Abstract: BACKGROUND: The occurrence of diabetic encephalopathy may be closely related to neuronal aging, but its underlying molecular mechanism is not fully understood. Therefore, exploring the role of neuronal aging in diabetic encephalopathy is of great significance for further revealing the pathogenesis of diabetic encephalopathy. 
OBJECTIVE: To explore role and mechanism of emodin in slowing down the senescence of HT-22 cells induced by high glucose.
METHODS: HT-22 cells were divided into a control group (glucose concentration of 25 mmol/L), a high glucose group (glucose concentration of 55 mmol/L), and a high glucose + emodin group (glucose concentration of 55 mmol/L, emodin concentration of 100 µmol/L) and cultured for 48 hours. Cell growth in each group was observed microscopically. Cell viability was assessed by CCK-8 assay. Telomerase reverse transcriptase activity was measured by ELISA in each group. Expression of senescence-related proteins P53, P21, and P16 in each group was determined by RT-qPCR and western blot assay. Expression of lamin A/C in each group was determined by immunofluorescence, RT-qPCR, and western blot assay.
RESULTS AND COUCLUSION: (1) Compared with the control group, the cells in the high-glucose group showed obvious growth inhibition under the microscope, which was manifested as a decrease in the number of cells, an increase in size, and a flattened morphology. Compared with the high-glucose group, the number of cells in the high-glucose emodin group increased significantly, and the morphology tended to be regular. (2) Compared with the control group, the cell viability of the high glucose group was significantly decreased (P < 0.000 1). Compared with the high glucose group, the cell viability in the high glucose + emodin group was significantly increased (P < 0.000 1). (3) Compared with the control group, the telomerase reverse transcriptase activity in the high glucose group was significantly decreased (P < 0.001). (4) Compared with the control group, the expression levels of P53, P21, and P16 in the high glucose group were significantly increased (P < 0.05). Compared with the high glucose group, the expression levels of P53, P21, and P16 in the high glucose + emodin group were significantly decreased (P < 0.05). (5) Compared with the control group, the expression level of lamin A/C in the high glucose group was significantly decreased (P < 0.000 1). Compared with the high glucose group, the expression levels of lamin A/C in the high glucose + emodin group were significantly increased (P < 0.05). These results suggest that emodin may mitigate high glucose-induced senescence in HT-22 cells by upregulating lamin A/C expression. 

Key words: diabetes encephalopathy, high-glucose environment, aging of hippocampal neurons, LaminA/C protein, emodin