This article is a correction to:
Neuroprotective Effects of Celastrol on Transient Global Cerebral Ischemia Rats via Regulating HMGB1/NF-κB Signaling Pathway
Bo Zhang
Qi Zhong1,3†
Rong Sha
Xiangdong Chen- 1Department of Anesthesiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
- 2Department of Anesthesiology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
- 3Department of Anesthesiology, Zhongnan Hospital, Wuhan University, Wuhan, China
- 4Department of Ophthalmology, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China
- 5Department of Rehabilitation Medicine, Enshi Autonomous Prefecture, Hospital of Traditional Chinese Medicine, Enshi, China
- 6Department of Quality Inspection, Wuhan Institute of Biological Products, Wuhan, China
A Corrigendum on
Neuroprotective Effects of Celastrol on Transient Global Cerebral Ischemia Rats via Regulating HMGB1/NF-κB Signaling Pathway
by Zhang, B., Zhong, Q., Chen, X., Wu, X., Sha, R., Song, G., et al. (2020). Front. Neurosci. 14:847. doi: 10.3389/fnins.2020.00847
In the original article, the image of Bax in Figure 2E was misused in the process of manuscript revision. Figure 3B (Iba-1) was inadvertently copied as Figure 2E (Bax). The corrected Figure 2E appears below.
FIGURE 2
Figure 2. Celastrol inhibits apoptotic hippocampal neuronal death. (A) Representative images of NeuN immunofluorescent staining sections (first row), cresyl violet-stained sections (second row) and TUNEL-stained sections (third row) in hippocampal CA1 region of tGCI/R rats, the built-in schematic diagram with red rectangular shows the area that we analyzed. Data were obtained from 4 independent animals, and the results of a typical experiment are exhibited. Scale bar = 200 μm. SO, stratum orients; SP, stratum pyramidal; SR, stratum radium. (B) Quantitative analysis of NeuN positive neurons. (C) Quantitative analysis of Nissl-positive neurons (D) The apoptosis index of hippocampal CA1 neurons. (E–H) Western blot analysis of apoptosis-related proteins Bcl-2, Bax and cleaved-caspase-3, β-actin was used as an internal control. The error bars represent mean ± S.E.M (n = 4, *P < 0.05 vs. Sham + Vehicle group; #P < 0.05 vs. IR+ Vehicle group; &P < 0.05 vs. IR + Celastrol (1 mg/kg) group; δ P < 0.05 vs. IR + Celastrol (2 mg/kg) group).
The authors apologize for this error and state that this does not change the scientific conclusions of the article in any way. The original article has been updated.
Keywords: celastrol, neuroinflammation, oxidative stress, neurological deficit, cerebral ischemia reperfusion
Citation: Zhang B, Zhong Q, Chen X, Wu X, Sha R, Song G, Zhang C and Chen X (2021) Corrigendum: Neuroprotective Effects of Celastrol on Transient Global Cerebral Ischemia Rats via Regulating HMGB1/NF-κB Signaling Pathway. Front. Neurosci. 15:637004. doi: 10.3389/fnins.2021.637004
Received: 02 December 2020; Accepted: 11 May 2021;
Published: 06 July 2021.
Edited and reviewed by: Dominique Massotte, Université de Strasbourg, France
Copyright © 2021 Zhang, Zhong, Chen, Wu, Sha, Song, Zhang and Chen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
*Correspondence: Chuanhan Zhang, Y2h1YW5oYW5femhhbmcmI3gwMDA0MDsxNjMuY29t; Xiangdong Chen, eGlhbmdkb25nY2hlbjIwMTMmI3gwMDA0MDsxNjMuY29t
†These authors have contributed equally to this work