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This document is a corrigendum for an article titled "Aloperine activates the Nrf2-ARE pathway when ameliorating early brain injury in a subarachnoid hemorrhage model." The corrigendum addresses an error in Figure 3 of the original article, where data panels for the SAH and SAH + vehicle groups appeared to be overlapping. The authors have re-examined their data and have now revised Figure 3 to incorporate data from one of the alternative experiments. The error in Figure 3 does not impact the results or conclusions of the original article. The authors apologize for any inconvenience caused. [Extracted from the article]

The effects of angiopoietin-like protein 2 (Angptl 2) and interleukin-6 (IL-6) in inflammatory mediators on the severity of coronary arterial lesion in patients with acute myocardial infarction were investigated. One hundred and twenty-six patients with acute myocardial infarction admitted to Tianjin Union Medical Center (the myocardial infarction group) and 133 healthy individuals (the control group) were selected for retrospective analysis from January 2013 to December 2015. The levels of Angptl 2 and IL-6 in serum of patients were detected by enzyme linked immunosorbent assay (ELISA), and the correlation analysis between the levels and the degree of coronary stenosis in patients with myocardial infarction was conducted. The expression level of Angptl 2 and IL-6 in the myocardial infarction group was significantly higher than that in the control group P<0.001. In the myocardial infarction group, the expression levels of Angptl 2 and IL-6 were the highest in the patients with severe stenosis, followed by the moderate stenosis, and the lowest in the patients with mild stenosis (P<0.050). Pearson's correlation analysis showed that Angptl 2 and IL-6 were positively correlated with the diameter of coronary stenosis (r=0.696, 0.750, P<0.001). In conclusion, both Angptl 2 and IL-6 are highly expressed in the peripheral blood of patients with acute myocardial infarction and involved in the occurrence and development of the disease. Moreover, Angptl2 and IL-6 are positively correlated with the severity of coronary arterial lesion in patients with acute myocardial infarction, and they are expected to become a target for the diagnosis and treatment of coronary atherosclerosis (CA) in the future. [ABSTRACT FROM AUTHOR]

Preeclampsia is a pregnancy-specific disease characterized by hypertension as well as proteinuria after the 20th week of pregnancy. Animal models are effective tools for studying the pathogenesis, diagnostic criteria and treatment methods of preeclampsia. The present study sought to establish and evaluate a preeclampsia-like Sprague Dawley (SD) rat model using N-nitro-L-arginine methyl ester (L-NAME). Rats were randomly assigned to 7 groups (n=10 in each): Control rats and rats treated with low-dose L-NAME (40 mg/kg body weight/day) starting from gestational day (GD) 9, medium-L-NAME (75 mg/kg body weight/day) starting from GD 9 (9D ML group), high-dose L-NAME (125 mg/kg body weight/day) starting from GD 9, low-dose L-NAME starting from GD 10, medium-dose L-NAME starting from GD 10 and high-dose L-NAME starting from GD 10. Blood pressure (BP), 24-h proteinuria, fetal intrauterine growth, histopathological changes, the plasma soluble fms-like tyrosine kinase-1 (sFlt-1)/placental growth factor (PLGF) ratio and cytokine levels were evaluated. Elevated BP, increased urinary albumin excretion, severe endotheliosis, mesangial expansion and increased sFlt-1/PLGF ratios were observed in the experimental groups compared with the control group (P<0.05), particularly in the 9D ML group. The results of the present study may optimize the conditions of the previously established L-NAME-induced preeclampsia SD rat model and aid further study into the pathogenesis of preeclampsia. [ABSTRACT FROM AUTHOR]

Aloperine (ALO) exhibits neuroprotective effects against oxidative stress in vitro; however, its protective effect in early brain injury (EBI) following experimental subarachnoid hemorrhage (SAH) remains to be elucidated. The aim of the current study was to evaluate the antioxidant activity of ALO in EBI, and its association with nuclear factor erythroid‑related factor 2 and the antioxidant responsive element (Nrf2‑ARE) survival pathway. In the present study, an experimental SAH model was induced in rats following a prechiasmatic cistern injection. All rats were randomly divided into five groups: Sham, SAH, SAH+ vehicle, and an SAH+ ALO group (including low and high doses). ALO was administrated intraperitoneally at 2 and 24 h following induction of the SAH model. Brain samples were collected from each group at 48 h after SAH induction. Subsequently, western blotting, immunohistochemistry and cell apoptosis assays were performed, along with assessments for brain edema, neurological deficit, and the activity of oxidant/antioxidant factors. It was observed that the expression of Nrf2‑ARE pathway‑associated agents, including Nrf2, and heme oxygenase‑1, were markedly increased in the high concentration ALO group compared with that of the SAH group. In addition, the level of oxidative damage was reduced. Furthermore, early brain damage, including brain edema, neurological deficit and cellular apoptosis were significantly ameliorated. In conclusion, the results of the present study indicate that ALO can ameliorate oxidative damage against EBI following SAH, most likely via the Nrf2‑ARE survival pathway. [ABSTRACT FROM AUTHOR]

Gliomas are the most common type of primary brain tumor in adults, where more than half of the cases are malignant, and the prognosis is poor. The early viral 1A (E1A) protein has been widely recognized to be essential for adenoviral replication and production of progeny virions in human cells, a process that is regulated by human telomerase reverse transcriptase. The p53 gene, as a tumor suppressor, regulates diverse cellular processes, including cell cycle arrest, cell autophagy, senescence and apoptosis. Dysfunction of the p53 pathways is common in malignant gliomas. Exogenous expression of p53 during adenovirus replication in human cancer cells may accelerate cell death and improve the release of early virus progeny. In the present study, a conditionally replicative adenovirus (CRAd) Ad‑Tp‑E1A‑Gp‑p53, which expressed functional p53 protein when replicating in cancer cells, was constructed. Next, the level of p53 expression in U251 cells was determined by western blot analysis, and the inhibitory effect of Ad‑Tp‑E1A‑Gp‑p53 on U251 cells was detected via an MTT assay. The results indicated that p53 expression was upregulated with an increase in the multiplicity of infection (MOI) of Ad‑Tp‑E1A‑Gp‑p53. Additionally, the inhibitory effects of Ad‑Tp‑E1A‑Gp‑p53 in different groups were significantly different (P<0.05), with the inhibition ratio of the experimental groups being higher, compared with the control group (P<0.05). Furthermore, the inhibition ratio increased with increases in the MOI of Ad‑Tp‑E1A‑Gp‑p53. Therefore, the expression of functional p53 and that of E1A may increase the potency of CRAd, and overexpression of p53 through CRAd is a promising approach to more effective treatments in a number of human cancer types. [ABSTRACT FROM AUTHOR]