The Injector, cilt.2, sa.3, ss.26, 2023 (Hakemli Dergi)
Objective: Parkinson's
disease (PD) represents a multifaceted neurodegenerative disorder characterised
by the progressive degeneration of dopaminergic neurons, ultimately resulting
in neurodegeneration. The hallmark pathological features of PD encompass the
reduction of dopaminergic neurons in the substantia nigra pars compacta and the
accumulation of misfolded α-synuclein within cytoplasmic inclusions known as
Lewy bodies. Rotenone, a naturally occurring toxin produced by tropical plants,
possesses the capacity to penetrate the blood-brain barrier. Upon neuronal
entry, it impedes proteasome activation, instigating α-synuclein
phosphorylation, aggregation, Lewy pathology formation, and subsequent
degeneration of nigrostriatal dopaminergic neurons. Boric acid (BA),
representing the primary form of boron in human tissues and bodily fluids,
assumes a pivotal role. A deficiency of BA in the human body is associated with
diminished motor and cognitive functions. The aim of our study is to examine the possible protective effect of BA
within a Rotenone-induced Parkinson's disease model established in the SH-SY5Y
human neuroblastoma cell line, serving as an in vitro experimental
paradigm.
Methods: The
cytotoxic effect of BA was determined by MTT experiment as a result of the
combined application of 200µM, 100 µM, 50 µM, 20 µM BA and 50 µM Rotenone
concentrations to the SH-SY5Y cell. Gene expression levels of signalling
pathways involved in the cytotoxicity of SH-SY5Y cells of the Rotenone, BA, and
Rotenone + BA groups were investigated by quantitative reverse transcriptase
polymerase chain reaction (RT-qPCR) and changes in protein expression
determined by the Western Blot method.
Results: The MTT
experiment revealed that the viability of the PH model generated with 50 µM
Rotenone was 64.58%, whereas the viability of the PH model generated with 200
µM BA was 116.36%, and a significant proliferation was observed. This specific
dosage was selectively used for RT-qPCR and Western blot analyses. Notably, the
co-administration of 50 µM Rotenone with 200 µM BA exhibited a marked
attenuation of apoptotic processes, as evidenced by a notable reduction in the
BAX/BCL-2 pro-apoptotic mRNA ratio, displaying a 0.54-fold change relative to
the Rotenone-only group.
Conclusion: Consequently,
these findings lead to the inference that boric acid (BA) may exert a
neuroprotective effect.
Keywords:
Apoptosis, boric acid, neuroprotective, Parkinson's disease, rotenone.