Background: Acute ischemic stroke (AIS) is a leading cause of death and disability worldwide. This study aimed to evaluate the efficacy and safety of anisodine hydrobromide (Ani) injection in the treatment of AIS.Methods: Randomized controlled trials (RCTs) based on Ani injection for the treatment of AIS were retrieved from both Chinese and English databases. The retrieval period was from the databases’ inception to May 2023. The Cochrane Collaboration Risk of Bias Tool was used to assess the methodological quality. The outcome indicators were analyzed using RevMan 5.3 software.Results: We included the findings of 11 RCTs encompassing 1,337 patients with AIS. Our meta-analysis revealed that Ani injection supplementation significantly reduced the National Institutes of Health Stroke Scale [MD = −1.53, 95%CI = (−1.94, −1.12), p < 0.00001], modified Rankin Scale [MD = −0.89, 95%CI = (−0.97, −0.81), p < 0.00001], and the relative time to peak [SMD = −0.81, 95%CI = (−1.08, −0.55), p < 0.00001] significantly. Additionally, Ani injection significantly increased the Barthel Index [MD = 10.65, 95%CI = (4.30, 17.00), p = 0.001], relative cerebral blood volume [SMD = 0.28, 95%CI = (0.02, 0.53), p = 0.03], and clinical efficacy [RR = 1.2, 95%CI = (1.08, 1.34), p = 0.001]. No statistically significant difference in the rate of adverse events was observed between the Ani injection supplemental group and the control group.Conclusion: Based on currently published evidence, Ani injection was found to be effective and safe in improving AIS outcome. Nevertheless, limitations of the included RCTs still exist, and thus, more multi-center, large-sample, high-quality RCTs are required to further verify the efficacy and safety of Ani injection in patients with AIS.Systematic Review Registration: [https://www.crd.york.ac.uk/prospero/display_record.php?ID=CRD42023427591], identifier [PROSPERO 2023 CRD42023427591].

The high global prevalence of anxiety disorders, coupled with the limitations of existing treatments, constitutes a severe public health challenge. Chronic stress, as a core environmental trigger, has garnered increasing attention for its mechanism of mediating brain-derived neurotrophic factor (BDNF) imbalance through neuroinflammation. BDNF dysregulation may contribute to anxiety disorders, particularly in subtypes with heightened neuroinflammation. The objective of this review is to comprehensively and methodically explores the potential role of the "M1-like microglia-A1-like astrocyte axis (M1-A1 axis)" in linking chronic stress to BDNF dysregulation in anxiety disorders, and to provide a theoretical basis for intervention strategies targeting this axis. By synthesizing recent relevant clinical and preclinical evidence, this review integrates evidence from molecular to systems levels, focusing on the activation mechanisms of neuroinflammation under chronic stress, the crosstalk between glial cells, and their regulatory network on BDNF. Chronic stress is associated with peripheral and central cascades through hypothalamic-pituitary-adrenal (HPA) axis activation and gut microbiota disruption. Within the central nervous system (CNS), stress induces microglial polarization toward the pro-inflammatory microglial subpopulations (hereinafter referred to as M1-like microglia). The signals released by M1-like microglia, such as Interleukin-1 alpha (IL-1α), Tumor Necrosis Factor-alpha (TNF-α), and Complement Component 1q (C1q) (ITC), drive astrocytes to transform into the neurotoxic astrocyte states (hereinafter referred to as A1-like astrocyte), forming the "M1-A1 axis". This axis contributes to BDNF dysregulation through the following mechanisms: (1) Release of pro-inflammatory cytokines inhibits BDNF transcription and translation; (2) Induction of astrocytic lactate metabolism disruption, which impairs neuronal energy supply and acidifies the microenvironment, further amplifying inflammation and affecting BDNF expression; (3) Compromise of the blood-brain barrier(BBB)enables peripheral immune cells to penetrate into the CNS, and these cells work in synergy with central glial cells to amplify inflammation. The reduction in BDNF and the imbalance in the ratio of its precursor to mature form ultimately lead to impaired synaptic plasticity in brain regions like the hippocampus (HIP) and amygdala, precipitating anxiety-like behaviors. Existing pharmacological interventions are inadequate to reverse this pathological process. The M1-A1 axis may serve as a key node linking chronic stress to BDNF dysregulation and anxiety disorders. Targeting the phenotypic transformation of glial cells, repairing the BBB, or modulating glial cell metabolism (e.g., lactate shuttle) may represent potential strategies requiring further validation. Future research should focus on the spatiotemporal dynamics of this axis and its clinical translation.

Tendinopathy is a common musculoskeletal disorder that markedly diminishes both physical performance and overall quality of life across age groups, imposing considerable socio‑economic burdens. Insulin‑like growth factor‑1 (IGF‑1) functions as a protective cytokine with significant involvement in multiple pathological conditions, including tendinopathy. The present review integrated current evidence on the role of IGF‑1 in tendon repair. IGF‑1 actively participates in every phase of tendon repair, making it a central driver of the injury response. When administered for tendon repair, IGF‑1 binds to IGF‑1R on target cell membranes, initiating sequential phosphorylation cascades that transmit signals from the membrane to the nucleus, while IGFBPs finely modulate this process. These intricate signaling pathways ultimately yield beneficial effects such as reduced inflammation, enhanced cell proliferation and migration and increased collagen synthesis, thereby promoting restoration of tendon structure and integrity. IGF‑1 has emerged as one of the most promising growth factors in tendon regenerative strategies. Nevertheless, clarification of critical parameters such as administration dosage and timing remains necessary to optimize its therapeutic value and to fully delineate its contribution to tendon repair.

Objective: This study aims to evaluate the efficacy of acupuncture as an adjunct to lifestyle interventions on weight loss in simple obesity. Methods: Potentially eligible studies that assessed anthropometric outcomes as well as glucose and lipid metabolism following acupuncture combined with lifestyle interventions in simple obesity patients were searched from eight databases from inception to October 2023. All analyses were performed using the Review Manager software v5.4 and Stata software v17.0. Results: Herein, 25 randomized controlled trials (RCTs) involving 2018 patients were included. Generally, acupuncture combined with lifestyle interventions outperformed lifestyle interventions alone in terms of body weight (MD = − 4.73, 95% CI [− 6.32, − 3.13], p < 0.00001), body mass index (BMI) (MD = − 2.11, 95% CI [− 2.75, − 1.48], p < 0.00001), waist circumference (WC) (MD = − 4.96, 95% CI [− 6.89, − 3.03], p < 0.00001), body fat percentage (BF %) (MD = − 2.61, 95% CI [− 4,51, − 0.71], p = 0.007), fasting plasma glucose (FPG) (SMD = − 0.66, 95% CI [− 1.02, − 0.31], p = 0.0002), fasting serum insulin (FINS) (SMD = − 1.12, 95% CI [− 1.44, − 0.81], p < 0.00001), homeostasis model assessment-insulin resistance (HOMA-IR) (MD = − 1.22, 95% CI [− 1.50, − 0.94], p < 0.00001), total cholesterol (TC) (SMD = − 1.14, 95% CI [− 1.83, − 0.45], p = 0.001), triglyceride (TG) (SMD = − 1.31, 95% CI [− 2.07, − 0.56], p = 0.0006), and low-density lipoprotein cholesterol (LDL-C) (SMD = − 1.81, 95% CI [− 3.11, − 0.51], p = 0.006). Subgroup analysis based on three subgroup variables (types of acupuncture and lifestyle interventions as well as treatment durations) could partially explain the heterogeneity of the results. Conclusion: Acupuncture demonstrated an enhancing effect on the benefits of lifestyle interventions for weight loss in patients with simple obesity, including reducing body weight and improving glucose and lipid metabolism. This finding suggests its potential value as a complementary therapy alongside lifestyle interventions in a clinical setting. However, further validation with rigorously designed and high-quality RCTs is still needed in the future.

Background Obesity is a major public health issue in China and around the world. While acupuncture is often used in clinical practice, there is a lack of conclusive evidence for its weight-loss effect. Thus we will conduct a parallel, randomised, sham-controlled trial to evaluate the efficacy and safety of acupuncture for treating obesity. Methods and analysis A total of 160 eligible participants with obesity will be randomly assigned to the verum acupuncture group or sham acupuncture group at a ratio of 1:1. All participants will be treated three times a week for a duration of 12 weeks, and followed up for another 16 weeks. The primary outcome is the percentage change in body weight from baseline to Week 12. The secondary outcomes include body mass index (BMI), waist circumference (WC), body fat percentage (BF%), blood pressure, fasting blood glucose, insulin, glycosylated haemoglobin A1c, blood lipids, and physical functioning score on the Short Form 36 Health Survey. Other secondary outcomes including psychological and social functions will also be evaluated using the body image scale, psychological function scale, and social function scale of the BODY-Q, Rosenberg Self-Esteem Scale, Patient Health Questionnaire-9, and Dutch Eating Behaviour Questionnaire . BMI, WC, BF% and blood pressure will be evaluated at Week 0, 4, 8, 12 and 28. Other secondary outcomes will be measured at Week 0, 12 and 28, respectively. Adverse events will be recorded in detail during the trial. Ethics and dissemination Ethical approval of this trial was granted by the Ethics Committee of Chengdu Sport University (2023–102). Written informed consent will be obtained from study participants before enrolment. The findings will be disseminated through peer-reviewed journals. Trial registration number Chinese Clinical Trial Registry (ChiCTR2200062092).

Background: Poststroke dysphagia impairs patients' quality of life and survival. Motor imagery (MI) is increasingly used as a rehabilitation adjunct, but its efficacy requires validation. This study aims to evaluate MI's effectiveness in treating poststroke dysphagia. Methods: An extensive literature search was conducted across eight English and Chinese electronic databases (from inception to April 2025) to identify randomized controlled trials (RCTs) comparing the effects of MI combined with conventional therapy (experimental group) versus conventional therapy alone (control group) on poststroke dysphagia. The methodological rigor was assessed using the Cochrane Collaboration Risk of Bias Tool. Data analysis of the outcome measures was conducted using RevMan 5.3 software, with bootstrapped analysis to test the accuracy of primary outcomes. Results: Pooled analysis of 13 RCTs involving 1053 patients with poststroke dysphagia demonstrated that, compared to the control group, the MI supplementation group showed significantly lower water swallowing test scores (MD: −0.64, 95% CI: −0.76, −0.51, p < 0.00001) and standardized swallowing assessment scores (MD: −2.26, 95% CI: −2.94, −1.57, p < 0.00001) and higher swallowing quality of life scores (MD: 22.03, 95% CI: 7.25, 36.81, p = 0.003). Bootstrapping analysis substantiated the precision of these results. Furthermore, the meta‐analysis revealed that add‐on MI therapy significantly reduced the incidence of aspiration pneumonia (RR: 0.25, 95% CI: 0.12, 0.53, p = 0.0003) and increased clinical efficacy (RR: 1.23, 95% CI: 1.08, 1.39, p = 0.001). However, no significant effects were observed on aspiration incidence, malnutrition, or nasogastric tube removal rates. Conclusion: Our findings support that MI therapy can be implemented as an add‐on approach for poststroke dysphagia. More high‐quality RCTs from multicenters are needed to provide more reliable evidence and explore the optimal treatment protocol.