Errors in Figures
The original publication [1] contains errors in two figures.
In Figure 4A, the Nissl image of the SAH + vehicle group was mistakenly selected and used during figure assembling. The other elements of the figure remain unchanged. The corrected Figure 4 is presented below.
Figure 4.
(A) Representative photomicrographs of Nissl (A1–D1) and TUNEL (A2–D2) staining in the cerebral cortex at 24 h after SAH and (B) quantitative analysis of neuronal survival (b1) and the apoptotic index (b2). As shown in the Nissl staining, in the sham group, the neuronal cell outline was clear and the structure compact, with abundant cytoplasm and Nissl bodies. However, evident neuronal loss and neuronal degeneration were observed in the SAH group and SAH + vehicle groups. Treatment with ATX significantly increased the proportion of surviving neurons. The TUNEL staining showed that the rats in the sham group display rare apoptotic cells in the cortex, while obvious TUNEL-positive cells could be observed in the SAH group and SAH + vehicle groups. In contrast, the proportion of apoptotic cell death decreased significantly in the SAH + ATX group. Values are represented as the mean ± SEM. *** p < 0.001, ** p < 0.01, * p < 0.05, ns p > 0.05.
In addition, the Bad blot in Figure 5A was mistakenly sourced from the P-Bad blot. The other elements of the figure remain unchanged. The corrected Figure 5 is presented below.
Figure 5.
Representative Western blots (A) and quantitative analysis of p-Akt, p-Bad and caspase-3 (B) in the cortex of the SAH + ATX and SAH + ATX + LY294002 groups. The levels of p-Akt and p-Bad were high in the SAH + ATX group. After LY294002 treatment, the high levels of p-Akt and p-Bad were significantly decreased. In contrast to the low level of caspase-3 in the SAH + ATX group, LY294002 treatment significantly upregulated the level of caspase-3 in the cortex. Results are expressed as the means ± SEM. ** p < 0.01, * p < 0.05.
These changes do not affect the results or conclusions of this study. The authors apologize for any inconvenience caused.
Reference
- Zhang, X.-S.; Zhang, X.; Wu, Q.; Li, W.; Zhang, Q.-R.; Wang, C.-X.; Zhou, X.-M.; Li, H.; Shi, J.-X.; Zhou, M.-L. Astaxanthin Alleviates Early Brain Injury Following Subarachnoid Hemorrhage in Rats: Possible Involvement of Akt/Bad Signaling. Mar. Drugs 2014, 12, 4291–4310. [Google Scholar] [CrossRef] [PubMed]
Disclaimer/Publisher’s Note: The statements, opinions and data contained in all publications are solely those of the individual author(s) and contributor(s) and not of MDPI and/or the editor(s). MDPI and/or the editor(s) disclaim responsibility for any injury to people or property resulting from any ideas, methods, instructions or products referred to in the content. |
© 2024 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).