Biochemical, histopathological, and immunohistochemical study on the ameliorative effect of crocin against lipopolysaccharide‑induced hippocampal toxicity in male albino rats.

BACKGROUND: Lipopolysaccharide (LPS)-induced neuroinflammation is widely used as an animal model for studying the mechanisms of neuroinflammation. Crocin, an active component of saffron (Crocus sativus L), possesses several beneficial properties. The present study aimed to investigate the role of crocin in alleviating hippocampal toxicity induced by LPS in rats. METHOD: Forty male albino rats were randomly divided into five groups. Group I served as a control. Group II intraperitoneally (i.p.) injected with LPS (1 mg/kg/day) for a week. Groups III, IV, and V were treated by oral gavage with captopril (50 mg/kg/day), crocin (50 mg/kg/day), and a combination of both captopril (50 mg/kg/day) and crocin (50 mg/kg/day), respectively for 30 consecutive days, starting on the 8th day after LPS i.p. injection. During the therapy schedule, rats were tested for memory and learning abilities. Hippocampal samples were collected for biochemical, histological, immunohistochemical, and morphometric studies. Biochemical evaluation included nuclear factor kappa B, inflammatory cytokines (tumor necrosis factor-α and interleukin-1β), amyloid beta, angiotensin-converting enzyme, markers of the cholinergic system (acetylcholinesterase and choline acetyltransferase), antioxidant enzymes (catalase and superoxide dismutase) and an oxidative stress indicator (malondialdehyde). Histological examinations, as well as immunohistochemical and histomorphometric analysis, were also performed on hippocampal tissue. RESULTS: The results revealed biochemical, histological, and immunohistochemical alterations in the hippocampus of the LPS group. Most of these alterations showed satisfactory improvements in hippocampal tissue when LPS-administered rats were treated with captopril and crocin, either separately or in combination. CONCLUSION: The present study suggests that crocin acts as a promising therapeutic agent for alleviating memory impairments and neuroinflammation induced by LPS.