Abstract
We aimed to test the therapeutic effects of baicalin on attention deficit hyperactivity disorder (ADHD) in an animal model and to explain the potential mechanism. We investigated the therapeutic effects and mechanisms of baicalin in a spontaneously hypertensive rat (SHR) model of ADHD depending on the dopamine (DA) deficit theory. In this study, fifty SHRs were randomly divided into five groups: methylphenidate (MPH), baicalin (50 mg/kg, 100 mg/kg, or 150 mg/kg), and saline-treated. Ten Wistar Kyoto (WKY) rats were used as controls. All rats were orally administered the treatment for four weeks. Motor activity, spatial learning and memory ability were assessed with the open-field and Morris water-maze tests. The mRNA and protein levels of tyrosine hydroxylase (TH), vesicular monoamine transporter 2 (VMAT2), synaptosomal-associated protein of molecular mass 25kD (SNAP25) and synataxin 1a in synaptosomes were detected with real-time polymerase chain reaction (PCR) and Western blot. In addition, DA levels were measured in the prefrontal cortex and striatum. The results indicated that both MPH and baicalin at doses of 150 mg/kg and 100 mg/kg significantly decreased the hyperactivity and improved the spatial learning memory deficit in the SHRs and increased the synaptosomal mRNA and protein levels of TH, SNAP25, VMAT2 and synataxin 1a compared with saline treatment. MPH significantly increased DA levels in both the prefrontal cortex (PFC) and striatum, while baicalin significantly increased DA levels only in the striatum. The results of the present study showed that baicalin treatment was effective for controlling the core symptoms of ADHD. Baicalin increased DA levels only in the striatum, which suggested that baicalin may target the striatum. The increased DA levels may partially be attributed to the increased mRNA and protein expression of TH, SNAP25, VMAT2, and syntaxin 1a. Therefore, these results suggested that the pharmacological effects of baicalin were associated with the synthesis, vesicular localization, and release of DA and might be effective in treating ADHD. However, further studies are required to better understand the molecular mechanisms underlying these findings.
Highlights
attention deficit hyperactivity disorder (ADHD), which has the core symptoms of inattention, hyperactivity, and/or increased impulsivity [1], is a common childhood neurodevelopment disorder with a 5.9% global annual incidence [2]
In the third week of the experiment, compared with the Wistar Kyoto (WKY) + saline group, except for the spontaneously hypertensive rat (SHR) + baicalin(50 mg/kg) group, the body weight of the other groups was significantly increased (p = 0.006, LSD), and the food intake in the SHR + baicalin(150 mg/kg) group was significantly higher than the other groups (p < 0.001, LSD); In the 4th week of the experiment, compared with the WKY + saline group, the weight of the other groups increased significantly (p < 0.001, LSD)
In a previous study, we hypothesized that baicalin would have therapeutic effects in patients with ADHD [23]
Summary
ADHD, which has the core symptoms of inattention, hyperactivity, and/or increased impulsivity [1], is a common childhood neurodevelopment disorder with a 5.9% global annual incidence [2]. Many studies have reported that the drug is effective in controlling the core symptoms in ADHD [3]; this drug has been reported to have many adverse reactions, such as loss of appetite, induced tics, drug dependence, and increased heart rate, that rebound after stopping treatment [6], which brings certain limitations to clinical medication.
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