Lipopolysaccharide (LPS) can induce neuroinflammation associated with Alzheimer's disease (AD). Crocin has neuroprotective properties due to its strong antioxidant, anti-inflammatory, and anti-apoptotic activities. The goal of this study is to find out if crocin can reverse the pathophysiological features of AD and the hippocampal neuroinflammation brought on by LPS. The rats were randomly divided into five equal groups. Group (I) served as a control, Group (II) received LPS (1 mg/kg/day) for one week, Following LPS exposure, Group III and IV received 50 mg/kg/day of captopril and 50 mg/kg/day of crocin, respectively, while Group V received a 30-day combination of both therapies. Nitric oxide (NO) and acetylcholine (Ach) levels were assessed in hippocampal samples, and Aurora kinase was found by immunohistochemical analysis. In the hippocampal homogenate, the LPS group exhibited a highly significant decrease in Ach level and a highly significant increase in NO concentration. Aurora expression in the hippocampus tissues increased concurrently with these results.. On the other hand, rats in the LPS+CAP group showed minor improvements in immunohistochemistry aurora expression along with a significantly higher Ach level and a significantly lower NO concentration.\. Rats in the LPS+CR and LPS+CAP+CR groups, however, exhibited a mild immunoreactivity to aurora expression along with a highly significant increase in Ach level and a decrease in NO concentration. Crocin co-treatment attenuates the LPS-induced neuroinflammation, which may be explained by increased NO, decreased Ach, and excessive aurora expression.