Abstract
Parkinson's disease (PD) is a prevailing neurodegenerative disorder. Baicalein has neuroprotective effects on PD animals, but its mechanism is not clarified. We explored baicalein effects on PD rats. PD rat models were established by injecting 6-hydroxydopamine into the striatum of substantia nigra on the left side of the rat brain and treated with baicalein. Dopamine (DA) content, neuronal apoptosis, neuronal injury, neuronal mitochondria, and autophagy were assessed. Baicalein-treated PD rats were treated with autophagy inhibitor 3-methyladenine to identify the role of autophagy in PD. PD rats were injected with AgomiR-30b-5p or sh-SIRT1 plasmids and treated with baicalein. PD rats elicited decreased neurological score and DA secretion of the striatum, increased neuronal apoptosis, and injury, and reduced number of mitochondria and autophagy, whereas baicalein alleviated neuronal injury and partly recovered mitochondrial dysfunction, 3-methyladenine inhibited the protection of baicalein. miR-30b-5p was elevated and SIRT1 was diminished in PD rats and inhibited by baicalein. miR-30b-5p targeted SIRT1. miR-30b-5p overexpression or SIRT1 silencing annulled the protection of baicalein. The phosphorylation level of AMPK in the substantia nigra of PD rats was decreased and mTOR was increased, whereas baicalein annulled these trends. Briefly, baicalein activated mitochondrial autophagy via miR-30b-5p and the SIRT1/AMPK/mTOR pathway, thus protecting PD rats.
Highlights
Parkinson’s disease (PD) is a prevailing progressive neurodegenerative disorder featured by Lewy body formation and dopaminergic neuronal death in the substantia nigra [1–3]
DA content in the striatum of rat brains was assessed by High-Performance Liquid Chromatography-Electrical Chemistry (HPLC-EC), which found decreased DA content in the striatum of PD rats, whereas baicalein restored DA content to some extent (Supplementary Figure S1B)
The rat brain neuronal apoptosis was further detected by TUNEL staining, which showed facilitated neuronal apoptosis in PD rats, whereas baicalein hindered the apoptosis (Supplementary Figure S1C)
Summary
Parkinson’s disease (PD) is a prevailing progressive neurodegenerative disorder featured by Lewy body formation and dopaminergic neuronal death in the substantia nigra [1–3]. It is a prevalent neurodegenerative disease that influences 1 to 2 out of 1,000 of the global population, especially in the aged population [4, 5]. PD is induced by dopaminergic neuron degeneration or pathophysiologic loss in the substantial nigra of midbrain and neuronal Lewy bodies development, with aging, family history, pesticide exposure, and environmental chemicals as the recognized risk factors [6]. The complicacy of PD has brought great clinical challenges, such as the difficulties in definitive early diagnosis, advanced-stage management, and treatment obstacles which delay the progression [7]. The progression of PD is affected by neuroinflammation [8].
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