The Therapeutic Potential of Dalbergia pinnata (Lour.) Prain Essential Oil in Alzheimer's Disease: EEG Signal Analysis In Vivo, SH-SY5Y Cell Model In Vitro, and Network Pharmacology

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder that is projected by the WHO to affect over 100 million people by 2050. Clinically, AD patients undergoing long-term antipsychotic treatment often experience severe anxiety or depression in later stages. Furthermore, early-stage AD manifests with weakened α waves in the brain, progressing to diminished α and β waves in late-stage disease, reflecting changes in emotional states and disease progression. In this study, EEG signal analysis revealed that inhalation of Dalbergia pinnata (Lour.) Prain essential oil (DPEO) enhanced δ, θ, α and β wave powers in the frontal and parietal lobes, with a rising trend in the β/α ratio in the temporal lobe. These findings suggest an alleviation of anxiety and an enhancement of cognitive functions. Treatment of the AD SH-SY5Y (human neuroblastoma cells) cell model with DPEO resulted in decreased intracellular levels of Aβ, GSK-3β, P-Tau, IL-1β, TNF-α, IL-6, COX-2, OFR, and HFR, alongside reduced AchE and BchE activities and increased SOD activity. Network pharmacology analysis indicated a potential pharmacological mechanism involving the JAK-STAT pathway. Our study provides evidence supporting DPEO's role in modulating anxiety and slowing AD pathological progression.

Keywords: Alzheimer’s disease; Dalbergia pinnata; SH-SY5Y cell; electroencephalography; essential oil; network pharmacology.

Figure 1

Main process of in vivo, in vitro, and network pharmacology.

Figure 2

EEG topographical maps for females. The changes in power across the four brainwaves from left to right (δ, θ, α, β, and β/α) before and after inhaling DPEO.

Figure 3

EEG topographical maps for males. The changes in power across the four brainwaves from left to right (δ, θ, α, β, and β/α) before and after inhaling DPEO.

Figure 4

SH-SY5Y cell viability. (a) DPEO cytotoxicity towards SH-SY5Y cells, (b) Aβ_1–42 cytotoxicity towards SH-SY5Y cells, (c) CCK-8 for control, model (10 μM Aβ_1–42), and treated (10 μM Aβ_1–42 and 0.04% DPEO) group. (p-value: ns (not significant), * < 0.05, *** < 0.001, **** < 0.0001).

Figure 5

Morphological images of SH-SY5Y cells following different treatments. (a) Control represents the normal cellular morphology. (b) Cellular morphology after treatment with 0.04% DPEO. (c) Cellular morphology following treatment with 10 μM Aβ_1–42 exhibiting rupture and shrinkage. (d) Cellular morphology after treatment with 10 μM Aβ_1–42 + 0.04% DPEO (v/v) (treated group) displaying relatively good cellular morphology.

Figure 6

Concentration of T-Tau, P-Tau, GSK-3β, Aβ_1–42, COX-2, IL-1β, TNF-α, and IL-6 in SH-SY5Y cells before and after treatment with 0.04% DPEO (v/v) at a concentration of 10 μM Aβ_1–42. (a) The concentration of T-Tau, (b) the concentration of P-Tau, (c) P-Tau concentration/T-Tau concentration, (d) the concentration of GSK-3β, (e) the concentration of Aβ_1–42, (f) the concentration of COX-2, (g) the concentration of IL-1β, (h) the concentration of TNF-α, and (i) the concentration of IL-6. (p-value: ns (not significant), *** < 0.001, **** < 0.0001).

Figure 7

SH-SY5Y cells’ OFR scavenging ratio, HFR scavenging ratio, and SOD activity before and after treatment with 0.04% DPEO (v/v) at a concentration of 10 μM Aβ_1–42. (a) OFR scavenging ratio, (b) HFR scavenging ratio, (c) SOD activity. (p-value: ** < 0.01, *** < 0.001, **** < 0.0001).

Figure 8

AchE and BchE activity in SH-SY5Y cells before and after treatment with 0.04% DPEO (v/v) at a concentration of 10 μM Aβ_1–42. (a) AchE activity, (b) BchE activity. (p-value: * < 0.05, *** < 0.001, **** < 0.0001).

Figure 9

(a) Venn diagram of intersection targets of elemicin, methyl eugenol, and Alzheimer’s disease. (b) Venn diagram of intersection targets of elemicin and methyl eugenol for Alzheimer’s Disease. (c) Drug AD targets PPI network. (d) Key targets PPI network.

Figure 10

Key targets GO/KEGG enrichment analysis and molecular docking. (a) GO function enrichment analysis. (b) KEGG pathway enrichment analysis. (c) Heatmap of molecular docking. They are elemicin-TYK2 methyl eugenol-PARP1, methyl eugenol-JAK2, and methyl eugenol-TYK2. (d) Structure of molecular docking (Vina score is ≤−5.0 kcal/mol, the molecular binding is relatively stable, Vina score is ≤−7.0 kcal/mol, and the molecular binding is highly stable).

Figure 11

DPEO in JAK-STAT signaling pathway.