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Article

Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats

  • Authors:
    • Ping He
    • Renmin Zhou
    • Guorui Hu
    • Zhifeng Liu
    • Yu Jin
    • Guang Yang
    • Mei Li
    • Qian Lin
  • View Affiliations / Copyright

    Affiliations: Department of Pediatrics, Medical College of Nanjing University, Nanjing, Jiangsu 210093, P.R. China, Department of Digestive Disease, Nanjing Children's Hospital, Nanjing Medical University, Nanjing, Jiangsu 210008, P.R. China
  • Pages: 1911-1916
    |
    Published online on: November 14, 2014
       https://doi.org/10.3892/mmr.2014.2958
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Abstract

Curcumin is known to possess anti‑inflammatory properties. Despite the fact that curcumin is known to be a strong inhibitor of H+, K+‑ATPase activity, the mechanism underlying the curcumin‑induced inhibition of the transcription of the H+, K+‑ATPase α subunit in gastric mucosal parietal cells remains unclear. The present study investigated the possible mechanism by which curcumin inhibits stomach H+, K+‑ATPase activity during the acute phase of gastric ulcer disease. A rat model of stress‑induced gastric ulcers was produced, in which the anti‑ulcer effects of curcumin were examined. Curcumin‑induced inhibition of the H+, K+‑ATPase promoter via histone acetylation, was verified using a chromatin immunoprecipitation assay. The results showed that curcumin improved stress‑induced gastric ulcer disease in rats, as demonstrated by increased pH values and reduced gastric mucosal hemorrhage and ulcer index. These effects were accompanied by a significant reduction in the level of histone H3 acetylation at the site of the H+, K+‑ATPase promoter and in the expression of the gastric H+,K+‑ATPase α subunit gene and protein. In conclusion, curcumin downregulated the acetylation of histone H3 at the site of the H+, K+‑ATPase promoter gene, thereby inhibiting the transcription and expression of the H+, K+‑ATPase gene. Curcumin was shown to have a preventive and therapeutic effect in gastric ulcer disease.
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Copy and paste a formatted citation
Spandidos Publications style
He P, Zhou R, Hu G, Liu Z, Jin Y, Yang G, Li M and Lin Q: Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats. Mol Med Rep 11: 1911-1916, 2015.
APA
He, P., Zhou, R., Hu, G., Liu, Z., Jin, Y., Yang, G. ... Lin, Q. (2015). Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats. Molecular Medicine Reports, 11, 1911-1916. https://doi.org/10.3892/mmr.2014.2958
MLA
He, P., Zhou, R., Hu, G., Liu, Z., Jin, Y., Yang, G., Li, M., Lin, Q."Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats". Molecular Medicine Reports 11.3 (2015): 1911-1916.
Chicago
He, P., Zhou, R., Hu, G., Liu, Z., Jin, Y., Yang, G., Li, M., Lin, Q."Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats". Molecular Medicine Reports 11, no. 3 (2015): 1911-1916. https://doi.org/10.3892/mmr.2014.2958
Copy and paste a formatted citation
x
Spandidos Publications style
He P, Zhou R, Hu G, Liu Z, Jin Y, Yang G, Li M and Lin Q: Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats. Mol Med Rep 11: 1911-1916, 2015.
APA
He, P., Zhou, R., Hu, G., Liu, Z., Jin, Y., Yang, G. ... Lin, Q. (2015). Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats. Molecular Medicine Reports, 11, 1911-1916. https://doi.org/10.3892/mmr.2014.2958
MLA
He, P., Zhou, R., Hu, G., Liu, Z., Jin, Y., Yang, G., Li, M., Lin, Q."Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats". Molecular Medicine Reports 11.3 (2015): 1911-1916.
Chicago
He, P., Zhou, R., Hu, G., Liu, Z., Jin, Y., Yang, G., Li, M., Lin, Q."Curcumin-induced histone acetylation inhibition improves stress-induced gastric ulcer disease in rats". Molecular Medicine Reports 11, no. 3 (2015): 1911-1916. https://doi.org/10.3892/mmr.2014.2958
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