ABSTRACT
Thromboembolism is a possible consequence of underlying atrial cardiopathy, which can occur even before the onset of atrial fibrillation. Our objective was to examine the association between biomarkers of atrial cardiopathy and outcomes of acute ischemic stroke (AIS) following endovascular treatment (EVT). We conducted a retrospective study that collected data from patients with AIS who underwent EVT and compared the outcomes between those with and without atrial cardiopathy. Neurological function was assessed using the modified Rankin Scale (mRS), with an mRS score >2 indicating poor function at day 90. Additionally, we evaluated secondary consequences, including symptomatic intracerebral hemorrhage (sICH), early neurological deterioration (END), and malignant cerebral edema (MCE). Our study included 87 patients (77.6 â% male; mean age 60.93 â± â12.47 years). Among these patients, 29 (33.3 â%) had atrial cardiopathy, while the remaining 58 (66.7 â%) did not. In the atrial cardiopathy group, 12 patients (41.4 â%) had poor functional outcomes (mRS>2), compared to 19 (32.8 â%) in the non-atrial cardiopathy group. We observed sICH in 22 (25.3 â%) patients, END in 14 (16.1 â%) patients, MCE in 11 (12.6 â%) patients, and two (2.3 â%) patients who died in the hospital. We found that patients with PTFV1>5000 âµV/ms (OR: 8.39, 95 â% CI: 1.43-105.95, P â= â0.02) and NT-proBNP>250 âpg/mL (OR: 5.09, 95 â% CI: 1.20-27.63, P â= â0.03) had significantly higher risk of END. After adjusting for covariates in the Firth logistic regression, we further found that atrial cardiopathy was significantly associated with END, as revealed by both univariate (OR: 6.31, 95 â% CI: 1.42-59.87, P â= â0.01) and multivariable firth regression models (Modle 1, OR: 7.10, 95 â% CI: 1.57-67.38, P â< â0.01; Modle 2, OR: 7.82, 95 â% CI: 1.69, 76.36, P â< â0.01; Modle 3, OR: 8.59, 95 â% CI: 1.72-91.70, P â< â0.01). Moreover, we observed that atrial cardiopathy was associated with an increased risk of END in AIS patients with large artery atherosclerosis (LAA) receiving EVT. Therefore, clinicians should consider atrial cardiopathy as a possible underlying cause of AIS in their patients. Further investigation is warranted to elucidate the relationship between atrial cardiopathy and AIS's occurrence, progression, and prognosis.
Subject(s)
Brain Ischemia , Ischemic Stroke , Stroke , Humans , Male , Middle Aged , Aged , Female , Stroke/therapy , Retrospective Studies , Prognosis , Biomarkers , Cerebral Hemorrhage , Treatment Outcome , Brain Ischemia/complicationsABSTRACT
Silibinin is a flavonoid extracted from milk thistle seeds which has been widely used as a hepatoprotective and antioxidant agent. Recently, accumulating evidence has demonstrated the anticancer effects of silibinin in various cancer models. It was previously reported that silibinin induced apoptosis and decreased metastasis by activating autophagy in renal cell carcinoma (RCC). However, the underlying molecular mechanisms by which silibinin regulates autophagy remain largely unknown. The aim of the present study was to investigate the effects of silibinin on RCC metastasis in vitro and in vivo, with a focus on autophagydependent Wnt/ßcatenin signaling. Human RCC 786O and ACHN cell lines were used as the model system in vitro and RCC xenografts of nude mice were used for in vivo studies. Silibinin inhibited metastasis and epithelialmesenchymal transition (EMT) of RCC in vitro and in vivo, by regulating the Wnt/ßcatenin signaling pathway. Furthermore, silibinin inhibited the Wnt/ßcatenin signaling pathway in an autophagydependent manner. Autophagic degradation of ßcatenin induced by silibinin was associated with the antimetastatic effects of silibinin against RCC. These findings identify a novel mechanism by which silibinin inhibits EMT and metastasis of RCC, highlighting a potential novel strategy for treating metastatic RCC.
