Hydrolysate of Oviductus Ranae Activates MAPK/ERK Signaling Apoptosis Pathway to Repair Corticosterone-induced Damage in HT-22 Cells
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Abstract:
To examine the protective mechanism of oviductus ranae (OR) on hippocampal neuronal cells, this study explored the protective effect and mechanism of OR hydrolysate in a corticosterone (CORT)-induced mouse hippocampal neuron (HT-22) model of cell injury. HT-22 cells were co-cultured with CORT to establish an injury model, then further incubated with OR hydrolysate, followed by the addition of the ERK signaling pathway inhibitor PD98059. MTT assay, Hoechst 33258 staining, flow cytometry and Western blot were employed to assess cell apoptosis, protein expression, and MAPK/ERK signaling pathway activity. Results demonstrated that elevated levels of CORT induced damage in HT-22 cells, while OR hydrolysate enhanced cell viability by 62.5%~87.5%, and reduced apoptosis rates by 50%~70%. Moreover, OR hydrolysate upregulated BCL-2 and P-ERK1/2 protein expression, and downregulated BAX, Caspase-3 and Caspase-9 protein expressions. These findings indicate that high CORT levels promote apoptosis by inhibiting the MAPK/ERK signaling pathway, leading to HT-22 cell damage. OR hydrolysate regulates the expression of apoptosis-related proteins, (BLC-2, BAX, Caspase-3 and Caspase-9) by activating the MAPK/ERK signaling pathway, thereby inhibiting apoptosis and reducing neuronal damage. This mechanism represents a key pathway through which OR exerts anti-depressive effects.
