Corrigendum to ‘Low, But Not High, Dose Triptolide Controls Neuroinflammation and Improves Behavioral Deficits in Toxic Model of Multiple Sclerosis by Dampening of Nf-Κb Activation and Acceleration of Intrinsic Myelin Repair’ [Toxicol. Appl. Pharmacol. 342 (2018), 86–98, (S0041008x18300309), (10.1016/J.Taap.2018.01.023)] Publisher Pubmed

Summary: Why were figures replaced in a published study? An erratum corrects microscopy panels; the authors state that the scientific conclusions remain unchanged. #ResearchIntegrity #Publishing

Sanadgol N ; Golab F ; Mostafaie A ; Mehdizadeh M ; Khalseh R ; Abdollahi M ; Vakilzadeh G ; Taghizadeh G ; Sharifzadeh M
Source: Toxicology and Applied Pharmacology Published:2026

Abstract

The authors regretfully acknowledge that during the final preparation of figures for this manuscript, incorrect images were mistakenly placed in the following figures and panels: Fig. 3, Panels G, J, M, and O. Fig. 5, Panel C. Fig. 7, Panel TP250 for GFAP staining. The authors have provided the correct figures as below. This oversight does not affect the scientific content or conclusions of the article, and all statements remain accurate. The authors also wish to correct the author list. Morteza Mahmoudi has been removed because they did not contribute to this article and was included in error. The corrected author list is shown above. The authors would like to apologize for these oversights and for any inconvenience caused.[Figure presented] Fig. 3. Effects of different doses of triptolide (TP) on PLP, myelin sheath and gliosis in C57BL/6 mice. PLP immunostaining (up panels), LFB staining (middle panels) and H&E staining (down panels) in coronal slices of CC. Pics A, D, G, J and M show PLP density and B, E, H, K and N show myelin patches, while C, F, I, L and O show presence of cellular bodies in different treatments. At Cup consumption, demyelination was evident, as is shown by the decrease in PLP (D), and was restricted to a few myelin patches (E). Demyelination was delayed after TP-125 treatment during last week (G and H). Maximal demyelination was observed after 1 week of TP-500 treatment in Cup-fed mice (M and N). Quantification analysis showed that TP-125 treated mice displayed significant increase while TP-500 treated mice displayed significant decrease in both PLP intensity (P) and myelin patches (Q). Quantification of H&E indicated significant decrease of cell infiltration after TP treatments (I, L, Q and R). Scale bar for (PLP) = 100 μm, for (LFB) and (H&E) = 50 μm. Data are presented as mean ± SEM. •••P < 0.001 compared to control mice; °P < 0.05, °°P < 0.01 and °°°P < 0.001 compared to Cup mice.[Figure presented] Fig. 5. Evaluation of oligodendrocytes precursor cells (OPCs) and apoptotic markers in C57BL/6 mice during triptolide (TP) treatment. Specific OPCs markers (O4 and NG2) (A) and markers of apoptotic cells (annexin-V and PI) were double-stained (B) and analyzed via flow cytometry. O4/NG2 double-staining assay revealed that although Cup consumption resulted in partial induction in this subset of OPCs, TP-125 significantly increased population of these cells (A). Annexin-V/PI double-staining assay revealed that although Cup consumption alone and in combination with TP-500 dramatically increased percentage of apoptotic cells (annexin V-FITC positive and PI negative), TP-125 treatment reduced number of these cells (B). Moreover, in situ detection of apoptotic cells was also performed via TUNEL assay (C). TUNEL assay confirmed that TP-125 significantly reduced population of apoptotic cells in the CC (C). The arrowhead indicates apoptotic cells. Scale bar = 50 μm. Using western blot technique, the effects of TP on Bax/Bcl-2 ratio was tested in different groups (D). The densities of Bax and Bcl-2 bands were measured, and their ratio to β-actin was calculated (D). Using q-PCR techniques the effects of TP on mRNA expression of Bax, Bcl-2 and Caspase-3 were measured in the CC region of mice brain after one week treatment (E, F and G, respectively). Quantitative RT-PCR was conducted and the results were normalized to β-actin and reported as fold changes to control. Data are presented as mean ± SEM. ••P < 0.01 and •••P < 0.001 compared to control mice; °P < 0.05 and °°P < 0.01 compared to Cup mice.[Figure presented] Fig. 7. Reactive gliosis and neuroglia specific NF-kB expression in C57BL/6 mice during triptolide (TP) treatment. IHC of coronal sections of the CC shows labeling with a monoclonal antibody that is specific to the mature OLGs marker (MOG, green), reactive astrocytes marker (GFAP, green), and microglial/macrophages marker (MAC-3, green) along with transcription factor NF-kB (red) and DAPI nuclear stain (blue). Images were taken of three coronal sections from three mice per group over four independent experiments. Scale bars = 25 μm. Quantification of MOG+, GFAP+ and MAC-3+ positive cells (A–C). Quantification of MOG, GFAP and MAC-3 mRNA expression (D-F) and Quantification of MOG+/NF-kB+, GFAP+/NF-kB+ and MAC-3+/NF-kB+ double positive cells (G-I) are depicted. Data are presented as mean ± SEM. •••P < 0.001 compared to control mice; °P < 0.05, °°P < 0.01 and °°°P < 0.001 compared to Cup mice. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.) © 2026 Elsevier Inc.