RESUMO
Background: To quantify the association between the free distal segment length of the internal carotid artery (FDS-ICA) and permanent cranial nerve injury (p-CNI) following carotid body tumor (CBT) resection. Methods: This study is a case-control study. We surveyed 109 consecutive patients who underwent CBT resection between June 2015 and June 2020 at our single center. A total of 89 patients met the inclusion criteria and were selected for analysis. The FDS-ICA was measured by image post-processing software for computed tomography angiography (CTA). Postoperative p-CNI complications were evaluated using comprehensive statistical approaches. Results: The cohort was divided into 2 groups depending on the presence of p-CNI, namely the p-CNI group (n=17) and the non-CNI group (n=79). The average FDS-ICA of patients with p-CNI complications was shorter than that of those without p-CNI complications (P<0.001). For every 1 mm increase in FDS-ICA, there was an associated decrease of 8% in the risk of p-CNI (0.92, 95% CI: 0.85 to 0.98, P<0.05). Threshold effect analysis of the FDS-ICA on p-CNI identified that the FDS-ICA was 28.7 (95% CI: 23.8 to 30.9) mm. Conclusions: The results of this study revealed a significant independent association between FDS-ICA and permanent postoperative cranial nerve injury complications of CBTs. Further study is warranted to confirm these results in a larger patient cohort.
RESUMO
The purpose of this study is to explore the antitumor properties of resibufogenin (RB) in non-small cell lung cancer (NSCLC) and elucidate its underlying mechanism. A549 and H520 cells were treated with various concentrations of RB with or without NLRP3 inhibitor (MCC950), caspase-1 inhibitor (VX765), or N-acetyl-l-cysteine (an ROS scavenger). Cell counting kit-8 and colony formation assays were conducted to determine cell viability. Cell invasion was detected by using the transwell assay. The release of lactate dehydrogenase (LDH) was determined by the LDH detection assay. The protein expression levels of related genes were measured by western blotting and immunohistochemistry. The reactive oxygen species (ROS) level was detected by using a 2,7-dichlorodihydrofluorescein diacetate ROS Assay Kit. The in vivo effects of RB were evaluated in a xenograft mouse model. RB treatment reduced cell viability and invasion in a dose-dependent manner. Furthermore, RB also enhanced pyroptosis levels in A549 and H520 cells, as indicated by the increased release of LDH and pyroptosis-related proteins. Interestingly, we also found that the antiproliferative and antimetastatic effects of RB were alleviated by the blockade of pyroptosis using NLRP3 inhibitor MCC950. Further study demonstrated that RB induced pyroptosis in a caspase-1-dependent manner, as evidenced by the finding that VX765 effectively reversed the effects of RB on A549 and H520 cells. We also found that RB could trigger caspase-1-dependent pyroptosis through ROS-mediated NF-κB suppression. In summary, our findings provide a potential antitumor agent and a novel insight into the mechanism of RB treatment of NSCLC.