Objectives: To explore the potential neuroprotective mechanism of crocin after cerebral infarction.
Methods: The murine hippocampal neuronal cell line HT-22, was used as the study model, with a control group, OGD-group, low-dose crocin group, middle-dose crocin group, and high-dose crocin group. Except for the control-group, cells in the other groups were treated with OGD for 6 h, in which 1 μg/mL, 2 μg/mL and 5 μg/mL of crocin were added in low-dose group, medium-dose group and high-dose group, respectively. Subsequently, the OGD cells were cultured for another 6 h. CCK-8 assay was carried out to detect the cell viability of each group, flow cytometry was used to detect cell apoptosis, immunofluorescence was conducted to detect the expression of reactive oxygen species, and Western Blot was performed to detect the protein expression of p-PI3K, p-Akt, p-mTOR, LC-3 I, LC-3 II, and Beclin-1.
Results: After hypoxia-reoxygenation treatment, the viability of HT22 cells was remarkably decreased, the apoptosis rate and expression of ROS were significantly increased, the protein expression of p-PI3K, p-Akt and p-mTOR were reduced, while the expression of LC-3 II/I and Beclin-1 were increased. After crocin treatment, the activity of hypoxic reoxygenated cells increased, the apoptosis rate decreased, the expression of reactive oxygen species dropped, the protein expression of p-PI3K, p-Akt and p-mTOR increased, and the expression of LC-3 II/I and Beclin-1 decreased.
Conclusion: At the cellular level, crocin can inhibit autophagy by activating the PI3K/Akt/mTOR pathway, and reduce the level of oxidative stress, thus playing a neuroprotective role.
Keywords: Crocin; PI3K/Akt/mTOR signaling pathway; cerebral infarction; neuroprotection.
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