Protective Effect of Casticin on Experimental Skin Wound Healing of Rats

The wound is known as damage to the skin structure by external stimuli, such as cut, bruises, and burn, which typically leaves the internal tissue exposed. The wound repair process when hampered leads to an excessive burden on the healthcare setting. Therefore, there is an urgent need to develop effective agents that can promote the wound healing process. In the present study, we intended to investigate the pharmacological benefit of Casticin (CST), a polymethylflavone against wound.

The wound in Wistar rats was induced by a surgical procedure. After surgery, the wound was examined for wound size over a period and for the expression of cyclooxygenase-2 and induced collagen III expressions. The effect of CST was examined on tumor necrosis factor α, interferon gamma, interleukin (IL)-10, transforming growth factor beta, and IL-7 by real-time polymerase chain reaction. The expression of matrix metalloproteinases (MMP)-2 and MMP-9 and its natural inhibitor (tissue inhibitors of metalloproteinases, TIMP1), level of macrophages, and lymphocytes were also quantified. The effect of CST was determined also on apoptosis of rats' splenocytes.

CST significantly enhances wound healing of rat postsurgery, with maximum activity achieved in the case of a 60 μM treated group. The expression of cyclooxygenase-2 was found reduced together with an increase in collagen III, tumor necrosis factor α, interferon gamma, IL-10, transforming growth factor beta, and IL-7 in the CST group. The levels of MMP-2 and MMP-9 were also found reduced together with an increase in TIMP1 level in CST-treated group. The levels of CD4⁺, CD8⁺, and CD11b⁺ cells at the wound site 24 and 120 h postsurgery was also found reduced in CST-treated group. However, it showed no apoptosis in murine splenocytes.

Collectively, CST can promote the wound healing process by modulation of inflammation and immune response, which induces tissue remodeling.