Antioxidative potential of a combined therapy of anti TNFα and Zn acetate in experimental colitis

Michela Barollo, Valentina Medici, Renata D'Incà, Antara Banerjee, Giuseppe Ingravallo, Marco Scarpa, Surajit Patak, Cesare Ruffolo, Romilda Cardin, Giacomo Carlo Sturniolo

Research output: Contribution to journalArticle

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Abstract

AIM: To evaluate whether combination therapy with anti-tumour necrosis factor α (TNFα) antibody and Zn acetate is beneficial in dextran sodium sulphate (DSS) colitis. METHODS: Colitis was induced in CD1-Swiss mice with 5% DSS for 7 d. The experimental mice were then randomised into the following subgroups: standard diet + DSS treated (induced colitis group); standard diet + DSS + subcutaneous 25 μg anti-TNFα treated group; Zn acetate treated group + DSS + subcutaneous 25 μg anti-TNFα; standard diet + DSS + subcutaneous 6.25 μg anti-TNFα treated group and Zn acetate treated group + DSS + subcutaneous 6.25 μg anti-TNFα. Each group of mice was matched with a similar group of sham control animals. Macroscopic and histological features were scored blindly. Homo genates of the colonic mu cosa were assessed for myeloperoxidase activity as a biochemical marker of inflamm ation and DNA adducts (8OH-dG) as a measure of oxidative damage. RESULTS: DSS produced submucosal erosions, ulcers, inflammatory cell infiltration and cryptic abscesses which were reduced in both groups of mice receiving either anti-TNFα alone or combined with zinc. The effect was more pronounced in the latter group (vs Zn diet, P < 0.02). Myeloperoxidase activity (vs controls, P < 0.02) and DNA adducts, greatly elevated in the DSS fed colitis group (vs controls, P < 0.05), were sig nificantly reduced in the treated groups, with a mor e remarkable effect in the group receiving combined therapy (vs standard diet, P < 0.04). CONCLUSION: DSS induces colonic inflammation which is modulated by the administration of anti-TNFα. Combining anti-TNFα with Zn acetate offers marginal benefit in colitis severity.

Original languageEnglish (US)
Pages (from-to)4099-4103
Number of pages5
JournalWorld Journal of Gastroenterology
Volume17
Issue number36
DOIs
StatePublished - Sep 28 2011

Fingerprint

Dextran Sulfate
Colitis
Acetates
Tumor Necrosis Factor-alpha
Diet
Therapeutics
DNA Adducts
Peroxidase
Control Groups
Hominidae
Abscess
Ulcer
Zinc
Biomarkers
Inflammation

Keywords

  • Anti tumor necrosis factor α
  • Experimental colitis
  • Inflammatory bowel disease
  • Oxidative dam age
  • Zinc

ASJC Scopus subject areas

  • Gastroenterology

Cite this

Antioxidative potential of a combined therapy of anti TNFα and Zn acetate in experimental colitis. / Barollo, Michela; Medici, Valentina; D'Incà, Renata; Banerjee, Antara; Ingravallo, Giuseppe; Scarpa, Marco; Patak, Surajit; Ruffolo, Cesare; Cardin, Romilda; Sturniolo, Giacomo Carlo.

In: World Journal of Gastroenterology, Vol. 17, No. 36, 28.09.2011, p. 4099-4103.

Research output: Contribution to journalArticle

Barollo, M, Medici, V, D'Incà, R, Banerjee, A, Ingravallo, G, Scarpa, M, Patak, S, Ruffolo, C, Cardin, R & Sturniolo, GC 2011, 'Antioxidative potential of a combined therapy of anti TNFα and Zn acetate in experimental colitis', World Journal of Gastroenterology, vol. 17, no. 36, pp. 4099-4103. https://doi.org/10.3748/wjg.v17.i36.4099
Barollo, Michela ; Medici, Valentina ; D'Incà, Renata ; Banerjee, Antara ; Ingravallo, Giuseppe ; Scarpa, Marco ; Patak, Surajit ; Ruffolo, Cesare ; Cardin, Romilda ; Sturniolo, Giacomo Carlo. / Antioxidative potential of a combined therapy of anti TNFα and Zn acetate in experimental colitis. In: World Journal of Gastroenterology. 2011 ; Vol. 17, No. 36. pp. 4099-4103.
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abstract = "AIM: To evaluate whether combination therapy with anti-tumour necrosis factor α (TNFα) antibody and Zn acetate is beneficial in dextran sodium sulphate (DSS) colitis. METHODS: Colitis was induced in CD1-Swiss mice with 5{\%} DSS for 7 d. The experimental mice were then randomised into the following subgroups: standard diet + DSS treated (induced colitis group); standard diet + DSS + subcutaneous 25 μg anti-TNFα treated group; Zn acetate treated group + DSS + subcutaneous 25 μg anti-TNFα; standard diet + DSS + subcutaneous 6.25 μg anti-TNFα treated group and Zn acetate treated group + DSS + subcutaneous 6.25 μg anti-TNFα. Each group of mice was matched with a similar group of sham control animals. Macroscopic and histological features were scored blindly. Homo genates of the colonic mu cosa were assessed for myeloperoxidase activity as a biochemical marker of inflamm ation and DNA adducts (8OH-dG) as a measure of oxidative damage. RESULTS: DSS produced submucosal erosions, ulcers, inflammatory cell infiltration and cryptic abscesses which were reduced in both groups of mice receiving either anti-TNFα alone or combined with zinc. The effect was more pronounced in the latter group (vs Zn diet, P < 0.02). Myeloperoxidase activity (vs controls, P < 0.02) and DNA adducts, greatly elevated in the DSS fed colitis group (vs controls, P < 0.05), were sig nificantly reduced in the treated groups, with a mor e remarkable effect in the group receiving combined therapy (vs standard diet, P < 0.04). CONCLUSION: DSS induces colonic inflammation which is modulated by the administration of anti-TNFα. Combining anti-TNFα with Zn acetate offers marginal benefit in colitis severity.",
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AU - Barollo, Michela

AU - Medici, Valentina

AU - D'Incà, Renata

AU - Banerjee, Antara

AU - Ingravallo, Giuseppe

AU - Scarpa, Marco

AU - Patak, Surajit

AU - Ruffolo, Cesare

AU - Cardin, Romilda

AU - Sturniolo, Giacomo Carlo

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N2 - AIM: To evaluate whether combination therapy with anti-tumour necrosis factor α (TNFα) antibody and Zn acetate is beneficial in dextran sodium sulphate (DSS) colitis. METHODS: Colitis was induced in CD1-Swiss mice with 5% DSS for 7 d. The experimental mice were then randomised into the following subgroups: standard diet + DSS treated (induced colitis group); standard diet + DSS + subcutaneous 25 μg anti-TNFα treated group; Zn acetate treated group + DSS + subcutaneous 25 μg anti-TNFα; standard diet + DSS + subcutaneous 6.25 μg anti-TNFα treated group and Zn acetate treated group + DSS + subcutaneous 6.25 μg anti-TNFα. Each group of mice was matched with a similar group of sham control animals. Macroscopic and histological features were scored blindly. Homo genates of the colonic mu cosa were assessed for myeloperoxidase activity as a biochemical marker of inflamm ation and DNA adducts (8OH-dG) as a measure of oxidative damage. RESULTS: DSS produced submucosal erosions, ulcers, inflammatory cell infiltration and cryptic abscesses which were reduced in both groups of mice receiving either anti-TNFα alone or combined with zinc. The effect was more pronounced in the latter group (vs Zn diet, P < 0.02). Myeloperoxidase activity (vs controls, P < 0.02) and DNA adducts, greatly elevated in the DSS fed colitis group (vs controls, P < 0.05), were sig nificantly reduced in the treated groups, with a mor e remarkable effect in the group receiving combined therapy (vs standard diet, P < 0.04). CONCLUSION: DSS induces colonic inflammation which is modulated by the administration of anti-TNFα. Combining anti-TNFα with Zn acetate offers marginal benefit in colitis severity.

AB - AIM: To evaluate whether combination therapy with anti-tumour necrosis factor α (TNFα) antibody and Zn acetate is beneficial in dextran sodium sulphate (DSS) colitis. METHODS: Colitis was induced in CD1-Swiss mice with 5% DSS for 7 d. The experimental mice were then randomised into the following subgroups: standard diet + DSS treated (induced colitis group); standard diet + DSS + subcutaneous 25 μg anti-TNFα treated group; Zn acetate treated group + DSS + subcutaneous 25 μg anti-TNFα; standard diet + DSS + subcutaneous 6.25 μg anti-TNFα treated group and Zn acetate treated group + DSS + subcutaneous 6.25 μg anti-TNFα. Each group of mice was matched with a similar group of sham control animals. Macroscopic and histological features were scored blindly. Homo genates of the colonic mu cosa were assessed for myeloperoxidase activity as a biochemical marker of inflamm ation and DNA adducts (8OH-dG) as a measure of oxidative damage. RESULTS: DSS produced submucosal erosions, ulcers, inflammatory cell infiltration and cryptic abscesses which were reduced in both groups of mice receiving either anti-TNFα alone or combined with zinc. The effect was more pronounced in the latter group (vs Zn diet, P < 0.02). Myeloperoxidase activity (vs controls, P < 0.02) and DNA adducts, greatly elevated in the DSS fed colitis group (vs controls, P < 0.05), were sig nificantly reduced in the treated groups, with a mor e remarkable effect in the group receiving combined therapy (vs standard diet, P < 0.04). CONCLUSION: DSS induces colonic inflammation which is modulated by the administration of anti-TNFα. Combining anti-TNFα with Zn acetate offers marginal benefit in colitis severity.

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