Role and mechanism of emodin in slowing down the senescence of HT-22 cells induced by high glucose

• High glucose induces senescence in HT-22 hippocampal neurons, characterized by reduced cell viability, decreased telomerase activity, and upregulation of senescence markers P53, P21, and P16. • Emodin treatment alleviates high glucose-induced senescence by restoring cell viability, increasing telomerase activity, and downregulating senescence markers. • High glucose downregulates lamin A/C expression, while emodin upregulates lamin A/C, suggesting a potential mechanism for its anti-senescence effect. • Emodin may serve as a therapeutic candidate for diabetic encephalopathy by targeting lamin A/C to mitigate neuronal senescence.