Evidence map›Paper›PMID 40893772›Full record

ArticleBiochemistry and biophysics reports2025

A study on the mechanism of Bushen Kaiqiao Formula in modulating microglial activation to alleviate neuroinflammation in ADHD.

Jiaqi Zhang, Ruxin Sun, Yu Xiong, Yuting Yang, Jing Wang, Kanglin Zhu, Xinqiang Ni, Min Huang

Abstract read
In one paragraph

Article in Biochemistry and biophysics reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

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3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Jiaqi ZhangDepartment of Neurology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.
Ruxin SunDepartment of Neurology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.
Yu XiongDepartment of Neurology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.
Yuting YangThe Fourth Clinical Medical College, Guangzhou University of Chinese Medicine, Shenzhen, China.
Jing WangThe Fourth Clinical Medical College, Guangzhou University of Chinese Medicine, Shenzhen, China.
Kanglin ZhuThe Fourth Clinical Medical College, Guangzhou University of Chinese Medicine, Shenzhen, China.
Xinqiang NiThe Fourth Clinical Medical College, Guangzhou University of Chinese Medicine, Shenzhen, China.
Min HuangDepartment of Neurology, The Seventh Affiliated Hospital, Sun Yat-sen University, Shenzhen, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Growing evidence suggests that dysregulated microglial activation and neuroinflammation in the prefrontal cortex may underlie the pathophysiology of Attention Deficit Hyperactivity Disorder. Utilizing spontaneously hypertensive rats-a well-validated animal model of ADHD-this study aimed to characterize ADHD-like behavioral phenotypes and prefrontal cortical neuronal development and elucidate the neuroimmunological mechanisms through which the Bushen Kaiqiao Formula (BSKQF) exerts its therapeutic effects by modulating microglial activation states. Methods: Ultra-high-performance liquid chromatography coupled with a tandem mass spectrometer (UHPLC-MS/MS) was used to qualitatively analyze the chemical composition of Bushen Kaiqiao Formula, and network pharmacology was applied to predict its potential therapeutic targets and ADHD-related pathways ADHD-like behaviors, including hyperactivity, impulsivity, spatial memory, and attention, were assessed using the Open Field Test, Elevated Plus Maze, and Y-Maze Test at weeks 2 and 4. Prefrontal cortical neuronal morphology and dendritic spine density were evaluated using Nissl staining and Golgi-Cox staining, respectively. Microglial activation (Iba-1+/iNOS + immunofluorescence), inflammatory cytokine levels (IL-1β and IL-6 by ELISA), and blood-brain barrier integrity (transmission electron microscopy) were examined. In vitro, primary prefrontal cortical neurons and microglia were isolated from neonatal rats and treated with BSKQF-containing serum at different concentrations, with Methylphenidate (MPH) as a control. An oxygen-glucose deprivation/reoxygenation (OGD/R) model was established to mimic neuroinflammatory conditions with inflammatory signaling pathways assessed. Results: UHPLC-MS/MS identified key bioactive components of Bushen Kaiqiao Formula. Network pharmacology analysis suggested that BSKQF may ameliorate ADHD-related behavioral deficits by inhibiting the NF-κB signaling pathway. Behavioral assessments demonstrated dose- and time-dependent effects. BSKQF significantly reduced neuronal loss, promoted synaptic plasticity, reduced the proportion of activated microglia (iNOS+/Iba-1+), and lowered IL-1β and IL-6 levels. Additionally, ultrastructural examination indicated restored blood-brain barrier integrity and reduced perivascular edema. In vitro, BSKQF-containing serum suppressed NF-κB pathway activation (p-NF-κB-p65, p-IκBα) and inflammasome-related proteins (NLRP3, caspase-1). Conclusion: BSKQF effectively alleviates ADHD-like behaviors in SHR rats by inhibiting prefrontal microglial activation and neuroinflammation, reducing neuronal apoptosis, restoring synaptic plasticity, and preserving blood-brain barrier integrity.

Indexed as

Attention deficit hyperactivity disorderBushen Kaiqiao FormulaMicroglial activationNeuroinflammationNF-κB pathway

Identifiers

PMID40893772
PMCPMC12396018

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.