Association Between Acupuncture's Neuroprotective Effects and Integrin Alpha 7.

Abstract

: Parkinson's disease (PD) entails the progressive degeneration of dopaminergic neurons in the substantia nigra (SN), accompanied by α-synuclein (α-syn)-enriched Lewy bodies. ITGA7 mediates cell-extracellular matrix adhesion and modulates apoptosis, though its involvement in PD pathogenesis warrants further investigation. Although acupuncture demonstrates neuroprotective effects in PD models, its precise molecular mechanisms remain incompletely understood; therefore, in this study, we explored the relationship between ITGA7 and α-synuclein expression in an MPTP-induced PD mouse model to determine the association between LR3/GB34 acupuncture-induced changes in α-synuclein levels and ITGA7 modulation.: In the in vivo model, MPTP-induced PD mice underwent immunohistochemistry, immunofluorescence, and Western blotting to assess ITGA7, α-synuclein, and TH levels in the SN and striatal tissues following LR3/GB34 acupuncture. In parallel, for the in vitro mechanistic study, SH-SY5Y neuroblastoma cells treated with MPPand transfected with ITGA7-siRNA were utilized to examine the involvement of apoptosis-related signaling pathways.: In the in vivo model, MPTP administration downregulated ITGA7 and upregulated α-synuclein in SN tissues. Similarly, in vitro exposure of SH-SY5Y cells to MPPyielded comparable results, revealing an inverse correlation between ITGA7 and α-synuclein. LR3/GB34 acupuncture treatment in the mouse model significantly increased ITGA7 and TH expression while reducing α-synuclein accumulation. To further understand the specific role of ITGA7 observed in these animal findings, we silenced ITGA7 in the MPP-treated cellular model. ITGA7 silencing exacerbated the neurotoxic effects, leading to further TH downregulation, α-synuclein upregulation, Bcl-2 reduction, and Bax/Bcl-2 ratio elevation.: Collectively, the histological preservation of dopaminergic neurons following LR3/GB34 acupuncture in the PD mouse model appears to be linked to ITGA7 upregulation. Furthermore, our in vitro findings implicate ITGA7 in the regulation of apoptosis-related signaling cascades, supporting its potential role in mitigating α-synuclein pathology.