrial function.
journal_name
Cell Biol Intjournal_title
Cell biology internationalauthors
Rong C,Chen FH,Jiang S,Hu W,Wu FR,Chen TY,Yuan FLdoi
10.1042/CBI20110432subject
Has Abstractpub_date
2012-07-01 00:00:00pages
635-41issue
7eissn
1065-6995issn
1095-8355pii
CBI20110432journal_volume
36pub_type
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