Correction: l-Arginine, as an essential amino acid, is a potential substitute for treating COPD via regulation of ROS/NLRP3/NF-κB signaling pathway

Abstract

Figures

Effects of l-arginine (LA) on KO COPD mice. Airway reaction (A). The percentage changes of the resistance of lung (RL) (B) and lung dynamic compliance (Cdyn) (C) in WT and KO COPD mice. Serum cytokines: The contents of interleukin-1β (IL-1β) (D), interleukin-6 (IL-6) (E), tumor necrosis factor-α (TNF-α) (F). BALF cytokines: the contents of Interleukin-1β (IL-1β) (G), interleukin-6 (IL-6) (H), tumor necrosis factor-α (TNF-α) (I). Reactive oxygen species (ROS) (J) and nitric oxide (NO) (K) contents in lung tissues. Pathological changes (HE staining) and Masson staining of lung in COPD rats: HE s

Role of l-arginine (LA) mediated ROS/NLRP3/NF-κB signaling pathway in cigarette smoke extract (CSE)-induced primary bronchial epithelial cell (BEC) injury and molecular docking of LA and NLRP3. Western blot of ROS/NLRP3/NF-κB signaling pathway in CES-induced BECs (A), Quantification of ROS/NLRP3/NF-κB signaling pathway in CES-induced BECs (B). The expression levels of NLRP3 (C) and p-NF-κBp65 (D) in CES-induced BECs by immunofluorescence (× 100). (n = 3). Molecular docking result of LA and NLRP3 (E): The binding energy predicted by Autodock is − 5.79 kcal/mol for LA-NLRP3 (The binding energy p

Effects of l-arginine (LA) on KO COPD mice. Airway reaction (A). The percentage changes of the resistance of lung (RL) (B) and lung dynamic compliance (Cdyn) (C) in WT and KO COPD mice. Serum cytokines: The contents of interleukin-1β (IL-1β) (D), interleukin-6 (IL-6) (E), tumor necrosis factor-α (TNF-α) (F). BALF cytokines: the contents of Interleukin-1β (IL-1β) (G), interleukin-6 (IL-6) (H), tumor necrosis factor-α (TNF-α) (I). Reactive oxygen species (ROS) (J) and nitric oxide (NO) (K) contents in lung tissues. Pathological changes (HE staining) and Masson staining of lung in COPD rats: HE s

Full text

Correction: Cell & Bioscience (2023) 13:152 10.1186/s13578-023-00994-9

In this article [1], the wrong figures appeared as Figs. 3 and 7; the figures should have appeared as shown below.

Incorrect Fig. 3

Correct Fig. 3Fig. 3. Effects of l-arginine (LA) on KO COPD mice. Airway reaction (A). The percentage changes of the resistance of lung (RL) (B) and lung dynamic compliance (Cdyn) (C) in WT and KO COPD mice. Serum cytokines: The contents of interleukin-1β (IL-1β) (D), interleukin-6 (IL-6) (E), tumor necrosis factor-α (TNF-α) (F). BALF cytokines: the contents of Interleukin-1β (IL-1β) (G), interleukin-6 (IL-6) (H), tumor necrosis factor-α (TNF-α) (I). Reactive oxygen species (ROS) (J) and nitric oxide (NO) (K) contents in lung tissues. Pathological changes (HE staining) and Masson staining of lung in COPD rats: HE staining of lung in COPD rats (× 200) (L), Masson staining of lung in COPD rats (× 200) (M), Collagen quantification of Masson staining and collagen I contents of lung in COPD KO mice (N). (n = 10). All data were presented as mean ± SD. Compared with WT mice: ^##^P < 0.01

Incorrect Fig. 7

Correct Fig. 7Fig. 7. Role of l-arginine (LA) mediated ROS/NLRP3/NF-κB signaling pathway in cigarette smoke extract (CSE)-induced primary bronchial epithelial cell (BEC) injury and molecular docking of LA and NLRP3. Western blot of ROS/NLRP3/NF-κB signaling pathway in CES-induced BECs (A), Quantification of ROS/NLRP3/NF-κB signaling pathway in CES-induced BECs (B). The expression levels of NLRP3 (C) and p-NF-κBp65 (D) in CES-induced BECs by immunofluorescence (× 100). (n = 3). Molecular docking result of LA and NLRP3 (E): The binding energy predicted by Autodock is − 5.79 kcal/mol for LA-NLRP3 (The binding energy predicted by Autodock <  − 6.00 is considered to be high degree of integration). All data were presented as mean ± SD. Compared with control: ^##^P < 0.01