Luteolin, a natural flavonoid compound, has demonstrated anti-inflammatory, antioxidant, and broad anti-tumor properties. Recent studies suggest that its anti-tumor effects are linked to enhanced CTL function—including proliferation, survival, and cytotoxicity-via inhibition of the YAP/Wnt signaling pathway in tumor cells. Consequently, luteolin has potential as an adjuvant in combination therapies with adoptive immunotherapy. This study first assessed luteolin’s tumor-inhibitory effects in vitro and in vivo using cytotoxicity assays, Transwell invasion tests, wound healing assays, and analyses of post-treatment tumor growth and survival time. Additionally, we explored whether luteolin combined with a DC/tumor fusion vaccine could synergistically enhance overall antitumor efficacy by boosting activation, proliferation, cytokines secretion, and cytotoxicity of effector T cells. Our findings indicate that luteolin, as a standalone agent, can inhibit the proliferation and invasion of colon and lung cancer cells both in vitro and in vivo to a certain extent. When combined with activated CTLs, it upregulated the expression of CD25 and CD69 in effector cells and resulted in higher levels of IL-2, TNF-α, and IFN-γ secretion in vitro. In vivo, this combination significantly curtailed subcutaneous tumor growth and extended the mean survival time of tumor-bearing mice (HCT116, A549), outperforming luteolin monotherapy. Furthermore, the efficacy of this combination therapy may be attributable to enhanced apoptosis in tumor cells, reduced proliferation, and decreased YAP expression. The combination of luteolin and DC/tumor fusion vaccine-activated CTLs presents a novel approach for cancer treatment. As an adjuvant, luteolin downregulates YAP expression in tumor cells, enhancing CTL proliferation, cytotoxicity, and survival, thus improving tumor recognition and selective targeting. This strategy is promising for safe and effective tumor treatment.

Appropriate formation of blood vessels is critical for tendon-bone healing during tendon injury, as excessive angiogenesis would exacerbate scar formation and lead to chronic pain and dysfunction. The mechanism to regulate inflammatory angiogenesis during tendon-bone healing remains to be elucidated. Here, we utilized lipopolysaccharide (LPS) to induce tenocyte inflammation and applied the conditioned medium from inflammatory tenocytes to treat rat aortic vascular endothelial cells (RAOECs). The results that indicated LPS treatment significantly induced the mRNA and protein upregulation of NLRP3, tumor necrosis factor α, IL-1β, and vascular endothelial growth factor A (VEGFA), as well as the secretion of VEGFA. Furthermore, the conditioned medium stimulated RAOEC angiogenesis. Celastrol, a quinone-methylated triterpenoid from Tripterygium wilfordii , has been reported to treat osteoarthritis. Here, celastrol could suppress LPS-induced upregulation of NLRP3 and IL-1β, and the secretion of VEGFA. Celastrol treatment also suppressed the conditioned medium-induced angiogenesis in RAOEC. Moreover, we established a rotator cuff tear rat model to stimulate tendon injury. Celastrol administration at the lesion significantly promoted tendon healing and functional recovery in injured mice by regulating NLRP3 and VEGFA levels. Taken together, these data suggest that the inflammation-induced tenocyte injury leads to angiogenesis, and that celastrol administration could suppress the inflammatory tenocyte-induced angiogenesis to promote tendon-bone healing via the NLRP3 pathway.

Cranial sutures play critical roles in load distribution and neuroprotection, with their biomechanical performance intimately linked to morphological complexity. The purpose of this study was to investigate the effect of different morphologies of cranial sutures on their biomechanical behavior. Based on the different morphologies of the cranial sutures, six groups of finite element models (closed, straight, sine wave, tight sinusoidal wave, layered sinusoidal wave, and layered sinusoidal wave + sutural bone) of the bone–suture–bone composite structures that ranged from simple to complex were constructed. Each model was subjected to 50 kPa impact and 98 N bilateral tensile loads to evaluate von Mises stress and total deformation variations across all groups under combined loading conditions. Key findings reveal that morphological complexity directly governs stress dynamics and mechanical adaptation; layered sinusoidal configurations delayed peak stress by 19–36% and generated elevated von Mises stresses compared to closed sutures, with stress concentrations correlating with interfacial roughness. Under impact, sutures exhibited localized energy dissipation ( 0.05), underscoring their dual roles in localized energy absorption and global strain redistribution. Craniosacral therapy relevant forces produced sub-micron deformations far below pathological thresholds (≥1 mm), which implies the biomechanical safety of recommended therapeutic force. Staggered suture–bone in open sutures (31.93% closure rate) enhances shear resistance, whereas closed sutures prioritize rigidity. The findings provide mechanistic explanations for suture pathological vulnerability and clinical intervention limitations, offering a quantitative foundation for future research on cranial biomechanics and therapeutic innovation.