Abstract
The objective of this study was to explore the neuroprotective effect of moxibustion on rats with Parkinson's disease (PD) and its mechanism. A Parkinson's disease model was established in rats using a two-point stereotactic 6-hydroxydopamine injection in the right substantia nigra (SN) and ventral tegmental area. The rats received moxibustion at the Baihui (GV20) and Sishencong (EX-HN1) acupoints for 20 minutes, six times a week, for 6 weeks. The right SN tissue was histologically and immunohistochemically examined. Differentially expressed genes (DEGs) were identified through RNA sequencing. In addition, the levels of tyrosine hydroxylase (TH), glutathione peroxidase 4 (GPX4), and ferritin heavy chain 1 (FTH1) in SN were measured. In comparison to the model group, the moxibustion group showed a significantly greater TH immunoreactivity and a higher behavioural score. In particular, moxibustion led to an increase in the number and morphological stability of SN neural cells. The functional pathway analysis showed that DEGs are closely related to the ferroptosis pathway. GPX4 and FTH1 in the SN were significantly overexpressed in the moxibustion-treated rats with PD. Moxibustion can effectively reduce the death of SN neurons, decrease the occurrence of ferroptosis, and increase the TH activity to protect the neurons in rats with PD. The protective mechanism may be associated with suppression of the ferroptosis.
Highlights
Parkinson’s disease (PD) is the second most common age-related neurodegenerative movement disorder after Alzheimer’s disease (AD) [1]
PD is primarily characterized by degeneration of the dopaminergic neurons in the substantia nigra pars compacta (SNpc) [3], which results in movement disorders, including tremor, rigidity, gait difficulty, and bradykinesia [4]
There was an obvious decrease in the number of dopaminergic neurons in the PD group that was often accompanied by a disordered neuronal distribution, nuclear condensation, or swelling
Summary
Parkinson’s disease (PD) is the second most common age-related neurodegenerative movement disorder after Alzheimer’s disease (AD) [1]. PD is primarily characterized by degeneration of the dopaminergic neurons in the substantia nigra pars compacta (SNpc) [3], which results in movement disorders, including tremor, rigidity, gait difficulty, and bradykinesia [4]. Ferritin heavy chain 1 (FTH1) is the target of iron death. As a major iron storage protein, FTH1 plays an important role in maintaining the iron balance in cells, and plays an important regulatory role in a variety of signalling pathways [8]. All of the motor complications have been found to occur in 40% and 70% of the patients after 5- and 15-year levodopa treatment, respectively [11]. The need for PD treatment strategies has led to the investigation of alternative therapies
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