Abstract
Parkinson's disease (PD) is regarded as a severe neurodegenerative disorder. Baicalein is involved in the treatment of PD. This study explored the mechanism of baicalein in PD. The PD rat model was established using 6-hydroxydopamine. The neurologic score, dopamine (DA) content, apoptotic cells, and neuronal damage were evaluated after rats were treated with baicalein. Autophagy in PD rats was inhibited using 3-methyladenine (3-MA). The mitochondrial membrane potential (MMP) and autophagy-related proteins (LC3, P62) were detected. Next, agomiR-30b was transfected into PD rats. The targeting relation between miR-30b and NIX was predicted and verified. Then, sh-NIX was transfected into PD rats, and the effects of miR-30b and NIX on MMP, LC3, and P62 were assessed. When miR-30b was overexpressed using agomiR-30b, the NIX and BNIP3 levels were detected. Baicalein increased the neurological score and restored DA content, neurons, MMP, and mitochondrial autophagy protein levels. Baicalein inhibited miR-30b expression and miR-30b targeted NIX. miR-30b upregulation or NIX silencing reversed the effect of baicalein on MMP and mitochondrial autophagy. Baicalein upregulated NIX and BNIP3 expressions, while miR-30b overexpression inhibited NIX and BNIP3 expressions. In summary, baicalein mediated mitochondrial autophagy and restored neuronal activity by downregulating miR-30b and activating the NIX/BNIP3 pathway, thus protecting against PD.
Highlights
Parkinson’s disease (PD) is a progressive neurodegenerative disorder that is characterized by motor and nonmotor symptoms [1]
It was found that the rats in the PD group showed severe neurological deficits, and the related motor and sensory coordination was decreased (P < 0.001), while the intervention of baicalein alleviated neurobehavioral defects caused by surgery-induced PD to some extent. e content of DA was detected by High Performance Liquid Chromatography-Electrical Chemistry (HPLC-EC) (Figure 1(b))
Our results showed that PD decreased membrane potential (MMP) in PD rats. e MMP returned to a certain level after baicalein intervention, while autophagy inhibitor 3-MA reversed the effect of baicalein in PD
Summary
Parkinson’s disease (PD) is a progressive neurodegenerative disorder that is characterized by motor and nonmotor symptoms [1]. Mitochondrial autophagy is a core cellular activity and insufficient autophagy of mitochondrial leads to various aging-related pathologies, especially PD [5, 7, 8]. Erefore, it is generally believed that the increase of LC3-II content represents the activation of autophagy flow, and the decrease of LC3-II content represents the inhibition of autophagy [9]. P62 is a Biochemistry Research International multifunctional protein, which plays an important role in autophagy. It consists of many domains and can bind to different proteins, such as UBA, LIr, and PB1 domains. Further study is needed to explore the pathogenesis of PD in terms of mitochondrial autophagy so as to provide new ideas for clinical treatment
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