Its selective toxicity is because susceptible parasite GABA receptors are distributed in the Peripheral Nervous System whereas the host GABA receptors are distributed in the CNS. Ivermectin is used in the field to treat mite infestation and maggot-infested wounds. Ivermectin eliminates parasites by inducing hyperpolarization through binding to the parasite-specific gamma-aminobutyric acid (GABA)-gated chloride ions and glutamate-gated ion channels dampening transmission of electrical impulses resulting in paralysis and death. Ivermectin was found to be so useful as an antiparasitic agent in many species and, it can be administered topically, orally, or parenterally.
Ivermectin is a macrolide belonging to the avermectin group which first received a wide application in human and veterinary medicine practice about three decades ago. TGF-β1 and VEGF are the two major growth factors that play a very significant role in the restoration of tissue function and integrity. The interleukins IL-1α, IL-1β, IL-4, and TNF-α are pro-inflammatory whilst IL-10 is anti-inflammatory during the wound healing process. They exhibit either pro-inflammatory or anti-inflammatory activity. Many cytokines and growth factors are implicated in the wound healing cascade. Eicosanoids such as Prostaglandin E 2 (PGE 2), Leukotriene B 4 (LTB 4) tend to enhance inflammation whereas Prostaglandin D 2 (PGD 2) shows anti-inflammatory actions during wound healing. Hydroxyproline, an integral component of collagen, serves as a precursor of tissue fibers MPO, an enzyme mainly released by neutrophils and monocytes, combats microbial invasion during injury and trigger inflammation. A clot formed as a result of tissue damage serves as an adhesion site for cells such as fibroblast, neutrophils, endothelial cells, and monocytes that migrate to the wounded site. Fibronectin, thrombin, and their derivatives from platelets interface with collagen leading to the release of growth factors and cytokines. Immediately after injury, the disrupted fibers activate platelet aggregation, resulting in degranulation and the release of clotting, chemotactic, and growth factors to initiate hemostasis. Wound repair is a critical yet entangled process in mammals, with many different features represented by successive yet interwoven phases hemostatic, inflammatory, proliferative, and maturation phases. Wound healing is, therefore, a progression of an intricate biochemical and physiological cascade that reestablishes the integral anatomy and functionality of the injured tissue. Low doses of ivermectin cream have the potential to be used in treating wounds with minimal scar tissue formation.Ī wound is a break in the structural continuity regarding the morphology and the functionality of an organ. Ivermectin promotes wound healing partly through modulation of the inflammatory process and the levels of Transforming Growth Factor-Beta 1 and Vascular Endothelial Growth Factor. Interestingly, low doses of ivermectin cream (0.03–0.1%) induced wound healing with minimal scarring compared to higher doses of the cream and the positive control, Silver Sulfadiazine. This corresponded with changes in cytokines (IL-1α, IL-4, IL-10, and TNF-α) and eicosanoids (LTB4, PGE 2, and PGD 2) levels on days 7 and 21. The levels of growth factors TGF-β1 and VEGF were significantly elevated on day 7 but decreased on day 21. This corresponded with a statistically significant wound contraction rate, hydroxyproline deposition, and a decreased time to heal rate. Non-irritant dose of ivermectin cream (0.03–1%) decreased wound macroscopic indices such as exudation, edge edema, hyperemia, and granulation tissue deposition by day 9 compared to day 13 for the vehicle-treated group. This study aimed to evaluate the wound healing property of ivermectin cream using histochemistry and enzyme-linked immunosorbent assay techniques. Here, we show that ivermectin exhibits wounding healing activity by mechanisms independent of its well-known antiparasitic activity. Ivermectin, a macrolide, has been used as an endectoparasiticide in human and veterinary medicine practice for decades.
Wound healing, therefore, seeks to re-establish the normal morphology and functionality through intertwined stages of hemostasis, inflammation, proliferation, and tissue remodelling. Wounds cause structural and functional discontinuity of an organ.
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