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The inflammatory environment and excessive chondrocyte apoptosis have been demonstrated to play crucial roles in the onset of osteoarthritis (OA). Hydrogen sulfide (H2S), a gaseous signalling molecule, exerts an inhibitory effect on inflammation and apoptosis in several degenerative diseases. However, the protective effect of H2S against OA has not been fully clarified, and its underlying mechanism should be examined further. In the current study, the role of endogenous H2S in the pathogenesis of OA and its protective effects on interleukin (IL)‐1β‐induced chondrocytes were identified. Our data revealed decreased H2S expression in both human degenerative OA cartilage tissue and IL‐1β‐induced chondrocytes. Pretreatment with the H2S donor sodium hydrosulfide (NaHS) dramatically attenuated IL‐1β‐induced overproduction of inflammatory cytokines and improved the balance between anabolic and catabolic chondrocyte capacities, and these effects were dependent on PI3K/AKT pathway‐mediated inhibition of nuclear factor kappa B (NF‐κB). Moreover, mitochondrial dysfunction‐related apoptosis was significantly reversed by NaHS in IL‐1β‐stimulated chondrocytes. Mechanistically, NaHS partially suppressed IL‐1β‐induced phosphorylation of the mitogen‐activated protein kinase (MAPK) cascades. Furthermore, in the destabilization of the medial meniscus mouse model, OA progression was ameliorated by NaHS administration. Taken together, these results suggest that H2S may antagonize IL‐1β‐induced inflammation and mitochondrial dysfunction‐related apoptosis via selective suppression of the PI3K/Akt/NF‐κB and MAPK signalling pathways, respectively, in chondrocytes and may be a potential therapeutic agent for the treatment of OA. [ABSTRACT FROM AUTHOR]

Background: Early dysphagia is a frequent complication of anterior cervical (AC) spine surgery. However, there are no reports that have discussed the correlation between early dysphagia and the positional relationship between thyroid cartilage and the surgical level. Methods: We retrospectively enrolled 82 patients in our hospital who underwent single-level AC discectomy performed by the same surgeon using the same internal fixation apparatus from 2015 to 2017. Swallowing difficulty was rated during the first five postoperative days using a 10-point scoring system. The positional relationship between the thyroid cartilage and the surgical level was defined as discectomy within the thyroid cartilage (IN group) or outside the thyroid cartilage (OUT group) using preoperative computed tomography (CT) images. The confounding factors such as gender, age, body mass index (BMI), hypertension, diabetes mellitus, drinking, smoking, operative level, operative time, and blood loss were analyzed by a binomial logistic regression. Results: The thyroid cartilage was most commonly located above the C5 level (65.1%). Early dysphagia developed in 47.6% of the patients during the first five postoperative days. The IN and OUT groups each contained 41 cases. The difference in the cumulative postoperative early dysphagia score between the IN and OUT groups was statistically significant (p <.05). The factors of gender, age, BMI, hypertension, diabetes mellitus, drinking, smoking, operative level, operative time, blood loss did not significantly influence the incidence of postoperative early dysphagia. Conclusions: We found that early dysphagia, which is a self-limiting complication, was correlated with surgery performed at levels outside the thyroid cartilage region. Preoperative review of the positional relationship between the thyroid cartilage and the surgical level can predict the incidence of postoperative transient dysphagia. [ABSTRACT FROM AUTHOR]

Steroid‐induced avascular necrosis of the femoral head (SANFH) is mainly induced by glucocorticoids. Fludarabine (Flu) is a specific signal transducer and activator of transcription 1 (STAT1) inhibitor. In this study, we investigated the effect of Flu on SANFH and the role played by the STAT1/caspase‐3 signaling pathway. Sprague‐Dawley rats were divided into control, SANFH, and Flu‐treated SANFH groups. Femoral head tissues were collected for hematoxylin‐eosin (H&E) staining and Western blot analysis. The latter was used to measure the levels of stat1, phospho‐stat1, caspase‐3, cleaved caspase‐3, caspase‐9, cleaved caspase‐9, Bax, cytochrome C, Bak, B‐cell lymphoma‐extra large, and B‐cell lymphoma‐2 protein expression. The results showed that Flu regulates protein expression in dexamethasone (Dex)‐induced SANFH. H&E staining showed a decrease in the ratio of empty lacunae induced by Dex. Taken together, our study demonstrated the involvement of the STAT1/caspase‐3 signaling pathway in SANFH and the potential of Flu as a therapeutic agent for patients with SANFH. [ABSTRACT FROM AUTHOR]

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