{'fraction_non_alphanumeric': 0.02869097429766886, 'fraction_numerical': 0.0035863717872086074, 'mean_word_length': 5.463320463320463, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Acetyl-11-Keto-β-Boswellic Acid Restrains Inflammation and Extracellular Matrix Degradation of Osteoarthritis via Suppression of NF-κB Pathway


 Background: Mechanical stress along with inflammation play causative roles in the development of osteoarthritis (OA), which decreases the quality of life and causes economic loss. Inflammation and extracellular matrix (ECM) degradation have been identified as key factors in the development of OA. As the main active component in frankincense, acetyl-11-keto-β-boswellic acid (AKBA) has been shown to have positive effects on inflammation. However, the effects of AKBA in cartilage inflammation and ECM degradation are currently elusive.Methods: We demonstrated the role of inflammation and ECM degradation in the pathogenesis of OA and determined the protective effect of AKBA on both Hulth-Telhag rat OA model and lipopolysaccharide (LPS)-induced rat chondrocytes.Results: We found increased inflammatory expression and decreased ECM expression in OA model cartilage and LPS-induced chondrocytes. Meanwhile, the protective effect of AKBA and its inhibitory effects on inflammation as well as ECM-related markers were also observed in the rat Hulth-Telhag model. Furthermore, activation of NF-κB attenuated nuclear p65 protein levels in chondrocytes upon LPS stimulation. In addition, AKBA was found to subsequently reversed the LPS-induced activation of NF- κB signal and inflammation-related ECM degradation in chondrocytes.Conclusions: Suppression of NF-κB pathway activation by AKBA restrains OA development via inhibition of inflammation and ECM degradation. AKBA is a promising therapeutic agent for the treatment of OA.