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Molecular Medicine Reports
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October-2025 Volume 32 Issue 4

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[Corrigendum] Cerebral ischemic post‑conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model

  • Authors:
    • Jue Wang
    • Dong Han
    • Miao Sun
    • Juan Feng

  • View Affiliations / Copyright

    Affiliations: Department of Neurology, Shengjing Hospital, Affiliated Hospital of China Medical University, Shenyang, Liaoning 110004, P.R. China
    Copyright: © Wang et al. This is an open access article distributed under the terms of Creative Commons Attribution License [CC BY 4.0].
  • Article Number: 276
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    Published online on: July 30, 2025
       https://doi.org/10.3892/mmr.2025.13641
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Figure 1

The effect of the autophagy activator, RAP, on IPOC (OGD/R plus 3 cycles of IPOC). (A) Cell viability evaluated using a CCK-8 assay; (B) expression levels of autophagy related proteins were detected by western blot; (C) quantitative analysis of LC3II protein relative to LC3I; (D) quantitative analysis of Beclin1 protein relative to GAPDH; (E) quantitative analysis of P62 protein relative to GAPDH; (F) cytoplasmic HMGB1 detected by western blot; (G) quantitative analysis of cytoplasmic HMGB1 protein relative to GAPDH; (H) quantitative analysis of cell supernatant HMGB1 protein detected by enzyme-linked immunosorbent assay. Data are presented as the mean ± standard deviation of 3 samples per group. *P<0.05 vs. normal control group, #P<0.05 vs. OGD/R group, &P<0.05 vs. IPOC group. N, normal control group; OGD/R (8 h OGD followed by 24 h reperfusion), oxygen and glucose deprivation and reperfusion; IPOC, ischemic post-conditioning; RAP, rapamycin; Int, Intralipid vehicle control; LC3, microtubule associated-protein 1A/1B-light chain 3; P62, sequestome 1; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; HMGB1, high mobility group box 1.

Figure 2

HMGB1 and Beclin1 co-immunoprecipitation. (A) Beclin1 and HMGB1 protein detected by western blot; (B) quantitative analysis of HMGB-bound Beclin1 relative to GAPDH; (C) quantitative analysis of HMGB1 protein relative to GAPDH; (D) quantitative analysis of free Beclin1 relative to GAPDH. Data are presented as the mean ± standard deviation of 3 samples per group. *P<0.05 vs. normal control group, #P<0.05 vs. OGD/R group. HMGB1, high mobility group box 1; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; N, normal control group; OGD/R (8 h OGD followed by 24 h reperfusion), oxygen and glucose deprivation and reperfusion; IPOC (OGD/R plus 3 cycles of IPOC), ischemic post-conditioning.

Figure 3

Analysis of protein expression levels of autophagy related proteins and HMGB1 following OGD/R (8 h OGD followed by 24 h reperfusion) and IPOC (OGD/R plus 3 cycles of IPOC). (A) Autophagy related proteins were detected by western blot; (B) quantitative analysis of LC3II protein relative to LC3I; (C) quantitative analysis of Beclin1 protein relative to GAPDH; (D) quantitative analysis of P62 protein relative to GAPDH; (E) cytoplasmic HMGB1 detected by western blot and quantitated relative to GAPDH; (F) quantitative analysis of cell supernatant HMGB1 protein detected by enzyme-linked immunosorbent assay. Data are presented as the mean ± standard deviation of 3 samples per group. *P<0.05 vs. normal control group, #P<0.05 vs. OGD/R group. LC3, microtubule associated-protein 1A/1B-light chain 3; P62, sequestome 1; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; HMGB1, high mobility group box 1; N, normal control group; OGD/R, oxygen and glucose deprivation and reperfusion; IPOC, ischemic post-conditioning.

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Copy and paste a formatted citation
Spandidos Publications style
Wang J, Han D, Sun M and Feng J: [Corrigendum] Cerebral ischemic post‑conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model. Mol Med Rep 32: 276, 2025.
APA
Wang, J., Han, D., Sun, M., & Feng, J. (2025). [Corrigendum] Cerebral ischemic post‑conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model. Molecular Medicine Reports, 32, 276. https://doi.org/10.3892/mmr.2025.13641
MLA
Wang, J., Han, D., Sun, M., Feng, J."[Corrigendum] Cerebral ischemic post‑conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model". Molecular Medicine Reports 32.4 (2025): 276.
Chicago
Wang, J., Han, D., Sun, M., Feng, J."[Corrigendum] Cerebral ischemic post‑conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model". Molecular Medicine Reports 32, no. 4 (2025): 276. https://doi.org/10.3892/mmr.2025.13641
Copy and paste a formatted citation
x
Spandidos Publications style
Wang J, Han D, Sun M and Feng J: [Corrigendum] Cerebral ischemic post‑conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model. Mol Med Rep 32: 276, 2025.
APA
Wang, J., Han, D., Sun, M., & Feng, J. (2025). [Corrigendum] Cerebral ischemic post‑conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model. Molecular Medicine Reports, 32, 276. https://doi.org/10.3892/mmr.2025.13641
MLA
Wang, J., Han, D., Sun, M., Feng, J."[Corrigendum] Cerebral ischemic post‑conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model". Molecular Medicine Reports 32.4 (2025): 276.
Chicago
Wang, J., Han, D., Sun, M., Feng, J."[Corrigendum] Cerebral ischemic post‑conditioning induces autophagy inhibition and a HMGB1 secretion attenuation feedback loop to protect against ischemia reperfusion injury in an oxygen glucose deprivation cellular model". Molecular Medicine Reports 32, no. 4 (2025): 276. https://doi.org/10.3892/mmr.2025.13641
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