Abstract
Inflammation plays an important role in the defense of the human body. The inflammatory response can suppress the spread of pathogens, accelerate the removal of necrotic cells, and repair the damaged tissues and organs. However, an excessive inflammatory response can be fatal as it may lead to cellular apoptosis, necrosis of tissues and organs, and systemic dysfunction. An inflammatory response occurs when the skin is burned or injured, causing more severe and extensive pathological damage to the injured area. For example, inflammation can damage the coagulation system in the capillaries, resulting in the formation of small blood clots in the affected areas. In severe cases, inflammation can lead to necrosis of the injured area and may even affect other uninjured areas, causing hypoxia and inadequate blood supply. The role of valproic acid (VPA), a histone deacetylase inhibitor, has been increasingly recognized in recent years. Evidence suggests that VPA can effectively alleviate tissue and organ injuries secondary to ischemia and hypoxia, and improve the body’s tolerance to ischemia-hypoxia and inflammatory insults, thus increasing the survival rates of the patients. This article reviews the latest research progress made in the mechanisms by which VPA regulates inflammatory response to burns.
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