Ethnopharmacological relevance: Moxibustion, a traditional Chinese healing method, uses mugwort (Artemisia argyi H.Lév. & Vaniot) to apply heat to specific points, treating conditions like "Bi Zheng", which is akin to rheumatoid arthritis (RA). According to traditional theory, its therapeutic actions are attributed to warming the meridians and regulating the flow of Qi and blood.
Aim of the study: To quantitatively evaluate the therapeutic efficacy of moxibustion and to map its anti-arthritic mechanisms in animal models of RA.
Materials and methods: The protocol was registered with PROSPERO (CRD42024503829) and reported according to PRISMA 2020. Eight databases were searched through 28 July 2025 for randomized controlled animal studies comparing moxibustion with the control in RA models. The primary outcome was arthritis severity, assessed by the arthritis index, paw volume, and histopathological score. Secondary endpoints included serum or tissue levels of pro-inflammatory cytokines (IL-1β, TNF-α, IL-6), immunomodulatory cytokines (IL-10, IL-4), and key signaling proteins (NF-κB, NLRP3, TLR4, MyD88). The SYRCLE tool was used to assess the risk of bias.
Results: Seventy-three studies were included. Meta-analysis showed that moxibustion significantly reduced arthritis severity (arthritis index: SMD -3.72, 95% CI -4.25 to -3.20; paw volume: SMD -4.59, 95% CI -5.54 to -3.63; histopathological score: SMD -2.24, 95% CI -2.80 to -1.67). Moxibustion also lowered the levels of pro-inflammatory cytokines: IL-1β (SMD -3.52, 95% CI -4.19 to -2.86), IL-6 (SMD -3.17, -4.17 to -2.16), and TNF-α (SMD -3.38, -3.97 to -2.79) and suppressed key signaling pathways, including NF-κB (SMD -2.29, 95% CI -3.20 to -1.37), NLRP3 (SMD -1.74, 95% CI -2.49 to -0.99), TLR4 (SMD -6.72, 95% CI -12.54 to -0.90), and MyD88 (SMD -9.16, 95% CI -15.28 to -3.04).
Conclusion: This meta-analysis suggests that moxibustion alleviates arthritis severity and histopathological damage in RA animal models, potentially through modulating inflammatory networks and inhibiting key pathways such as NF-κB and NLRP3. These findings provide preclinical evidence supporting the rationale for future clinical investigation of moxibustion as a potential adjunct therapy for RA.
Ethnopharmacological relevance: Buyang Huanwu Decoction (BYHWD), a traditional Chinese medicine (TCM) formulation renowned for its properties in replenishing qi and promoting blood circulation, corresponds closely with the pathophysiological framework of "qi deficiency and blood stasis" observed in vascular cognitive impairment (VCI). Consequently, there is a critical need to validate its therapeutic efficacy and elucidate the pharmacological mechanisms underlying its use in VCI treatment.
Aim of the study: This investigation aimed to systematically assess the therapeutic effects of BYHWD on VCI and to clarify the molecular mechanisms involved.
Materials and methods: The bioactive constituents of BYHWD were characterized via UHPLC-MS/MS. A rat model of VCI was established through two-vessel occlusion (2VO). Experimental groups received oral gavage administration of BYHWD at dosages of 6.4, 12.8, and 25.6 g/kg daily for four weeks, with Ginaton (14.4 mg/kg) employed as a positive control. Cerebral blood flow was assessed using laser speckle imaging. Cognitive performance was evaluated through the Morris water maze (MWM) test. Histopathological changes in brain tissue were assessed by Nissl and LFB staining. To investigate pharmacological mechanisms, ELISA, immunohistochemistry, Western blot, and immunofluorescence analyses were conducted. Additionally, in vitro studies utilized an oxygen-glucose deprivation (OGD) model in BV2 microglial cells, with intervention by the p53 activator Nutlin-3 to further validate mechanistic pathways.
Results: Administration of BYHWD markedly enhanced learning and memory functions, increased cerebral perfusion, and mitigated neuronal loss and white matter injury in 2VO rats. Furthermore, BYHWD significantly inhibited microglial activation and decreased the secretion of pro-inflammatory cytokines. Mechanistic investigations demonstrated that BYHWD downregulated the expression of proteins associated with the p53/cGAS/STING signaling pathway in the 2VO model. In vitro, activation of p53 by Nutlin-3 negated the neuroprotective effects of BYHWD on OGD-induced BV2 cells and concurrently intensified inflammatory responses.
Conclusion: BYHWD ameliorates cognitive deficits and neuropathological damage in 2VO rats primarily through suppression of the p53/cGAS/STING signaling cascade and attenuation of neuroinflammation. This study provides strong pharmacological evidence for the early prevention and clinical treatment of VCI.
Ethnopharmacological relevance: Xiehuang San (XHS) is a classical Chinese herbal formula with analgesic, anti-inflammatory, gastrointestinal-regulating and hypoglycemic effects, but its specific regulatory mechanisms remain incompletely understood.
Aim of the study: To evaluate the effects of XHS on T2DM, with a particular focus on its metabolic and molecular mechanisms.
Materials and methods: C57BL/6J mice were induced with T2DM using a high-fat diet combined with streptozotocin. T2DM mice were treated with XHS for 4 weeks to assess blood glucose control and metabolism. Serum metabolomics were analyzed by UPLC-Q-TOF/MS. Network pharmacology integrated drug-metabolite-disease associations. Molecular docking and dynamics simulations assessed the binding of active compounds to targets. RT-qPCR and Western blot were used to determine gene and protein expression levels. An in vitro model was established to validate the effects of XHS on T2DM.
Results: XHS significantly improved T2DM pathology. Compared to the diabetic Mod group, XHS reduced fasting blood glucose levels, enhances glucose tolerance and improves insulin resistance and sensitivity. 24 dysregulated metabolites were corrected after treatment. Network pharmacology predicted that the key target of XHS in T2DM treatment is the CLCF1-STAT3 pathway. Licochalcone B, Wogonin and Apigenin are predicted to exhibit strong binding affinity for this pathway. Both in vitro and in vivo models, XHS effectively inhibits the activation of the CLCF1-STAT3 signalling pathway and protects insulin signalling.
Conclusion: This study combines metabolomics and network pharmacology to reveal that XHS exerts anti-diabetic effects by remodeling glycerophospholipid metabolism and inhibiting CLCF1-STAT3 signaling. These findings support the application of XHS in the treatment of T2DM.

