Chronic pain is a complex condition shaped by long-standing alterations in both physiological and psychological processes. Rather than representing a simple continuation of acute nociceptive signaling, chronic pain is increasingly understood as the outcome of progressive dysregulation within distributed neural systems that govern sensation, affect, motivation, and cognitive control. Neuroimaging and electrophysiological studies indicate that this state is accompanied by extensive plastic changes in deep brain structures and large-scale networks. Beyond well-described central sensitization processes, chronic pain is characterized by disrupted oscillatory rhythms and altered connectivity within large-scale brain networks, including thalamo-cortical circuits and prefrontal-limbic-reward networks. These findings support a conceptual shift from viewing chronic pain as a focal, lesion-driven phenomenon toward recognizing it as a disorder of distributed network pathology. Pharmacological treatments remain central to clinical practice, yet their long-term efficacy is often limited and frequently accompanied by substantial side effects. The ongoing concerns about opioid-related risks and the inadequate therapeutic response in a subset of patients highlight the need for safe, non-pharmacological approaches that can address not only pain but also comorbid disturbances in mood, sleep, and social functioning. Neuromodulation provides a promising path toward mechanism-based and non-pharmacological management of chronic pain by employing physical or chemical stimulation to alter the excitability and synchrony of specific neural populations within central, peripheral, and autonomic systems. While invasive deep brain stimulation demonstrates that targeting deep brain structures can be effective, its clinical application is restricted by surgical risks and cost, highlighting the importance of non-invasive techniques capable of reaching deep targets. Current non-invasive approaches, such as transcranial electric stimulation, are constrained by limited penetration depth and insufficient spatial precision. These limitations hinder reliable engagement of deep regions implicated in pain, including the thalamus and nucleus accumbens, and tend to produce broad, non-specific modulation of cross-network oscillatory activity. Temporal interference (TI) stimulation has emerged as a means of overcoming these obstacles. By delivering interacting high-frequency currents that generate a low-frequency envelope within the head, TI enables focal stimulation of deep targets while minimizing superficial current delivery. Recent multiscale modeling and animal studies indicate that TI exploits the nonlinear rectification properties of neuronal membranes in response to high-frequency carriers, as well as their phase-locked responses to low-frequency envelopes, to generate “peak-focused” electric fields in deep regions under relatively low superficial current loads. Moreover, TI appears to exhibit potential advantages in terms of cell-type selectivity and rhythm-specific engagement, including differential responses across neuronal subtypes and distinct coupling to θ-, β-, and γ-band oscillations. These features suggest a promising avenue for correcting abnormal rhythms and network dynamics that contribute to chronic pain. This review summarizes current knowledge of the neural mechanisms underlying chronic pain and recent advances in TI research. It examines functional disturbances across key pain-related regions and networks, outlines the principles and technical characteristics of TI, and discusses potential deep-brain targets and stimulation strategies relevant to chronic pain. Evidence to date indicates that TI, with its non-invasiveness, tolerability, and capacity for precise deep brain modulation, holds great promise for the management of treatment-resistant chronic pain and may evolve into a new generation of precise and efficient non-pharmacological analgesic strategies.

Chronic pain is a complex condition shaped by long-standing alterations in both physiological and psychological processes. Rather than representing a simple continuation of acute nociceptive signaling, chronic pain is increasingly understood as the outcome of progressive dysregulation within distributed neural systems that govern sensation, affect, motivation, and cognitive control. Neuroimaging and electrophysiological studies indicate that this state is accompanied by extensive plastic changes in deep brain structures and large-scale networks. Beyond well-described central sensitization processes, chronic pain is characterized by disrupted oscillatory rhythms and altered connectivity within large-scale brain networks, including thalamo-cortical circuits and prefrontal-limbic-reward networks. These findings support a conceptual shift from viewing chronic pain as a focal, lesion-driven phenomenon toward recognizing it as a disorder of distributed network pathology. Pharmacological treatments remain central to clinical practice, yet their long-term efficacy is often limited and frequently accompanied by substantial side effects. The ongoing concerns about opioid-related risks and the inadequate therapeutic response in a subset of patients highlight the need for safe, non-pharmacological approaches that can address not only pain but also comorbid disturbances in mood, sleep, and social functioning. Neuromodulation provides a promising path toward mechanism-based and non-pharmacological management of chronic pain by employing physical or chemical stimulation to alter the excitability and synchrony of specific neural populations within central, peripheral, and autonomic systems. While invasive deep brain stimulation demonstrates that targeting deep brain structures can be effective, its clinical application is restricted by surgical risks and cost, highlighting the importance of non-invasive techniques capable of reaching deep targets. Current non-invasive approaches, such as transcranial electric stimulation, are constrained by limited penetration depth and insufficient spatial precision. These limitations hinder reliable engagement of deep regions implicated in pain, including the thalamus and nucleus accumbens, and tend to produce broad, non-specific modulation of cross-network oscillatory activity. Temporal interference (TI) stimulation has emerged as a means of overcoming these obstacles. By delivering interacting high-frequency currents that generate a low-frequency envelope within the head, TI enables focal stimulation of deep targets while minimizing superficial current delivery. Recent multiscale modeling and animal studies indicate that TI exploits the nonlinear rectification properties of neuronal membranes in response to high-frequency carriers, as well as their phase-locked responses to low-frequency envelopes, to generate “peak-focused” electric fields in deep regions under relatively low superficial current loads. Moreover, TI appears to exhibit potential advantages in terms of cell-type selectivity and rhythm-specific engagement, including differential responses across neuronal subtypes and distinct coupling to θ-, β-, and γ-band oscillations. These features suggest a promising avenue for correcting abnormal rhythms and network dynamics that contribute to chronic pain. This review summarizes current knowledge of the neural mechanisms underlying chronic pain and recent advances in TI research. It examines functional disturbances across key pain-related regions and networks, outlines the principles and technical characteristics of TI, and discusses potential deep-brain targets and stimulation strategies relevant to chronic pain. Evidence to date indicates that TI, with its non-invasiveness, tolerability, and capacity for precise deep brain modulation, holds great promise for the management of treatment-resistant chronic pain and may evolve into a new generation of precise and efficient non-pharmacological analgesic strategies.

Objective: To develop and validate a clinically actionable prediction model for postoperative pulmonary complications (PPCs) in cardiac surgery patients, focusing on modifiable preoperative risk factors amenable to targeted optimization. Methods: In this prospective observational cohort study, 492 adults undergoing open-chest cardiac surgery between August 15, 2023 and December 31, 2023 were analyzed. Prespecified predictors included gas exchange variables, pulmonary function, inspiratory muscle strength, and physical performance. Univariable and multivariable logistic regression analyses were used to develop the prediction model. Discrimination was assessed by the area under the receiver operating characteristic curve (AUC). Results: A total of 90 patients (14.1%) developed PPCs after surgery. Five independent predictors were identified: elevated arterial PaCO2 (odds ratio [OR] 1.12, 95% confidence interval [CI] 1.00–1.26), oxygen desaturation (SpO2<93%) (OR 12.47, 95% CI 3.51–48.13), reduced gait speed (OR 0.17, 95% CI 0.04–0.71), lower FEV1/FVC ratio (OR 0.96, 95% CI 0.92–1.00), and diminished inspiratory muscle strength (MIP % predicted) (OR 0.96, 95% CI 0.92–0.99). The model demonstrated good discriminative ability with an AUC of 0.86 (95% CI 0.80–0.93) in the training cohort and 0.87 (95% CI 0.74–0.93) in the validation cohort. Conclusion This parsimonious model achieved high predictive accuracy using five modifiable physiological variables. By targeting abnormalities in gas exchange, pulmonary mechanics, muscle strength, and functional reserve, the model offers a practical tool to guide individualized prehabilitation strategies for reducing PPC risk in cardiac surgery patients.

Objective This study aims to assess the impact of four-dimensional cone-beam computed tomography (4D-CBCT) image guidance on setup error correction and target dose distribution optimization in patients receiving stereotactic body radiotherapy for lung cancer. Methods A total of 82 lung cancer patients treated with SBRT in our hospital between February 2023 and February 2025 were randomly selected as study subjects. Using a random number table, they were divided into two groups. The conventional group underwent positioning verification using traditional three-dimensional cone-beam CT, while the study group underwent verification using 4D-CBCT. Setup errors, target dose-volume parameters, organ at risk dose-volume parameters, and adverse reactions were compared between the two groups. Results The setup errors in the X, Y, and Z axes in the study group were 0.21, 0.19, and 0.23 mm, respectively, which were significantly lower than 0.58, 0.62, and 0.59 mm in the conventional group (P<0.05). The three-dimensional vector error was 0.34 (0.21, 0.48) mm in the study group, which was significantly lower than 0.98 (0.65, 1.32) mm in the conventional group (P<0.05). The rotational errors in left-right, anteroposterior, and superior-inferior directions in the study group were (0.25±0.12)°, (0.21±0.10)°, and (0.23±0.11)°, respectively; these values were significantly lower than (0.48±0.18)°, (0.42±0.15)°, and (0.45±0.16)° in the conventional group (P<0.05). The minimum dose received by 95% of the target volume [(59.45±0.85) Gy] and the percentage of the target volume receiving at least 100% of the prescription dose [(95.82±2.65)%] in the study group were higher than those in the conventional group [(58.90±1.20) Gy and (93.65±3.85)%]. The homogeneity index and conformity index in the study group were 1.07±0.03 and 1.15±0.05, respectively, which were lower than 1.12±0.05 and 1.23±0.08 in the conventional group (P<0.05). No significant differences were observed between the two groups in the volume of the lung receiving 5 Gy [(28.11±5.52)% vs. (28.85±6.24)%], the volume of the lung receiving 20 Gy [(12.84±3.56)% vs. (13.45±3.90)%], mean lung dose [(8.65±2.11) Gy vs. (8.95±2.34) Gy], maximum spinal cord dose [(18.54±3.62) Gy vs. (19.13±4.25) Gy], or mean heart dose[(14.85±4.22) Gy vs. (16.27±4.83) Gy](P>0.05). The incidence rates of radiation pneumonitis, radiation esophagitis, and skin reactions in the study group were 12.20%, 7.32%, and 4.88%, respectively, which were not significantly different from 17.07%, 9.76%, and 7.32% in the conventional group (P>0.05). Conclusion The 4D-CBCT can reduce setup errors, improve target dose accuracy and conformity in lung cancer patients undergoing SBRT, and minimize radiation exposure to normal tissues, making it worthy of clinical promotion.

Objective This study aims to assess the impact of four-dimensional cone-beam computed tomography (4D-CBCT) image guidance on setup error correction and target dose distribution optimization in patients receiving stereotactic body radiotherapy for lung cancer. Methods A total of 82 lung cancer patients treated with SBRT in our hospital between February 2023 and February 2025 were randomly selected as study subjects. Using a random number table, they were divided into two groups. The conventional group underwent positioning verification using traditional three-dimensional cone-beam CT, while the study group underwent verification using 4D-CBCT. Setup errors, target dose-volume parameters, organ at risk dose-volume parameters, and adverse reactions were compared between the two groups. Results The setup errors in the X, Y, and Z axes in the study group were 0.21, 0.19, and 0.23 mm, respectively, which were significantly lower than 0.58, 0.62, and 0.59 mm in the conventional group (P<0.05). The three-dimensional vector error was 0.34 (0.21, 0.48) mm in the study group, which was significantly lower than 0.98 (0.65, 1.32) mm in the conventional group (P<0.05). The rotational errors in left-right, anteroposterior, and superior-inferior directions in the study group were (0.25±0.12)°, (0.21±0.10)°, and (0.23±0.11)°, respectively; these values were significantly lower than (0.48±0.18)°, (0.42±0.15)°, and (0.45±0.16)° in the conventional group (P<0.05). The minimum dose received by 95% of the target volume [(59.45±0.85) Gy] and the percentage of the target volume receiving at least 100% of the prescription dose [(95.82±2.65)%] in the study group were higher than those in the conventional group [(58.90±1.20) Gy and (93.65±3.85)%]. The homogeneity index and conformity index in the study group were 1.07±0.03 and 1.15±0.05, respectively, which were lower than 1.12±0.05 and 1.23±0.08 in the conventional group (P<0.05). No significant differences were observed between the two groups in the volume of the lung receiving 5 Gy [(28.11±5.52)% vs. (28.85±6.24)%], the volume of the lung receiving 20 Gy [(12.84±3.56)% vs. (13.45±3.90)%], mean lung dose [(8.65±2.11) Gy vs. (8.95±2.34) Gy], maximum spinal cord dose [(18.54±3.62) Gy vs. (19.13±4.25) Gy], or mean heart dose[(14.85±4.22) Gy vs. (16.27±4.83) Gy](P>0.05). The incidence rates of radiation pneumonitis, radiation esophagitis, and skin reactions in the study group were 12.20%, 7.32%, and 4.88%, respectively, which were not significantly different from 17.07%, 9.76%, and 7.32% in the conventional group (P>0.05). Conclusion The 4D-CBCT can reduce setup errors, improve target dose accuracy and conformity in lung cancer patients undergoing SBRT, and minimize radiation exposure to normal tissues, making it worthy of clinical promotion.

Objective This study aims to assess the impact of four-dimensional cone-beam computed tomography (4D-CBCT) image guidance on setup error correction and target dose distribution optimization in patients receiving stereotactic body radiotherapy for lung cancer. Methods A total of 82 lung cancer patients treated with SBRT in our hospital between February 2023 and February 2025 were randomly selected as study subjects. Using a random number table, they were divided into two groups. The conventional group underwent positioning verification using traditional three-dimensional cone-beam CT, while the study group underwent verification using 4D-CBCT. Setup errors, target dose-volume parameters, organ at risk dose-volume parameters, and adverse reactions were compared between the two groups. Results The setup errors in the X, Y, and Z axes in the study group were 0.21, 0.19, and 0.23 mm, respectively, which were significantly lower than 0.58, 0.62, and 0.59 mm in the conventional group (P<0.05). The three-dimensional vector error was 0.34 (0.21, 0.48) mm in the study group, which was significantly lower than 0.98 (0.65, 1.32) mm in the conventional group (P<0.05). The rotational errors in left-right, anteroposterior, and superior-inferior directions in the study group were (0.25±0.12)°, (0.21±0.10)°, and (0.23±0.11)°, respectively; these values were significantly lower than (0.48±0.18)°, (0.42±0.15)°, and (0.45±0.16)° in the conventional group (P<0.05). The minimum dose received by 95% of the target volume [(59.45±0.85) Gy] and the percentage of the target volume receiving at least 100% of the prescription dose [(95.82±2.65)%] in the study group were higher than those in the conventional group [(58.90±1.20) Gy and (93.65±3.85)%]. The homogeneity index and conformity index in the study group were 1.07±0.03 and 1.15±0.05, respectively, which were lower than 1.12±0.05 and 1.23±0.08 in the conventional group (P<0.05). No significant differences were observed between the two groups in the volume of the lung receiving 5 Gy [(28.11±5.52)% vs. (28.85±6.24)%], the volume of the lung receiving 20 Gy [(12.84±3.56)% vs. (13.45±3.90)%], mean lung dose [(8.65±2.11) Gy vs. (8.95±2.34) Gy], maximum spinal cord dose [(18.54±3.62) Gy vs. (19.13±4.25) Gy], or mean heart dose[(14.85±4.22) Gy vs. (16.27±4.83) Gy](P>0.05). The incidence rates of radiation pneumonitis, radiation esophagitis, and skin reactions in the study group were 12.20%, 7.32%, and 4.88%, respectively, which were not significantly different from 17.07%, 9.76%, and 7.32% in the conventional group (P>0.05). Conclusion The 4D-CBCT can reduce setup errors, improve target dose accuracy and conformity in lung cancer patients undergoing SBRT, and minimize radiation exposure to normal tissues, making it worthy of clinical promotion.

ObjectiveTreadmill exercise intervention was evaluated for its effects on addictive behavior, learning and memory, and hippocampal neuroinflammation in methamphetamine (MA)-addicted mice, and transcriptomic screening was performed to identify candidate molecules involved in exercise-mediated attenuation of MA-related neuronal injury. MethodsTwo-month-old male C57BL/6 mice were randomly assigned to four groups: control (C), exercise control (CE), methamphetamine (M), and methamphetamine plus exercise (ME). Mice in the M and ME groups received intraperitoneal injections of MA (1 mg/kg) once daily for 7 consecutive days to establish the addiction model, whereas mice in the C and CE groups received equal volumes of saline. Subsequently, mice in the CE and ME groups underwent treadmill exercise at 12 m/min for 60 min/d for 2 weeks. Conditioned place preference (CPP), the Y-maze, and the Morris water maze (MWM) were used to assess addictive behavior, spatial recognition memory, and spatial learning and memory, respectively. Hippocampal neuronal ultrastructure was examined by transmission electron microscopy (TEM), and microglia-related responses were evaluated by immunofluorescence staining for ionized calcium-binding adapter molecule 1 (Iba-1) in the hippocampal CA1 region. Previously generated and publicly available RNA-seq data from brain tissue of the C, M, and ME groups were reanalyzed, with three biological samples per group. Differentially expressed genes (DEGs) were re-screened using the criteria of P<0.05 and fold change>1.5 or <0.67, followed by gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses. NLR family CARD domain containing 5 (Nlrc5) was further validated by reverse transcription-quantitative polymerase chain reaction (RT-qPCR), and Western blot was used to determine the protein expression of NLRC5, nuclear factor kappa B (NF‑κB), interleukin-1β (IL-1β), postsynaptic density-95 (PSD-95), and synaptophysin. ResultsTreadmill exercise significantly attenuated MA-induced conditioned place preference and improved learning and memory performance in both the Y-maze and MWM tests. Exercise increased exploration time and distance in the novel arm of the Y-maze, shortened escape latency, and increased the number of platform crossings in the MWM. Average swimming speed during the probe trial did not differ significantly among groups, suggesting that the MWM differences were not attributable to obvious differences in swimming performance. TEM revealed that MA exposure induced mitochondrial swelling, disrupted cristae, reduced organelle abundance, and nuclear envelope abnormalities in hippocampal neurons, whereas these ultrastructural changes were alleviated after exercise. Immunofluorescence staining showed that MA increased Iba-1 fluorescence intensity in the hippocampal CA1 region, while treadmill exercise significantly reduced this change. Transcriptomic analysis identified 160 DEGs associated with MA exposure and 58 DEGs associated with exercise intervention, with 9 overlapping DEGs. KEGG enrichment analysis showed that MA-related DEGs were enriched in the NOD-like receptor signaling pathway. Among the overlapping DEGs, Nlrc5, which was downregulated after MA exposure and restored following exercise intervention, was selected as a candidate gene for further validation. RT-qPCR confirmed that treadmill exercise reversed the MA-induced decrease in Nlrc5 mRNA expression. Western blot analysis further showed that treadmill exercise increased NLRC5, PSD-95, and synaptophysin protein expression while reducing NF-κB and IL-1β expression. ConclusionTwo weeks of treadmill exercise attenuated MA-induced conditioned place preference and ameliorated learning and memory impairment, alleviated hippocampal neuroinflammation and neuronal ultrastructural damage, and restored the expression of synapse-related proteins. Transcriptomic screening combined with molecular validation demonstrated that exercise intervention was accompanied by restoration of NLRC5 expression, reduced NF‑κB and IL-1β expression, and increased PSD-95 and synaptophysin expression. These findings suggest that NLRC5 may represent a candidate molecule involved in exercise-mediated amelioration of MA-related neuronal injury. However, the present results mainly demonstrate coordinated changes in NLRC5 expression, inflammatory indicators, and cognitive outcomes rather than a direct causal relationship, and the specific role of NLRC5 requires further functional validation.

OBJECTIVES: To explore the measures to improve the follow-up rate of preterm infants after discharge, and to evaluate the effectiveness of these measures using quality improvement methodology. METHODS: The follow-up status of preterm infants discharged from March to May 2017 was used as the baseline before quality improvement, and a specific quality improvement goal for the follow-up rate was proposed. The Pareto chart was used to analyze the causes of follow-up failure, and a key driver diagram was constructed based on the links involved in improving follow-up rate. The causes of failure were analyzed to determine the key links and intervention measures for quality improvement, and the follow-up rate was monitored weekly using a control chart until the quality improvement goal was achieved. RESULTS: The follow-up rate of preterm infants after discharge was 57.92% (117/202) at baseline before quality improvement, and the quality improvement goal was set to increase the follow-up rate of preterm infants from baseline to more than 80% within 12 months. The Pareto chart analysis showed that the main causes of follow-up failure were deficiencies in follow-up file management and irregular follow-up times (33.70%, 31/92), insufficient follow-up education and poor communication (25.00%, 23/92), and the inability to meet the diverse needs of parents (18.48%, 17/92). Based on the key links for quality improvement and the main causes of follow-up failure, the following intervention measures were adopted: (1) strengthen follow-up publicity and education; (2) build a follow-up team; and (3) establish a follow-up platform and system. The control chart indicated that with the implementation of the above intervention measures, the weekly follow-up rate increased to 74.09% (306/413) in July 2017 and 83.09% (511/615) in December 2017, finally achieving the quality improvement goal. During the COVID-19 pandemic, the follow-up rate of preterm infants fluctuated between 23.54% (460/1 954) and 70.97% (1 931/2 721), and subsequently, it returned to pre-pandemic levels starting in February 2023. CONCLUSIONS The application of quality improvement methodology can help to formulate intervention measures based on the main causes of follow-up failure, thereby improving the follow-up rate of preterm infants after discharge. This quality improvement method is feasible and practical and thus holds promise for clinical application.
Humans ; Quality Improvement ; Infant, Premature ; Infant, Newborn ; Patient Discharge ; Follow-Up Studies ; Female ; Male

OBJECTIVES: To explore the application of the colloidal gold method and chemiluminescence method in detecting gonadotropin (Gn) in morning urine for assessing pubertal development status in children. METHODS: A total of 132 children diagnosed with central precocious puberty (CPP), early and fast puberty (EFP), and premature thelarche (PT) at Ruijin Hospital Affiliated to Shanghai Jiao Tong University School of Medicine from November 2021 to December 2022 were included, along with 685 healthy children who underwent routine health examinations at the hospital's pediatric health care department during the same period. All 132 patients underwent a gonadotropin-releasing hormone (GnRH) stimulation test. Both patients and healthy children had their urinary Gn levels measured using the colloidal gold method and chemiluminescence method, including levels of luteinizing hormone (LH) and follicle-stimulating hormone (FSH). The correlation between serum Gn and urinary Gn detected by the two methods, as well as the correlation between Tanner stages of healthy children and urinary Gn, was analyzed. RESULTS: Urine Gn levels detected by both the colloidal gold method and chemiluminescence method showed a positive correlation with serum LH baseline values, LH peak values, baseline LH/FSH ratios, and peak LH/FSH ratios (P<0.05). In healthy children, urinary LH levels detected by the chemiluminescence method gradually increased from Tanner stage Ⅰ to Ⅳ (P<0.05), while urinary FSH levels were lower in Tanner stage I than in stages Ⅱ, Ⅲ, and IV (P<0.05). Urinary LH levels detected by the colloidal gold method were lower in Tanner stage I compared to stages Ⅱ, Ⅲ, and IV, with the highest levels observed in Tanner stage Ⅳ (P<0.05). Additionally, urinary FSH levels in Tanner stage Ⅲ were higher than in stages Ⅰ and Ⅱ (P<0.05). The area under the receiver operating characteristic curve for evaluating Tanner stages I and II in healthy children using urinary LH and FSH levels by the chemiluminescence method and urinary LH levels by the colloidal gold method were 0.730, 0.699, and 0.783, respectively. CONCLUSIONS The colloidal gold method and chemiluminescence method for detecting Gn in morning urine show good correlation with serum Gn levels. As a non-invasive and convenient detection method, the colloidal gold method can serve as a useful tool for screening the onset of pubertal development in children.
Humans ; Child ; Male ; Female ; Gold Colloid ; Luminescent Measurements/methods* ; Gonadotropins/urine* ; Puberty ; Luteinizing Hormone/urine* ; Child, Preschool ; Adolescent ; Follicle Stimulating Hormone/urine*

Objective To investigate the neuroprotective effects and mechanisms of abscisic acid(ABA)in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine(MPTP)-induced Parkinson's disease(PD)mouse models.Methods Eight-week-old C57BL/6J mice were randomly divided into three groups,control group(Ctrl),MPTP group,and MPTP+ABA group,12 mice in each group.Except for the control group,mice in the other groups were intraperitoneally injected with MPTP 25 mg/kg daily for 8 consecutive days to establish a subacute PD model.The MPTP+ABA group received intraperitoneal injections of ABA 25 mg/kg daily for 11 consecutive days,starting 3 days prior to MPTP administration.Behavioral tests were performed 24 hours after the last administration.On day 3,the expression of tyrosine hydroxylase(TH)and glial fibrillary acidic protein(GFAP)in the substantia nigra pars compacta(SNc)and striatum(STR)was analyzed by Western blotting,and mRNA levels of inflammatory factors were measured by Real-time PCR.Immunofluorescent staining was used to detect the expression of TH,GFAP,and ionized calcium-binding adapter molecule 1(Iba1).Results Compared with the control group,MPTP-treated mice exhibited impaired motor function,a reduced number of TH-positive dopaminergic neurons in the SNc,down-regulated TH protein expression in both the SNc and striatum,up-regulated GFAP protein expression,increased numbers of GFAP-and Iba1-positive cells,and elevated levels of pro-inflammatory factors.In contrast,the MPTP+ABA group showed improved motor function,increased TH-positive neurons in the SNc,up-regulated TH protein expression,down-regulated GFAP protein expression,reduced numbers of GFAP-and Iba1-positive cells,and decreased pro-inflammatory factor levels compared to the MPTP group.Conclusion ABA ameliorates motor dysfunction in MPTP-induced PD model mice,reduces degeneration and death of dopaminergic neurons in the SNc,suppresses the proliferation and activation of astrocytes and microglia in the SNc and striatum,and alleviates neuroinflammation.These results suggest that ABA exerts neuroprotective effects in MPTP-induced PD model mice.