Search

This document is a corrigendum for an article titled "miR-590-5p may regulate colorectal cancer cell viability and migration by targeting PDCD4." The corrigendum acknowledges that certain data panels in Figure 3 of the original article contained overlapping sections of data, which were assembled incorrectly. The revised version of Figure 3, featuring alternative data from one of the repeated experiments, is provided. The authors state that these errors did not significantly impact the overall results or conclusions of the study. They apologize for any inconvenience caused and express gratitude to the editor for allowing them to publish this corrigendum. [Extracted from the article]

The blood-brain barrier (BBB) is critical for proper cerebral homeostasis and its dysfunction during ischemic stroke can result in significant neurological injury. The major goal of the present study was to identify whether curcumin pretreatment possessed protective effects on BBB integrity during the 24 h of acute ischemic brain injury. To investigate the protective effects of curcumin, male Sprague-Dawley rats were divided into multiple groups, including sham, middle cerebral artery occlusion/reperfusion (MCAO/R) vehicle and curcumin pretreated MCAO/R groups. The effects of curcumin were measured by analyzing neurological deficits, infarct size, BBB permeability and expression levels of permeability-related proteins in the brain. It was found that curcumin pretreatment significantly improved neurological scores, decreased infarct size, and protected synaptic remodeling of hippocampal neurons and upregulated the protein expression level of tight junction proteins, ZO-1, occludin and claudin-5 in ischemic rat brains. Furthermore, curcumin pretreatment before stroke was shown to downregulate the phosphorylation of NF-κB and MMP-9, which are central mediators of inflammation. The results from the present study indicated that curcumin pretreatment ameliorated ischemic stroke injury by protecting BBB integrity and synaptic remodeling, as well as inhibiting inflammatory responses. [ABSTRACT FROM AUTHOR]

Cerebral ischemic stroke is the primary cause of stroke-associated mortality and disability, and current therapeutic options are limited and ineffective. The present study aimed to investigate the potential of apoptotic therapy and the role of microRNA (miR)-424 in cerebral ischemic stroke. PC12 cells, a cloned cell line from rat adrenal pheochromocytoma, were treated with CoCl2 to construct a cellular ischemia model. mRNA and protein levels of programmed cell death protein 4 (PDCD4), Bcl-2, Bax, caspase-3, PI3K and AKT were evaluated using reverse transcription-quantitative PCR and western blot analyses, respectively. Cell Counting Kit-8 assays were performed to examine cell viability in the ischemia model. Flow cytometry was conducted to evaluate the apoptosis of ischemic cells. Furthermore, a luciferase assay was performed to verify the target gene of miR-424. It was revealed that the expression level of miR-424 was downregulated in the ischemia model, while the expression of PDCD4 was upregulated. Moreover, the expression of miR-424 was increased after treatment with miR-424 mimics. The mRNA and protein expression of PDCD4 was upregulated after transfection with pcDNA3.1-PDCD4. PDCD4 was predicted and demonstrated to be a target of miR-424. Notably, overexpression of miR-424 increased cell viability and inhibited apoptosis in the ischemia model, which was reversed by co-treatment with pcDNA3.1-PDCD4. Furthermore, overexpression of miR-424 regulated the expression of PDCD4, Bax, Bcl-2, phosphorylated-PI3K/AKT and caspase-3, which was restored after co-transfection with pcDNA3.1-PDCD4. Collectively, the results indicated that miR-424 regulated the progression of cerebral ischemic stroke in a cellular model by targeting PDCD4. [ABSTRACT FROM AUTHOR]