RESUMO
Background: Growing evidence suggests an association between thyroid stimulating hormone (TSH) and severity of acute ischemic stroke (AIS). However, few studies have ruled out the potential influences of abnormal thyroid hormones when assessing this association. This study aimed to investigate the association between TSH levels and the severity of AIS patients with euthyroidism, and to explore the potential mechanism of TSH on this disease by analyzing the correlation of TSH with lipid profiles. Methods: This retrospective study consisted of 345 patients with normal T3 and T4 levels admitted for first-ever cerebral ischemic stroke. Baseline data of participant were collecte. Laboratory data, including serum levels of TSH and lipid profiles were measured in our hospital's clinical laboratory on admission. Stroke severity was recorded using the National Institutes of Health Stroke Scale (NIHSS). Associations between TSH levels and disease severity were analyzed with logistic regression analysis. Correlations between TSH and lipid profiles were analyzed with Spearman's rank correlation analysis. Results: Among the 345 patients with AIS, the median age was 63 years (63±12 years), 106 patients (30.7%) were female, 237 (68.7%) patients were mild-severity and 108 (31.3%) patients were severity. Data analysis showed that higher serum TSH levels were associated with the mild severity of patients with AIS (P=0.042 in Kruskal-Wallis test, P=0.025 in logistic regression analysis, and P=0.044 in multiple logistic regression), but not in AIS patients with euthyroidism (P=0.078, P=0.337, respectively). Furthermore, TSH levels were correlated with triglycerides (TG) levels not only in total patients (r=0.135, P=0.012) but also in the patients with euthyroidism (r=0.133, P=0.018). Conclusions: TSH levels are associated with the severity of AIS patients, but not in patients with euthyroidism, predicting that stratified management of TSH may be beneficial in patients with AIS. Moreover, TSH levels are correlated with TG levels in patients with AIS.
RESUMO
Cerebral ischemia is a leading cause of death and long-term disability in the world. Tripartite motif-47 (Trim47), a member of the TRIM family proteins, has been reported to be involved in apoptosis and inflammation in various types of diseases. Nevertheless, the underlying molecular mechanism of Trim47 in cerebral ischemia/reperfusion (I/R) injury remains unclear. This study aimed to explore the role of Trim47 in cerebral I/R injury and the potential underlying mechanisms. The results indicated that Trim47 expression was markedly induced in rats after stroke onset. By the use of genetic approaches, we indicated that Trim47 knockdown significantly reduced the infarct size, mitigated the neurological deficits scores and decreased brain water contents in rats with cerebral I/R injury induced by middle cerebral artery occlusion (MCAO). In addition, Trim47 knockdown-alleviated cerebral I/R was correlated with the suppression of apoptosis through inhibiting Caspase-3 cleavage. Furthermore, reducing Trim47 apparently decreased the release of pro-inflammatory factors, including interleukin 6 (IL-6), tumor necrosis factor-α (TNF-α) and inducible nitric oxide synthase (iNOS), in brain samples of MCAO rats, which was partly by the blockage of nuclear factor-kappa B (NF-κB) signaling. However, Trim47 over-expression markedly accelerated cerebral ischemia injury through promoting apoptosis and inflammation. The suppressive effects of Trim47 knockdown on cerebral I/R were verified in human neuron-like cells stimulated by oxygen and glucose deprivation (OGD). Thus, this study demonstrated a new mechanism for the effect of Trim47 on cerebral I/R injury, and targeting Trim47 might provide feasible therapies for stroke treatment.
