Neuroprotective Role of Amentoflavone on LPS-Induced Parkinsons Disease Animal Model via Inhibition of Microglia-Mediated Inflammation

Abstract

Background: Amentoflavone (AF) is a polyphenolic compound present in Selaginella tamariscina, exhibiting various activities. Nevertheless, the potential neuroprotective effects of AF in animal models of Parkinsons disease (PD) induced by lipopolysaccharide (LPS) remain unexplored. Methods: In the PD animal model, induced by LPS, the experimental procedure involved establishing the model through LPS administration, followed by animal euthanasia. Brain samples were then collected for subsequent analysis. Protein and mRNA expressions of tumor necrosis factor-alpha (TNF-α), interleukin (IL)-1β, IL-6, inducible nitric oxide synthase (iNOS), cyclooxygenase-2 (COX-2), IL-4, transforming growth factor-beta (TGF-β), arginase-1 (Arg-1), and cluster of differentiation (CD)206 were assessed using Western blot and Quantitative Real-Time Polymerase Chain Reaction (qRT-PCR) assays, respectively. Immunohistochemical staining and confocal laser scanning microscopy were employed to detect the expression of tyrosine hydroxylase (TH), the key enzyme responsible for dopamine (DA) synthesis, and alpha-synuclein (α-syn), which serves as the pathological basis of PD. Results: The LPS-induced PD animal model successfully replicated functional deficits resembling those observed in human PD. AF was shown to ameliorate the reduction in excitability, motor dysfunction, depression-like behavior, and anxiety-like behavior. Conclusions: In LPS-induced PD animal models, AF demonstrates a neuroprotective effect on DA neurons by suppressing the microglia-mediated inflammatory response. In terms of effectiveness, early prophylactic administration of AF appears to yield better results compared to late therapeutic administration.