Abstract

Induced ulcer wound repair needs re-epithelialisation to replace necrotised and/or damaged tissue and to re-establish its integrity. Transforming growth factor-β (TGF-β) affects all cell types that are involved in all stages of wound healing. The assessment of induced ulcer wound healing activity was carried out through three models: First, excision model, second, induced ulcer wound using 50 mg Aspirin, and third by using 10 mg Nicorandil wound model. The animals were divided into eight groups; and were treated with different concentrations of Zinc sulphate, compared to their controls. The efficacy of Zinc sulphate on healing process of lesion induced was assessed by; body weight change, macroscopical appearance of the induced ulcers (ulcer area and wound contraction), microscopically appearance and histopathology; as well as qualitative assessment Moreover, the effect of ulcer induction on the serum levels of TGF-β according to the procedure of the kit was assessed in all groups. Different concentrations of topical Zinc sulphate have not significantly enhanced the healing of excision wounds. Thirty milligram Zinc sulphate has not significantly enhanced the healing of lesion ulcer induced by 50 mg Aspirin or 10 mg Nicorandil. Nevertheless, the 50 mg Aspirin and 10 mg Nicorandil caused delay in healing. In all groups, a significant reduction in ulcer area was observed compared to that of the baseline. Besides, a significant elevation in wound contraction was noticed compared to that of the baseline. Qualitative assessment of the healing process of the induced ulcer confirms that Aspirin or Nicorandil delay healing. Assessment of serum TGF-β level in serum showed no statistical significant elevation in those groups treated with different concentrations of Zinc sulphate compared to their control, while TGF-β level showed non-significant reduction in the group of induced ulcer by Aspirin or Nicorandil and treatment with 30 mg Zinc sulphate, compared to their controls. In conclusion, Nicorandil cause ulceration in the same manner of Aspirin, which delay the healing process, and TGF-β appears to play a more profound role in the healing process perforations than in the healing of induced ulcers in skin.

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