[Corrigendum] TLR4-mediated NF-κB signaling pathway mediates HMGB1-induced pancreatic injury in mice with severe acute pancreatitis.

Following the publication of the article, the authors noted that there were certain errors in Fig. 5. In particular, the published Fig. 5A-a contains an image of H&E-stained micrographs from wild-type mice after the administration of a low dose of rhHMGB1, and not after the administration of a high dose of rhHMGB1, as should be shown. In addition, the data in the published graph of Fig. 5C-a is not correct and in Fig. 5C‑b, the significance marker is merged with the error bars and is not evident. [the original article was published in the International Journal of Molecular Medicine 37: 99-107, 2016; DOI: 10.3892/ijmm.2015.2410].

Int J Mol Med 37: 99–107, 2016; DOI: 10.3892/ijmm.2015.2410

Following the publication of the article, the authors noted that there were certain errors in Fig. 5. In particular, the published Fig. 5A-a contains an image of H&E-stained micrographs from wild-type mice after the administration of a low dose of rhH-MGB1, and not after the administration of a high dose of rhH-MGB1, as should be shown. In addition, the data in the published graph of Fig. 5C-a is not correct and in Fig. 5C-b, the significance marker is merged with the error bars and is not evident. Shown below is the new version of Fig. 5 with the correct images:

Figure 5

Response of Toll-like receptor 4 (TLR4)-deficient mice to recombinant human high-mobility group box 1 (rhHMGB1) administration. (A) Pancreatic histopathological changes in wild-type (WT) and TLR4-deficient mice 48 h after the administration of a high dose of rhHMGB1. Representative H&E-stained micrographs (original magnification, ×200) from the (a) WT and (b) TLR4−/− groups. The pancreatic tissues in the wild-type group exhibited marked edema, infiltration of inflammatory cells, a mass of necrotic acinar cells and the disappearance of the normal lobe structure in the pancreas; there was a significant reduction in the TLR4-deficient group. (B-a) Histological scores of the pancreas and (b) serum amylase and lipase changes in the WT and TLR4−/− groups. (C) The activation of nuclear factor-κB (NF-κB) was assessed from the nuclear p65 [(a) western blot analysis] and its downstream, relative levels of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) [(b) ELISA] in the pancreatic tissue from the WT and TLR4−/− groups. *P<0.01 compared to the WT group. The relative levels of nuclear p65 protein compared to the control group are normalized to histone 3 (H3). The relative levels of TNF-α and IL-1β compared to the control group are normalized to the total protein concentration of each sample. Data are expressed as the means ± SD (n=6/group). Blots shown are from a representative experiment that was repeated 3 times with similar results (n=6/group). WT, WT mice given a high dose of rhHMGB1; TLR4−/−, TLR4-deficient mice administered a high dose of rhHMGB1.