Abstract
7,8-Dihydroxyflavone (7,8-DHF) is thought to be a promising therapeutic agent for various neurodegenerative diseases. The major purpose of this study was to investigate the neuroprotective effects of 7,8-DHF on the rotenone-induced motor deficit of Parkinson's disease. Nine-month-old rats were treated with rotenone (2 mg/kg/day, i.h.) for 5 weeks to establish the animal model of Parkinson's disease (PD), and 7,8-DHF (5 mg/kg, i.p.) was administrated daily throughout the whole period of rotenone injection. Five weeks later, an open field test was used to assess the motor ability of the animals. TH immunostaining was performed to evaluate rotenone-induced neurotoxicity on substantia nigra (SN) dopaminergic neurons and the DA terminals in the striatum. Western blot analyses were used to examine the expressions of TH, BDNF/TrkB signaling cascades, phospho-α-synuclein (Ser129), α-synuclein, and phospho-tau (Ser396) in SN. The results revealed that treatment with 7,8-DHF improved PD model's behavioral performance and reduced dopaminergic neuron loss in the SN and striatum, associated with the activation of TrkB receptors and its signaling cascades, and reduced p-MAPK, p-α-synuclein, and p-tau. Collectively, these results indicated that 7,8-DHF displayed prominent neuroprotective properties, providing a promising therapeutic strategy for PD treatment.
Highlights
Neurons and glial cells have been shown to synthesize and secrete a wide variety of neurotrophins, such as nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF), and play an important role in the survival of neurons and the growth of neurites [1]. e expression of BDNF is upregulated after a traumatic brain injury [2]
Tremendous basic and clinical studies have confirmed the essential role of BDNF in the survival of dopamine neurons and the pathophysiological mechanisms of Parkinson’s disease (PD) [3, 4]. e level of serum BDNF in patients with PD was significantly lower than those in normal subjects, and the decreased level of serum BDNF was closely related to the degree of apoptosis in striatal dopaminergic neurons [5]
Rats in the 7,8-DHF group were administered 7,8DHF (5 mg/kg, i.p.) once a day for 5 weeks. e other two groups were given an equal volume vehicle. ree animals in the rotenone group and one animal in the 7,8-DHF group were excluded from the study and were euthanized using CO2 followed by decapitation, due to sharp weight loss caused by the toxicity of rotenone
Summary
7,8-Dihydroxyflavone Protects Nigrostriatal Dopaminergic Neurons from Rotenone-Induced Neurotoxicity in Rodents. E major purpose of this study was to investigate the neuroprotective effects of 7,8-DHF on the rotenone-induced motor deficit of Parkinson’s disease. TH immunostaining was performed to evaluate rotenone-induced neurotoxicity on substantia nigra (SN) dopaminergic neurons and the DA terminals in the striatum. E results revealed that treatment with 7,8-DHF improved PD model’s behavioral performance and reduced dopaminergic neuron loss in the SN and striatum, associated with the activation of TrkB receptors and its signaling cascades, and reduced p-MAPK, p-α-synuclein, and p-tau. These results indicated that 7,8-DHF displayed prominent neuroprotective properties, providing a promising therapeutic strategy for PD treatment
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