{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,7,2]],"date-time":"2025-07-02T15:10:11Z","timestamp":1751469011191,"version":"3.41.0"},"reference-count":36,"publisher":"Canadian Science Publishing","issue":"11","license":[{"start":{"date-parts":[[2018,11,1]],"date-time":"2018-11-01T00:00:00Z","timestamp":1541030400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/www.nrcresearchpress.com\/page\/about\/CorporateTextAndDataMining"}],"content-domain":{"domain":["cdnsciencepub.com"],"crossmark-restriction":false},"short-container-title":["Can. J. Physiol. Pharmacol."],"published-print":{"date-parts":[[2018,11]]},"abstract":"<jats:p> Because the excessive apoptosis of articular chondrocytes contributes to extracellular matrix (ECM) loss and cartilage damage in rheumatoid arthritis (RA), inhibiting chondrocyte apoptosis might be a promising strategy for RA. Aquaporin1 (AQP1) is overexpressed in RA cartilage and synovial tissues, and play a vital pathogenic role in RA development. Particularly, we previously reported that acetazolamide (AZ) as an AQP1 inhibitor suppressed secondary inflammation and promoted ECM production in cartilage of adjuvant-induced arthritis rats. Here, we investigated the antiapoptotic effect of AZ on interleukin-1\u03b2 (IL-1\u03b2)-induced apoptosis, a classic in vitro model of chondrocyte apoptosis. AZ treatment could inhibit IL-1\u03b2-induced apoptosis, evidenced by increasing cell viability, relieving apoptotic nuclear morphology, decreasing apoptosis rates, and restoring mitochondrial membrane potential. Additionally, AZ reversed IL-1\u03b2-induced decrease of Bcl-2 protein and reduced IL-1\u03b2-induced increases of Bax and caspase 3 protein, accompanied by inhibiting I\u03baB\u03b1 degradation and phosphorylation in cytoplasm, reducing NF-\u03baB p65 protein level in nucleus and preventing NF-\u03baB p65 translocation from cytoplasm to nucleus. In conclusion, our findings indicated that AZ could effectively attenuate IL-1\u03b2-induced chondrocyte apoptosis mediated by regulating the protein levels of apoptosis-related genes and inhibiting the activation of NF-\u03baB signal pathway, suggesting that AZ might be of potential clinical interest in RA treatment. <\/jats:p>","DOI":"10.1139\/cjpp-2018-0334","type":"journal-article","created":{"date-parts":[[2018,8,1]],"date-time":"2018-08-01T13:48:05Z","timestamp":1533131285000},"page":"1104-1111","update-policy":"https:\/\/doi.org\/10.1139\/csp-crossmark-policy","source":"Crossref","is-referenced-by-count":6,"title":["Acetazolamide protects rat articular chondrocytes from IL-1\u03b2-induced apoptosis by inhibiting the activation of NF-\u03baB signal pathway"],"prefix":"10.1139","volume":"96","author":[{"given":"Li","family":"Cai","sequence":"first","affiliation":[{"name":"Department of Pathology, School of Basic Medicine, Anhui Medical University, 81 Meishan Road, Hefei 230032, 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