Strokes are preceded by oxidative stress and inflammation, two processes linked to atherosclerosis and hypertension. Statins have been widely employed to control atherosclerosis; however, there could be neurological implications to its use—including cognitive impairment. Thus,we aimed to determine whether alpha-tocopherol is capable of reversing the neurological side effects of statins and enhancing its anti-inflammatory properties. To assess these effects, 15-week-old stroke-prone spontaneously hypertensive rats (SHRSPs) were divided into four groups (n = 6, each): alpha-tocopherol (AT), lovastatin (LoV), alpha-tocopherol + lovastatin (AT + LoV), and control (C).We administered 120 IU of alpha-tocopherol diluted in 0.1 ml of coconut oil,whereas the dose of lovastatin was administered at a ratio of 1 mg/kg of rat body weight. The control group received 0.1 ml coconut oil. All animals received the treatments via orogastric gavage.We assessed body weight, diuresis, food and water intake, oxidative stress (malondialdehyde levels), the total cellular injury marker (lactate dehydrogenase), short and long-term memory, cognition, and histopathological changes in the hippocampus. The results demonstrated that lovastatin treatment did not negatively affect the memory of our animal model. In fact, the animals treated with AT and LoV showed improvement in memory and cognition. Additionally, both treatments decrease lactate dehydrogenase and oxidative stress levels. Furthermore, our study also demonstrated hippocampal tissue preservation in the treated groups.

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