Neuroprotective effects of Tiliacora triandra (Colebr.) Diels leaf extract against lipopolysaccharide-induced memory impairment via anti-neuroinflammation.

Neurodegenerative diseases are characterized by progressive neuronal loss associated with neuroinflammation. Lipopolysaccharide (LPS) is used as a proinflammatory stimulus in neurodegenerative models, as it induces neuroinflammatory responses and activates microglia and astrocytes, leading to the release of cytokines [such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6] that exacerbate neuronal damage. Tiliacora triandra, a medicinal plant native to Southeast Asia, has antioxidant and anti-inflammatory properties. The present study investigated the neuroprotective effects of T. triandra leaf extract (TTE) against LPS-induced memory impairment and neuroinflammation in rats. Animals were randomly divided into five treatment groups, namely a vehicle-control, vehicle plus LPS, ibuprofen plus LPS (positive control) and TTE-treated plus LPS groups receiving 200 or 400 mg/kg body weight (BW) TTE for 14 consecutive days. Starting on day 8, LPS (250 µg/kg BW) was administered intraperitoneally for 7 days to induce neuroinflammation. At the end of the treatment period, animals were sacrificed and hippocampal tissues were collected for histological and biochemical analyses. The results demonstrated that TTE significantly ameliorated LPS-induced memory deficits and sickness-like behavior. TTE treatment reduced neuroinflammatory responses, as evidenced by decreased levels of proinflammatory cytokines, such as TNF-α and IL-1β, compared with the vehicle plus LPS group. Additionally, compared with the vehicle plus LPS group, TTE treatment resulted in a reduced number of activated microglia and astrocytes, as indicated by a reduced number of positive cells of ionized calcium-binding adapter molecule 1 and glial fibrillary acidic protein in the hippocampus, respectively. Furthermore, the results of the present study suggested that TTE treatment promoted neuronal survival in hippocampal regions affected by LPS administration. Overall, these findings suggested that TTE mitigated the LPS-induced neuroinflammation and cognitive impairment, which indicates that it may have potential as a therapeutic agent for neuroinflammatory and memory-related disorders.