Selenium Nanorods from Lawsonia inermis Flowers: Enhancing Anti-Diabetic Effects and Cognitive Function Via mTOR/Akt and BDNF/pTrKB/CREB Pathways in High Glucose-Induced Neuroblastoma SH-SY5Y Cells

Cognitive impairment and brain cell death are linked to the harmful effects of high hyperglycemia. This work examines the antioxidant and cognitive-boosting properties of selenium nanorods derived from Lawsonia inermis (Henna) flower extract in protecting SH-SY5Y neuroblastoma cells from oxidative damage generated by high glucose (HG). The selenium nanorods (HF-SeNRs) were produced by employing the henna flower extract (HFE) as both a stabilizer and reductant. The pharmacokinetic behavior of the phytocompounds present in the HFE explored using computational approaches. The physico-chemicals properties of nanorods were then examined utilizing a range of spectral and microscopic methods, including FTIR, XRD, EDX, HR-TEM, DSC and FFT. HF-SeNRs, measuring 17–20 nm in size and having a rod-shaped structure, demonstrated notable antioxidant properties and effectively inhibited the acetylcholinesterase enzyme activity. Pre-treatment of SH-SY5Y cells exposed to high glucose with HF-SeNRs (at concentrations ranging from 6.25 to 25 µg/mL) resulted in a dose-dependent preservation of cell viability. This pre-treatment also postponed the onset of oxidative damage-induced mitochondrion-related impairment, DNA breakage, and programmed cell death. In addition, HF-SeNRs decreased the expression of cell death promotor proteins (p53, Bax, caspase 3) and increased the expression of the cell death inhibiting protein Bcl-2 in high glucose circumstances. They regulated the AKT/mTOR and BDNF/TrkB/CREB signaling pathways, which are linked to cellular development, proliferation, and cognitive function. HF-SeNRs showed potential in mitigating oxidative damage and cell death induced by high glucose exposure in SH-SY5Y cells. This was achieved by increasing antioxidant activity and modulating signaling proteins related to cell death and cognitive function.