Table of Content

20 May 2026, Volume 21 Issue 5

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Challenges and Breakthroughs in Basic and Clinical Research of Brain Cytoprotective Agents for Acute Ischemic Stroke in China

HE Dandan, LI Jian, WANG Chunjuan, LI Shuya

2026, 21(5):  517-524.  DOI: 10.3969/j.issn.1673-5765.2026.05.001

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Brain cytoprotection therapy serves as an important adjunct to reperfusion therapy for acute ischemic stroke, yet it has long faced challenges in clinical translation. In recent years, research teams in China, guided by clinical needs, have made notable progress in this field. This article systematically reviews the progress of basic and clinical research on brain cytoprotection. Firstly, it elaborates on the core therapeutic targets, and the guiding role of the stroke treatment academic industry roundtable (STAIR) and the stroke preclinical assessment network (SPAN). Secondly, it highlights the breakthrough achievements in clinical research in China, including the research data and clinical application value of representative drugs such as edaravone dexborneol, minocycline, and loberamisal. Finally, it analyzes the current challenges faced in this field and looks forward to future development strategies, aiming to provide a reference for promoting the innovation and clinical translation of brain cytoprotection therapy for acute ischemic stroke. 

Brain cytoprotection

WANG Chunjuan, LI Shuya

2026, 21(5):  525-525. 

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Research Progress of Edaravone Dexborneol in Brain Cytoprotection for Acute Ischemic Stroke

CHENG Xiyue, ZHAO Jingyan, WANG Chunjuan

2026, 21(5):  526-532.  DOI: 10.3969/j.issn.1673-5765.2026.05.002

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Brain cytoprotection has long been a highly regarded yet challenging research direction in the field of acute ischemic stroke treatment. In the era of reperfusion therapy, with continuous advances in intravenous thrombolysis and endovascular therapy, the therapeutic goals of ischemic stroke have extended beyond large vessel recanalization to meaningful tissue-level benefit. Practical clinical demands such as alleviating ischemia-reperfusion injury, stabilizing the neurovascular unit, and expanding salvageable brain tissue have brought brain cytoprotection research back to the clinical forefront. Edaravone dexborneol, a compound preparation of edaravone and dexborneol, exerts multi-target effects including scavenging oxygen free radicals and inhibiting the inflammatory cascade, and has become one of the most evidence-based agents for brain cytoprotection in ischemic stroke in China. In recent years, relevant Chinese guidelines have gradually recommended it as an available brain cytoprotective agent, whereas international guidelines have not yet made routine recommendations for the clinical use of brain cytoprotective agents but have acknowledged renewed research opportunities in the context of reperfusion therapy for ischemic stroke. This review summarises the research background of brain cytoprotective agents, the positioning of brain cytoprotective strategies in international guidelines, and the pharmacological basis and current evidence for edaravone dexborneol. It summarises the design features, main findings, and clinical implications of key randomized controlled trials and real‑world cohort studies in this field. Additionally, based on ongoing registered studies, it discusses future prospects of edaravone dexborneol in pre‑hospital ultra-early intervention for ischemic stroke, combination treatment with reperfusion therapy, and application in precisely stratified or special populations, aiming to provide a reference for research and clinical practice in brain cytoprotection for ischemic stroke.

Research Progress on the Anti-Neuroinflammatory Effects and Brain Cytoprotection of Minocycline in Acute Ischemic Stroke: From Mechanisms to Clinical Evidence

YANG Qianqian, ZHANG Meiyang, LU Yao, ZHOU Dongyang, WANG Zhengyilei, Shan Shuyi, LIU Chenhui, WANG Yilong, GUAN Ling

2026, 21(5):  533-542.  DOI: 10.3969/j.issn.1673-5765.2026.05.003

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Acute ischemic stroke is a major cause of disability and mortality. Despite continuous improvements in reperfusion therapy and secondary prevention strategies, some patients still experience varying degrees of neurological dysfunction after stroke. Neuroinflammation is involved in the onset, progression, and recovery of acute ischemic stroke and has emerged as an important therapeutic target for brain cytoprotection in recent years. Minocycline, a classic tetracycline antibiotic, exerts multiple anti-neuroinflammatory effects beyond its antimicrobial activity, including modulation of microglial activation, suppression of inflammatory cytokine release, inhibition of matrix metalloproteinase activity, and attenuation of peripheral immune-cell infiltration into the central nervous system. Preclinical studies have shown that minocycline reduces infarct volume and attenuates neurological deficits in various animal models of cerebral ischemia. Preliminary clinical studies have suggested that minocycline is generally safe and well tolerated in patients with acute ischemic stroke, although evidence for its efficacy remains inconsistent. More recently, a large-scale randomized controlled trial—EMPHASIS (efficacy and safety of minocycline in patients with moderate to severe acute ischemic stroke) trial showed that short-course minocycline treatment improves 90-day functional outcomes in patients with acute ischemic stroke, without significantly increasing safety risks. Future studies should focus on identifying the target populations most likely to benefit, optimizing the therapeutic time window, dose, and treatment duration, evaluating combination strategies with reperfusion therapy, and developing novel drug-delivery approaches as well as imaging and biomarker-based evaluation systems, thereby clarifying the clinical role and translational value of minocycline in acute ischemic stroke.

Research Progress of PSD-95-Targeted Brain Cytoprotective Agents in Acute Ischemic Stroke Based on STAIR Principles

HE Dandan, LI Shuya

2026, 21(5):  543-552.  DOI: 10.3969/j.issn.1673-5765.2026.05.004

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Brain cytoprotection serves as an important complementary strategy to reperfusion therapy in acute ischemic stroke. To overcome the challenges in the clinical translation of brain cytoprotective agents, the stroke therapy academic industry roundtable (STAIR) was established in 1999 in the United States with the aim of developing a systematic framework to guide drug research and development in stroke. Since its inception, STAIR has continuously refined strategy-specific recommendations for brain cytoprotective agents, providing structured guidance for preclinical experimentation and clinical research. Postsynaptic density protein-95 (PSD-95) has emerged as a key target in the brain cytoprotection field owing to its well-defined mechanisms and high target specificity. Under the guidance of STAIR principles, PSD-95-based brain cytoprotective agents have undergone a series of preclinical and clinical studies. This paper systematically reviews the key points of STAIR principles for the development of brain cytoprotective agents and summarizes the status of preclinical and clinical studies of PSD-95-targeting agents under STAIR guidance. It also outlines the research progress on the brain cytoprotective effects of these agents in acute ischemic stroke, thereby providing a reference for the clinical translation of brain cytoprotective agents.

Research and Perspectives on Brain Cytoprotective Agents Delivery via the Skull Bone Marrow Pathway

CHEN Zhuangzhuang, XU Liu, WANG Nanxing, ZHANG Meiyang, JI Ruobing, YANG Mo, LIU Xiangrong, WANG Yilong

2026, 21(5):  553-560.  DOI: 10.3969/j.issn.1673-5765.2026.05.005

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The blood-brain barrier (BBB) prevents peripheral pathogenic microorganisms from entering the brain, yet simultaneously blocks macromolecular and polypeptide drugs from reaching the central nervous system. Commonly used brain cytoprotective agents, such as free radical scavengers, calcium antagonists, and anti-inflammatory modulators, have demonstrated clear brain cytoprotective effects in preclinical stroke studies, yet their clinical translation has often been disappointing owing to insufficient BBB penetration. The novel drug delivery route via the skull bone marrow-cerebral dura mater-glymphatic system for intracerebral drug delivery holds promise for bypassing the BBB, offering a novel strategy for efficient brain delivery of brain cytoprotective agents. In recent years, multiple preclinical and clinical studies have progressively demonstrated that skull bone marrow administration has good feasibility, safety, and efficacy in the treatment of stroke, traumatic brain injury, and other conditions. Moreover, given the important immune surveillance function of the skull bone marrow, this route holds promise for combining multimodal delivery strategies, such as nano‑drug delivery systems and immune cell‑based drug delivery, to achieve precise and efficient intracerebral drug delivery. This review systematically summarizes recent advances in the delivery of brain cytoprotective agents via the skull bone marrow route, with a focus on the novel delivery mode of drug transport via this approach. It highlights the unique advantages of this route in bypassing the BBB, rapidly targeting cerebral lesions, and enhancing local drug concentration. 

Stem Cell Derivatives: Multi-Target Brain Cytoprotective Biological Products Beyond the Limitations of Live Cell Therapy

CHEN Weiqi, JIANG Lingling, HE Di, CHEN Yanbo, ZHANG Ruinan, LIU Xinru, LIU Wenzhu, GUO Lei, WANG Ling, WANG Yilong

2026, 21(5):  561-569.  DOI: 10.3969/j.issn.1673-5765.2026.05.006

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For neurological deficits caused by nervous system diseases, the clinical efficacy of conventional single-target brain cytoprotective agents is limited. Although stem cell therapy holds the potential for multi-target brain cytoprotection, its clinical translation is hindered by challenges such as a low in vivo survival rate, potential to induce intracerebral inflammation, and risks of tumorigenicity. Stem cell derivatives are acellular biological products that, by enriching the paracrine active components (including stem cell secretome and extracellular vesicles), retain the pleiotropic brain cytoprotective functions of stem cells while significantly circumventing the safety and heterogeneity risks associated with live cell therapy. This article systematically reviews the mechanisms of action of stem cell derivatives and the current status of related basic and clinical research. Regarding the mechanisms of action, these derivatives can modulate the inflammatory and immune microenvironment, promote angiogenesis and neuroregeneration, and mediate intercellular substance transport, thereby establishing a new paradigm for systemic neural repair and regeneration in brain cytoprotection. Currently, stem cell derivatives have shown preliminary brain cytoprotective potential and favorable safety in research on diseases such as amyotrophic lateral sclerosis, multiple system atrophy, and ischemic stroke. Notably, in the context of increasingly stringent biomedical research and translational regulatory frameworks, as an “off-the-shelf” strategy with greater potential for standardization and industrialization, stem cell derivatives are expected to overcome the current druggability limitations in brain cytoprotection therapy and usher the field into an era of noncellular biological products.

Research Progress on the Relationship between the Apolipoprotein E Gene and Brain Injury after Ischemic Stroke 

CHANG-CAO Wenjing, XU Shuhong, LI Jian, LI Shuya

2026, 21(5):  570-576.  DOI: 10.3969/j.issn.1673-5765.2026.05.007

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The apolipoprotein E (APOE) gene and its encoded protein ApoE represent promising targets worthy of attention in studies of brain cytoprotection for ischemic stroke. The ApoE protein is involved in pathophysiological processes closely linked to tissue injury and repair after cerebral ischemia, including cerebral lipid transport, glia-neuron support, regulation of inflammatory responses, and maintenance of the neurovascular unit and the blood-brain barrier homeostasis. Preclinical studies have demonstrated that endogenous ApoE deficiency in Apoe gene knockout mice aggravates experimental ischemic brain injury. Humanized APOE2, APOE3, and APOE4 knock-in mouse models further indicate that mice expressing the human ApoE4 protein isoform may develop more severe cerebral infarction and neurological deficits. In addition, interventional studies have verified that ApoE mimetic peptides CN-105 and COG1410 exert effects of regulating inflammatory responses, stabilizing the blood-brain barrier, and improving neurological function in animal models of ischemic stroke. Clinical studies have yielded inconsistent findings regarding the associations between APOE genotype and ischemic stroke risk, age at onset, short-term functional outcomes, and post-stroke cognitive outcomes. Current evidence is insufficient to support APOE genotype as an independent predictive biomarker or a well-established therapeutic target for ischemic stroke. This review summarizes the potential mechanisms, preclinical and clinical research evidence regarding the APOE gene and ApoE protein-related pathways in post-ischemic brain injury, as well as therapeutic strategies targeting ApoE-associated pathways.

A Study on the Correlation between Apolipoprotein E Gene Polymorphism and Cognitive Function Changes after Stroke

LI Wenyi, JIANG Jiwei, REN Qiwei, WANG Linlin, ZHAO Min, XU Jun

2026, 21(5):  577-584.  DOI: 10.3969/j.issn.1673-5765.2026.05.008

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Objective  To investigate the differences in clinical characteristics among various apolipoprotein E (APOE) genotypes in patients with acute ischemic stroke, and to explore the association between APOE gene polymorphism and changes in cognitive function after stroke. 
Methods  This study was based on a multicenter, prospective study (predictive, preventive and personalized project of vascular cognitive impairment in China). Patients with acute ischemic stroke admitted to six medical institutions in China from September 1, 2022 to August 31, 2023 were enrolled. Baseline data collected at enrollment included age, sex, years of education, BMI, medical history (hypertension, diabetes mellitus, heart disease, hyperlipidemia, stroke or TIA), smoking history, drinking history, medication history, NIHSS score, MoCA score, Hamilton depression scale (HAMD) score, Hamilton anxiety scale (HAMA) score, imaging data (whether critical site infarction, infarct size grade), TOAST classification, and APOE genotype. Patients were categorized into three groups based on their APOE genotypes: APOE ε3 homozygotes (ε3/ε3), APOE ε2 carriers (ε2/ε3, ε2/ε2), and APOE ε4 carriers (ε3/ε4, ε4/ε4). The patients were followed up 6 to 12 months after stroke onset. One-factor analysis of variance was performed to compare the above baseline clinical data among the three groups. Additionally, generalized linear mixed models were utilized to analyze the correlation between APOE genotypes and the longitudinal changes in MoCA scores after stroke. 
Results  A total of 202 patients with acute ischemic stroke were included at baseline, including 155 males and 47 females, with a mean age of (58.5±10.4) years. There were no statistically significant differences in baseline age, sex, years of education, BMI, medical history, smoking history, drinking history, medication history, NIHSS score, MoCA score, HAMD score, HAMA score, proportion of critical site infarction, infarct size grade, or TOAST classification among the three groups of patients with different APOE genotypes (all P>0.05). A total of 151 patients completed the follow-up, and the median follow-up period was 8.0 (7.0-10.0) months. After adjusting for sex, age, years of education, and center effect, it was found that compared with the APOE ε3 homozygotes, the APOE ε4 carriers showed a significant negative correlation with MoCA score at baseline (β=-1.682, P=0.029), and the interaction between follow-up period and APOE ε4 carrier status was also significantly negatively correlated with MoCA score (β=-0.322, P<0.001). 
Conclusions  The polymorphism of the APOE gene is related to the changes in cognitive function scores after stroke. Compared with the APOE ε3 homozygotes, APOE ε4 carriers exhibit lower cognitive function scores at stroke onset, and show a more rapid decline in cognitive function scores after stroke.




Value of Transesophageal Echocardiography in the Etiological Screening of Cardioembolic Stroke

ZHANG Huiqin, DU Lijuan, ZHANG Meng, LYU Yifei, HE Wen, ZHANG Wei

2026, 21(5):  585-592.  DOI: 10.3969/j.issn.1673-5765.2026.05.009

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Objective  To evaluate the value of transesophageal echocardiography (TEE) combined with contrast-enhanced TEE in the etiological screening of cardioembolic stroke.
Methods  This prospective study consecutively enrolled patients with clinically suspected cardioembolic stroke who were admitted to the Beijing Tiantan Hospital, Capital Medical University, between March 2023 and May 2025. All enrolled patients underwent routine transthoracic echocardiography (TTE) and TEE examinations. Among them, patients with atrial fibrillation underwent left heart contrast enhanced-TEE (LHCE-TEE), and patients with right-to-left shunt (RLS) indicated by TCD underwent agitated saline contrast enhanced-TEE (ASCE-TEE). The observed indicators included intracardiac and atrial appendage thrombi, the source and grade of RLS, prosthetic valve thrombus, and aortic arch plaque condition.
Results  A total of 256 patients with suspected cardioembolic stroke were enrolled, including 80 patients with atrial fibrillation, 150 patients with RLS, and 26 patients with other etiologies. Among the 80 patients with atrial fibrillation, 16 patients were diagnosed with left atrial appendage thrombi. The initial examination results showed that the number of left atrial appendage thrombi detected by TTE, TEE, and LHCE-TEE was 1, 8, and 16, respectively. LHCE-TEE was superior to TEE in detecting hypoechoic thrombi (9 cases vs. 1 case, P<0.01) and non-active thrombi (9 cases vs. 1 case, P<0.01). Among the 150 patients with RLS, ASCE-TEE detected more cases of patent foramen ovale (PFO) (125 cases) than TTE (15 cases) and TEE (65 cases) and was able to identify smaller PFOs, with statistically significant differences (both P<0.01). ASCE-TEE detected 125 cases of PFO-RLS, 55 cases of pulmonary vein-related RLS (P-RLS), and 45 cases with both PFO-RLS and P-RLS. Semiquantitative analysis of RLS showed that the proportion of patients with grade 3 shunt volumes was higher than that with grade 1 and 2 shunt volumes in both PFO-RLS and P-RLS (both P<0.05). Additionally, TTE demonstrated a higher detection rate for left ventricular thrombi than TEE (12 cases vs. 8 cases), while TEE outperformed TTE in detecting prosthetic valve thrombi (6 cases vs. 1 case) and unstable aortic arch and/or descending aortic plaques (25 cases vs. 10 cases).
Conclusions  LHCE-TEE can clearly delineate the borders of hypoechoic left atrial appendage thrombi and significantly improve the detection rate of hypoechoic and non-active thrombi. ASCE-TEE accurately identifies PFO and effectively differentiates the source and grade of RLS. TEE has important clinical value in detecting prosthetic valve thrombi, unstable aortic arch and/or descending aortic plaques.


Research on Electroencephalography Microstates in Acute Post-Stroke Accompanying Cognitive Impairment

LIU Yanxiang, LI Ying, CHANG Jingling

2026, 21(5):  593-602.  DOI: 10.3969/j.issn.1673-5765.2026.05.010

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Objective To explore the underlying neuroelectrophysiological mechanisms in patients with acute post-stroke accompanying cognitive impairment (APSACI) and to identify the associated specific electroencephalography microstates.
Methods Patients with acute ischemic stroke who were admitted to Tongzhou Campus of Dongzhimen Hospital, Beijing University of Chinese Medicine from October 1, 2024 to June 30, 2025 were consecutively enrolled. According to the MoCA score, patients were divided into two groups: those with a score≥26 were assigned to the acute post-stroke non-cognitive impairment (APSNCI) group, and those with a score<26 were assigned to the APSACI group. Resting-state electroencephalography data were collected to analyze temporal parameters of four typical microstates: duration, occurrence, coverage, and transition probability. Pearson correlation analysis was employed to investigate the associations between these temporal parameters and MoCA scores, and ROC curve analysis was adopted to verify the results with significant correlations.
Results A total of 31 patients with acute ischemic stroke were enrolled in this study, including 14 cases in the APSNCI group (11 males and 3 females) and 17 cases in the APSACI group (13 males and 4 females). There were significant differences between the two groups in the duration of microstate C and D, as well as the occurrence and coverage of microstate D (all P<0.05). After Bonferroni correction, the between-group difference in the duration of microstate D  emained statistically significant (P=0.002). Significant differences were observed in the transition probabilities of microstate A→D, B→C, B→D, and D→B between the two groups (all P<0.05). The duration, occurrence, and coverage of microstate D, as well as the transition probability of microstate D→B showed significant positive correlations with MoCA scores (all P<0.05). The AUC values of duration-D and coverage-D were relatively high, while the AUC value of microstate D→B was relatively low.
Conclusions Patients with APSACI exhibit specific large-scale brain network dysfunctions, particularly involving microstate C/D-related networks, as well as abnormalities in dynamic coordination. Parameters associated with microstate D show significant correlations with the severity of cognitive impairment. Electroencephalography microstate features could serve as potential biomarkers reflecting the neuroelectrophysiological mechanisms of APSACI and assessing its severity of cognitive impairment. These findings are helpful for understanding the pathological basis of APSACI and developing auxiliary diagnostic tools in the future.




Association of Allostatic Load Score with Imaging Progression of Cerebral Small Vessel Disease in Individuals with COVID-19: A Community-Based Cohort Study

WANG Luyan, ZHOU Mengyuan, GUO Yijia, PAN Yuesong, WANG Yilong

2026, 21(5):  603-611.  DOI: 10.3969/j.issn.1673-5765.2026.05.011

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Objective  To explore the association between baseline allostatic load score (ALS) and imaging progression of cerebral small vessel disease (CSVD) in individuals with coronavirus disease 2019 (COVID‑19).
Methods  This study was conducted based on the polyvascular evaluation for cognitive impairment and vascular events (PRECISE) cohort, with community residents in Lishui, Zhejiang as research participants. Baseline assessment of the cohort was conducted from May 2017 to September 2019, with centralized follow‑up every two years, and a special survey on COVID-19 was completed between May and June 2024. Participants with a history of COVID‑19 who completed the second follow‑up [median follow-up duration of 4.7 (4.4-4.8) years] and underwent cranial MRI were enrolled in the present study. ALS was calculated from ten baseline clinical indicators: systolic and diastolic blood pressure, resting pulse, BMI, waist-to-hip ratio, TC, HDL-C, glycated hemoglobin, serum albumin, and high‑sensitivity C‑reactive protein. According to the total ALS score, participants were classified into low‑ALS (0-1 points), moderate‑ALS (2-3 points), and high‑ALS (≥4 points) groups. CSVD imaging markers were assessed based on cranial MRI, including lacunes, cerebral microbleeds, enlarged perivascular spaces (EPVS), and white matter hyperintensities. By comparing cranial MRI findings at baseline and follow-up, progression was determined for each individual CSVD imaging marker, for overall CSVD imaging progression (defined as progression of any of the above markers), and for total CSVD burden progression according to the Wardlaw criteria and the modified Rothwell criteria. Associations between ALS groups and CSVD progression were estimated using generalized linear models.
Results  A total of 1663 participants were included in this study, including 555 in the low‑ALS group, 697 in the moderate‑ALS group, and 411 in the high‑ALS group. After adjustment for covariates, compared with the low‑ALS group, the high‑ALS group had a 90% higher risk of incident lacunes (RR 1.90, 95%CI 1.24-2.90, P=0.003). Each 1‑point increment in ALS was associated with an 18% higher risk of incident lacunes (RR 1.18, 95%CI 1.09-1.29, P<0.001). In terms of EPVS grading progression, each 1‑point increase in ALS was associated with a 5% higher risk of EPVS grading progression in the basal ganglia (RR 1.05, 95%CI 1.01-1.10, P=0.030). Compared with the low-ALS group, both the moderate‑ALS group (RR 1.14, 95%CI 1.03-1.25, P=0.010) and the high‑ALS group (RR 1.13, 95%CI 1.01-1.26, P=0.028) showed a higher risk of overall CSVD imaging progression. Each 1‑point increase in ALS was associated with a 3% higher risk (RR 1.03, 95%CI 1.01-1.05, P=0.007). According to the Wardlaw criteria, both the moderate‑ALS group (RR 1.18, 95%CI 1.04-1.35, P=0.012) and the high‑ALS group (RR 1.22, 95%CI 1.05-1.40, P=0.008) also exhibited a higher risk of total CSVD burden progression than the low-ALS group. Each 1‑point ALS increment was associated with a 4% higher risk (RR 1.04, 95%CI 1.01-1.07, P=0.007).
Conclusions  Among individuals with COVID‑19, higher ALS levels were associated with increased risks of imaging progression and total burden progression of CSVD, primarily manifested as an increased risk of incident lacunes. These findings suggest that long‑term physiological stress may contribute to COVID‑19-related cerebral microvascular injury.


Mechanistic Study on Rat miR-664-1-5p Targeting the PTEN/Akt/Nrf2 Pathway to Attenuate Oxidative Damage in PC12 Cells Induced by Hypoxia/Reoxygenation

PENG Yan, FENG Wenzhan, LIU Qin, TANG Hongmei, LIU Yi, GAO Li, WANG Sijia, BAI Xue

2026, 21(5):  612-623.  DOI: 10.3969/j.issn.1673-5765.2026.05.012

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Objective  To investigate the effect and mechanism of rat micro ribonucleic acid (miRNA) -664-1-5p (hereinafter referred to as miR-664-1-5p) on injury induced by hypoxia/reoxygenation in adrenal pheochromocytoma (PC12) cells. 
Methods  PC12 cells were cultured in vitro and divided into the control group, the hypoxia/reoxygenation group, the hypoxia/reoxygenation+negative control (NC) mimic group, and the hypoxia/reoxygenation+miR-664-1-5p mimic group. The expression level of miR-664-1-5p was detected by real-time fluorogenic quantitative PCR. Cell viability was measured using cell counting kit-8. Apoptosis rate was determined by flow cytometry. The levels of superoxide dismutase (SOD) and malondialdehyde (MDA) were detected by enzyme linked immunosorbent assay. The protein relative expression levels of phosphatase and tensin homolog (PTEN), protein kinase B (Akt), phosphorylated Akt (p-Akt), and nuclear factor-erythroid 2-related factor 2 (Nrf2) were detected by Western blotting. The targeted binding between miR-664-1-5p and PTEN was verified by dual-luciferase reporter assay. The regulatory relationship between miR-664-1-5p and PTEN was confirmed by PTEN overexpression. 
Results  Compared with the control group, the expression of miR-664-1-5p (P<0.01), cell viability (P<0.05), SOD level (P<0.05), and protein expression of Nrf2 (P<0.05) and p-Akt (P<0.01) were significantly decreased in the hypoxia/reoxygenation group, while MDA level (P<0.05), apoptosis rate (P<0.05), and PTEN protein expression (P<0.01) were significantly increased. Overexpression of miR-664-1-5p reversed these changes. Dual-luciferase reporter assay confirmed that miR-664-1-5p directly targeted PTEN and inhibited luciferase activity. Furthermore, transfection with the plasmid cytomegalovirus DNA-PTEN overexpression plasmid reduced SOD level, Nrf2 and p-Akt protein expression, and elevated MDA level and apoptosis rate in PC12 cells (all P<0.01). 
Conclusions  Rat miR-664-1-5p alleviates oxidative stress injury and apoptosis induced by hypoxia/reoxygenation in PC12 cells by targeting PTEN and activating the Akt/Nrf2 signaling pathway, which provides a novel potential target for the prevention and treatment of cerebral ischemia reperfusion injury.


Chinese Expert Consensus on Respiratory Function Reconstruction in Patients with Neurological Critical Illnesses

The Respiratory Critical Care Group of the Critical Care Rehabilitation Professional Committee of the Chinese Rehabilitation Medical Association, The Intensive Rehabilitation Group of the Rehabilitation Physicians’ Branch of the Chinese Medical Doctor Association, Beijing Rehabilitation Medical Association-Critical Care Rehabilitation Professional Committee

2026, 21(5):  624-649.  DOI: 10.3969/j.issn.1673-5765.2026.05.013

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Patients with neurological critical illness often suffer from severe respiratory dysfunction, which significantly affects their prognosis and survival rates. The consensus working group was jointly established by the Respiratory Critical Care Group of the Critical Care Rehabilitation Professional Committee of the Chinese Rehabilitation Medical Association, the Intensive Rehabilitation Group of the Rehabilitation Physicians’ Branch of the Chinese Medical Doctor Association, and Beijing Rehabilitation Medical Association-Critical Care Rehabilitation Professional Committee. Based on practical clinical problems, the working group used the grading of recommendations assessment, development and evaluation (GRADE) system to evaluate the quality of evidence (graded into four levels: high, moderate, low, and very low) and the strength of recommendations (strong recommendation and weak recommendation). A consensus was reached through the modified Delphi method, and finally, the Chinese Expert Consensus on Respiratory Function Reconstruction in Patients with Neurological Critical Illnesses was formulated. This consensus systematically elaborates on the pathophysiological mechanisms, multimodal assessment methods, core treatment technologies, and complication management strategies for respiratory dysfunction in patients with neurological critical illness, aiming to standardize the process of respiratory function reconstruction, promote multidisciplinary collaboration, and improve the quality of life and rehabilitation outcomes.

A Case Report of Cerebellar Infarction Manifested as Acute Isolated Positional Headache

ZHANG Xiaoliang, LIU Yan

2026, 21(5):  650-656.  DOI: 10.3969/j.issn.1673-5765.2026.05.014

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The clinical manifestations of cerebellar infarction are complex and varied. In addition to typical signs of cerebellar ataxia, patients may present with atypical symptoms without definite neurological localization signs, which easily lead to misdiagnosis or missed diagnosis. This article reports a 37-year-old male patient with acute isolated positional headache (occurring in an upright position and relieved when lying down) as the only symptom, without typical signs of cerebellar ataxia. The initial diagnosis was intracranial hypotension headache. Cranial MRI-DWI revealed an acute infarction in the inferior left cerebellar hemisphere, accompanied by mild cerebellar tonsillar descent of 2 mm, and normal cerebrospinal fluid pressure. Combined with the patient’s cerebrovascular risk factors such as hypertension, long-term smoking, and sleep apnea syndrome, the diagnosis was revised to acute cerebellar infarction. After treatment with antiplatelet therapy, dehydration, and circulation improvement, the patient’s positional headache was rapidly alleviated. This case suggests that in young patients with risk factors for cerebrovascular disease who present with sudden positional headache without typical neurological localization signs, the possibility of cerebellar infarction should be considered. Early cranial MRI, especially the DWI sequence, is crucial for accurate diagnosis. This case provides valuable clinical reference for recognizing atypical presentations of cerebellar infarction and emphasizes the importance of multimodal imaging in the differential diagnosis of positional headache.