Induced ulcer wound repair needs re-epithelialisation to replace necrotised and/or damaged tissue and to reestablish 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.

Herpes labialis is an infection caused by the herpes simplex virus, characterized by an eruption of small and usually painful blisters on the skin of the lips, mouth, gums, or the skin around the mouth. Although there is no successful treatment available, the local use of compounds with effective anti-inflammatory and cytoprotective effects may be of value in this respect. This project was designed to evaluate clinically the local use of silymarin, a group of flavonoids with powerful antioxidant, anti-inflammatory and cytoprotective activity, in the treatment of herpes simplex ulcer. Fifty three patients with herpes labialis ulcers (HLU) were enrolled in this randomized, single blinded, placebo controlled clinical study, and they were allocated into 4 groups, treated with 1%, 3% and 5% silymarin paste and placebo formula respectively. Patient's responses to treatment were followed by clinical evaluation of healing time, size of the ulcers and pain sensation, in addition to evaluating biochemical and immunological markers of the oxidative stress and inflammatory response. HLU patients showed dose dependent improvement in the healing time, pain score and size of ulcer as a result of treatment with various concentrations (1%, 3% and 5%) of silymarin paste, associated with improvement in the oxidative stress state and immunological parameters. In conclusion, silymarin can be used locally as paste formula for the treatment of HLU, an effect which may be attributed to its antioxidant, anti-inflammatory and cytoprotective properties. Keywords: Herpes labialis, ulcers, silymarin

Many reports confirm ulcers as an adverse effect of drugs such as nicorandil and aspirin. The exact responsible mechanisms of ulceration have until now not proved. Mucosal ulcers associated with the onset of ulcer are manifested by an increase in proinflammatory cytokine, excessive prostaglandin, and up-regulation of Endothilin-1 level, which directly impacts the release of leptin. These, released locally within mucosal tissues, have played a role in controlling the extent of local inflammatory responses and processes of mucosal repair.This study was designed to find out the correlation of plasma leptin and prostaglandin levels as a possible mechanism of oral ulcer formation as an adverse effect of nicorandil. The effect of nicorandil for inducing ulceration was assessed. The plasma leptin and prostaglandin E2 for the tested groups in relation to the studied parameters (gender, and daily body weight change) were estimated in albino rats.Nicorandil causes mucous membrane damage, inflammation, and ulceration. A significant reduction of plasma leptin level, which was dose-dependent, and a non-significant reduction of serum prostaglandin E2 level. The mechanisms of ulcer induction as an adverse effect of nicorandil can be related to dose-dependant leptin and prostaglandin E2 levels, which affects on repair and healing process.Keywords: Nicorandil, Leptin, Prostaglandin E2, Ulcer.