The antidepressant-like properties of corilagin on SH-SY5Y neuroblastoma cells and a forced swimming test animal model.

Corilagin, a member of the phenolic tannin family, exhibits both anti-inflammatory and anti-oxidative properties. Depression is a mental disorder caused by an imbalance in brain neurotransmitters, excessive stress, and chronic inflammatory responses. The present study aims to estimate the antidepressant-like effect of corilagin using amyloid-β (Aβ)-stimulated neuroblastoma SH-SY5Y cells and forced swimming test (FST)-induced depression model in mice. Corilagin prevented Aβ-induced damage to SH-SY5Y cells by enhancing cell viability and lowering levels of lactate dehydrogenase, interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. During the FST, corilagin demonstrated a dual effect by decreasing immobility duration while simultaneously elevating levels of neurotransmitters (dopamine, NE, and 5-HT) and neuroprotective factors (brain-derived neurotrophic factor and cyclic adenosine monophosphate response element-binding protein) within the hippocampus. By increasing the activities of superoxide dismutase and catalase and decreasing malondialdehyde amounts, corilagin reduced oxidative stress in the hippocampus. Corilagin decreased amounts of IL-1β, IL-6, and TNF-α, while increasing the amounts of IL-10. Furthermore, corilagin administration led to a substantial reduction in hippocampal Aβ and total tau protein levels without causing any adverse effects. These findings suggest that corilagin exerts antidepressant-like effects by enhancing neurotransmitter function and reducing oxidative stress and inflammation. Hence, we propose corilagin as a potential treatment for depression.