Acetyl-11-keto-beta-boswellic Acid (AKBA) Ameliorates Histopathological and Oxidative Stress Brain Disorders in the Experimental Model of Cuprizone-induced Demyelination

Background: Multiple sclerosis is an inflammatory autoimmune disease that destroys the myelin sheath (demyelination) and neurons of the central nervous system (CNS), with several factors contributing to its development. Objectives: This study investigated the impact of administering acetyl 11-keto-beta boswellic acid (AKBA) in an animal model of cuprizone-induced demyelination. Methods: Thirty-two C57BL/6 female mice (WT; 20 - 25 g, 8 - 10 weeks old) were randomly divided into four groups: (1) Control (CO), (2) Cuprizone-treated (CPZ, 0.3%), (3) AKBA + CPZ (50 mg/kg, pre-treatment), and (4) CPZ + AKBA (50 mg/kg, post-treatment). At the end of the study, the weight and movement balance of the animals were assessed using the rotarod test. After sampling the brain, the extent of the demyelination area in the corpus callosum was measured with Luxol Fast Blue staining, the number of oligodendrocyte cells was determined by immunohistochemistry, and the levels of malondialdehyde (MDA) and total antioxidant capacity (TAC) as oxidative stress factors in the brain tissue were measured. Results: The use of acetyl-11-keto-beta boswellic acid in the cuprizone-induced demyelination model prevented weight loss, increased animal resistance in the rotarod test, and reduced the demyelination rate in the corpus callosum. Additionally, AKBA elevated the number of oligodendrocytes and total antioxidant capacity levels while reducing malondialdehyde levels in brain tissue. Pretreatment with AKBA exhibited a more significant effect. Conclusions: This study showed that acetyl-11-keto-beta boswellic acid, an important active substance of the frankincense plant, likely protects the nervous system and neurons in the cuprizone-induced demyelination model by preventing the decrease in the number of oligodendrocytes, reducing oxidative stress, and preventing the destruction of myelin.