Lipoxin A4 Inhibits NLRP3 Inflammasome Activation in Rats With Non-compressive Disc Herniation Through the JNK1/Beclin-1/PI3KC3 Pathway
- 1Department of Pain Management, Shandong Provincial Hospital, Cheeloo College of Medicine, Shandong University, Jinan, China
- 2Department of Anesthesiology, The Affiliated Yantai Yuhuangding Hospital of Qingdao University, Yantai, China
- 3Department of Anesthesiology, Qingdao Municipal Hospital, Qingdao, China
A Corrigendum on
Lipoxin A4 Inhibits NLRP3 Inflammasome Activation in Rats With Non-compressive Disc Herniation Through the JNK1/Beclin-1/PI3KC3 Pathway
by Jin, J., Xie, Y., Shi, C., Ma, J., Wang, Y., Qiao, L., et al. (2020). Front. Neurosci. 14:799. doi: 10.3389/fnins.2020.00799
In the original article, there was a mistake in the legend for **Figure 6** as published. **The results were error in Figure 6A, so the legend of Figure 6 was revised**. The correct legend appears below.
**Figure 6. The expression of autophagy- and apoptosis-related protein expression in spinal neuron cells by western blot. *p < 0.05 compared with the control group; #p < 0.05 compared with the model group; ∧p < 0.05 compared with the LXA4 group. Experiments were repeated three times for each group. Data are presented as means ± SD. One-way analysis of variance (ANOVA) was used for comparisons among groups followed by Dunnett's t-test. **
In the original article, there was a mistake in **Figure 6** as published. **The results of Figure 6A were error, so the results of Figure 6A were deleted in Figure 6 **. The corrected *Figure 6** appears below.
Figure 6. The expression of autophagy- and apoptosis-related protein expression in spinal neuron cells by western blot. *p < 0.05 compared with the control group; #p < 0.05 compared with the model group; ∧p < 0.05 compared with the LXA4 group. Experiments were repeated three times for each group. Data are presented as means ± SD. One-way analysis of variance (ANOVA) was used for comparisons among groups followed by Dunnett's t-test.
In the original article, there was an error. **The levels of TNF (orb79138-480), IL-1β (orb79117), IL-18 (orb107403), IL-4 (orb303658), IL-10 (orb76364), and TGF-β1 (orb7087) (all from Biorbyt, Cambridge, United Kingdom) in the spinal dorsal horn, dorsal root ganglion, and spinal neurons were measured following the instructions of the respective ELISA kits.**
A correction has been made to **Materials and Methods**, **ELISA**, **Page 3**:
**The levels of TNF-α (orb452907), IL-1β (orb453587), IL-18 (orb107403), IL-4 (orb303658), IL-10 (orb76364), and TGF-β1 (orb7087) (all from Biorbyt, Cambridge, United Kingdom) in the spinal dorsal horn and dorsal root ganglion were measured following the instructions of the respective ELISA kits. **
In the original article, there was an error. **The Effect of LXA4 on the Expression of the NLRP3 Inflammasome and Autophagy-Related Proteins in TNF-α-Induced Neuronal Cells in vitro**
A correction has been made to **Results**, **The Effect of LXA4 on the Expression of the NLRP3 Inflammasome and Autophagy-Related Proteins in TNF-α-Induced Neuronal Cells in vitro**, **Page 9**:
**The Effect of LXA4 on the Expression of Autophagy-Related Proteins in TNF-α-Induced Neuronal Cells in vitro**
In the original article, there was an error. **The levels of proinflammatory (TNF-α, IL-1β, and IL-18) and anti-inflammatory (IL-4, IL-10, TGF-β) mediators are shown in Figure 6A. Compared with control group, the levels of TNF-α, IL-1β, and IL-18 clearly increased in other groups (p < 0.05). Administration of LXA4 led to a marked reduction in the expression levels of TNF-α, IL-1β, and IL-18 compared with the model group, while the effect of LXA4 was weakened by LY294002 (p < 0.05). Compared with control group, the levels of TNF-α, IL-1β, and IL-18 clearly obviously decreased in other groups (p < 0.05). Meanwhile, the expression of IL-4, IL-10, and TGF-β was significantly increased in the LXA4 group compared with the model group (p < 0.05). Similar to the in vivo results, LAX4 treatment markedly upregulated the contents of anti-inflammatory factors and weakened the effect of LY294002. The expression of autophagy-related proteins were also measured in vitro (Figure 6B). Compared with the control group, the expression of MAP1LC3B/MAP1LC3A, Beclin-1, and PI3KC3 was significantly decreased in other groups (p < 0.05). The expression of caspase-1 was significantly increased after TNF-α stimulated, compared with control group (p < 0.05). LY294002 administration further decreased the expression levels of these proteins. Meanwhile, treatment with LXA4 significantly increased the expression of autophagy-related proteins and weakened the effect of LY294002 (p < 0.05).**
A correction has been made to **Results**, **The Effect of LXA4 on the Expression of Autophagy-Related Proteins in TNF-α-Induced Neuronal Cells in vitro**, **Page 10**:
**The expression of autophagy-related proteins were also measured in vitro (Figure 6). Compared with the control group, the expression of MAP1LC3B/MAP1LC3A, Beclin-1, and PI3KC3 was significantly decreased in other groups (p < 0.05). The expression of caspase-1 was significantly increased after TNF-α stimulated, compared with control group (p < 0.05). LY294002 administration further decreased the expression levels of these proteins. Meanwhile, treatment with LXA4 significantly increased the expression of autophagy-related proteins and weakened the effect of LY294002 (p < 0.05). **
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: lipoxin A4, non-compressive disc herniation, NLRP3, JNK1, beclin-1, PI3KC3
Citation: Jin J, Xie Y, Shi C, Ma J, Wang Y, Qiao L, Li K and Sun T (2020) Corrigendum: Lipoxin A4 Inhibits NLRP3 Inflammasome Activation in Rats With Non-compressive Disc Herniation Through the JNK1/Beclin-1/PI3KC3 Pathway. Front. Neurosci. 14:608184. doi: 10.3389/fnins.2020.608184
Received: 19 September 2020; Accepted: 16 October 2020;
Published: 16 November 2020.
Edited by:
Rajeev K. Singla, Sichuan University, ChinaReviewed by:
Shengwei Jin, Wenzhou Medical University, ChinaManoj Kumar Sabnani, University of Texas at Arlington, United States
Copyright © 2020 Jin, Xie, Shi, Ma, Wang, Qiao, Li and Sun. 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: Kezhong Li, lkviiwej@163.com; Tao Sun, suntaosdph@163.com
†These authors have contributed equally to this work