Objective. Here, we aimed to explore the main mechanism of Yaobishu (YBS) in lumbar disc herniation (LDH). Methods and Results. Eighteen compounds that might act on LDH were obtained through a combination of network pharmacology prediction and identification by high‐performance liquid chromatography‐mass spectrometry. The key compounds were palmitic acid and trans‐4‐hydroxy‐3‐methoxycinnamate (cinnamate). KEGG analysis demonstrated that palmitic acid target genes mainly regulate the PPAR signaling pathway, Ras signaling pathway, and fatty acid metabolism. Cinnamate target genes were primarily involved in chemical carcinogenesis‐receptor activation, lipid and atherosclerosis, the HIF‐1 signaling pathway, and nitrogen metabolism. The rat LDH model was constructed using autologous nucleus pulposus tissue implantation. Differential expression gene (DEGs) related to metabolism (CDKN1A and UHRF1), inflammation (S100A9 and SOCS3), autophagy (DCN and LEPR), and apoptosis (CTSW and BCL2A1) in dorsal root ganglion (DRG) tissues of the control and LDH groups was evaluated by RNA‐Seq. TNF‐α stimulated DRG neuronal cells were used to establish an in vitro LDH model. YBS, palmitic acid, and cinnamate reduced the expression of substance P, CGRP, S100A9, CTSW, and cleaved caspase‐3, while enhancing the expression of CDKN1A, UHRF1, PCNA, Ki67, SOCS3, DCN, LEPR, and BCL2A1, as well as telomerase activity. Pearson’s correlation analysis confirmed that DCN was positively correlated with BCL2A1, indicating that autophagy might be negatively correlated with apoptosis in LDH. YBS, palmitic acid, and cinnamate reduced the Siegal neurological score and serum IL‐1β and IL‐18 levels, while increasing changes in the hind paw mechanical withdrawal threshold. The RNA‐Seq results further showed that YBS downregulated S100A9 and CTSW expression, while upregulating SOCS3, CDKN1A, UHRF1, DCN, LEPR, and BCL2A1 expression. Conclusion. YBS and its compounds, palmitic acid, and cinnamate, attenuated LDH by regulating the inflammatory, metabolic, autophagic, and apoptotic pathways. Our results might improve the theoretical and experimental basis for clinical applications of LDH disease treatment.

Background: This study aimed to investigate the feasibility and precision of using a 3D-printed template for femoral tunnel placement in guiding the optimal positioning of the Internal anatomical stop and Low tension maintenance (IDEAL) bone tunnel during single-bundle anterior cruciate ligament (ACL) reconstruction. Methods: A retrospective analysis was conducted on 40 patients who underwent arthroscopic single-bundle ACL reconstruction at our hospital between April 2021 and November 2021. In the direct vision group, the IDEAL bone tunnel was positioned using radiofrequency localization directly visualized at the stump. In the 3D-printed positioning group, preoperative CT scans and Digital Imaging and Communications in Medicine (DICOM) data were employed. Following the Quadrant method by Bernard, the femoral tunnel’s depth was set at 25% and its height at 29%. Postoperative plain CT scans enabled the reconstruction of 3D models for both groups. The accuracy of femoral tunnel placement was then compared. Results: The central locations of the bone tunnels in the direct vision group were at a mean depth of 25.74 ± 1.84% and a height of 29.22 ± 2.97%. In the 3D printing localization group, these values were 25.39 ± 2.98% for depth and 28.89 ± 2.50% for height, respectively. No significant differences were found in tunnel positioning between the groups. Both groups demonstrated statistically significant improvements in International Knee Documentation Committee Subjective Knee Form (IKDC) and Lysholm scores postoperatively, with no significant differences observed 12 months post-surgery. Conclusion: The findings of this study suggest that 3D printing-assisted arthroscopic IDEAL point femoral tunnel positioning and conventional arthroscopic positioning are feasible and effective for ACL reconstruction. Using 3D printing technology to design femoral anchor points in ACL reconstruction allows for the customization of anterior fork reconstruction and precise bone tunnel positioning, supporting the goal of individualized and accurate reconstruction.

Background: Osteoid osteoma (OO) is a benign lesion characterized by an increased fibrous component in the bone marrow, presence of bone-like structures within the medullary cavity, and a surrounding sclerotic bone rim. Reports on OO located in the posterior proximal tibia are rare. Case summary: Herein, we report the case of an 18-year-old male, admitted for the evaluation of right knee pain. The right knee pain had started 6 months prior without any apparent cause, which was notably severe at night, affecting sleep, and was exacerbated while climbing stairs or bearing weight. The patient also experienced pain on flexion. Three-dimensional computed tomography and magnetic resonance imaging revealed a nodular lesion beneath the cortical bone of the posterior medial plateau of the right tibia and an abnormal signal focus on the posterior lateral aspect of the right tibial plateau associated with extensive bone marrow edema. A small amount of fluid was present in the right knee joint capsule. The patient subsequently underwent arthroscopic excision of the OO. Postoperatively, there was significant relief of pain, and the knee range of motion returned to normal. Conclusion: Although OO in the posterior proximal tibia is a rare occurrence, it can be effectively excised through minimally invasive arthroscopic visualization.

Background: This study aimed to evaluate the effect of Shenbing Decoction III (SBD III) and its key Apigenin on peritoneal dialysis (PD)–induced peritoneal fibrosis and explore the underlying mechanisms. Methods: Liquid chromatography–mass spectrometry confirmed the presence of Apigenin in SBD III. Human peritoneal mesothelial cells (HMrSV5) were stimulated with PD solution (PDS) to induce fibrosis, and treatment with SBD III and Apigenin was administered. Results: PDS decreased cell viability and increased the migration and invasion capabilities of HMrSV5 cells. It also reduced E‐cadherin expression, while increasing the expression of α‐SMA, fibronectin, collagen I, and TGF‐β1. SBD III and Apigenin effectively counteracted these effects. Additionally, SBD III and Apigenin inhibited the PDS‐induced upregulation and phosphorylation of transforming growth factor‐β‐activated kinase 1 (TAK1), p38, and nuclear factor‐κB (NF‐κB), similar to the effects of 5z‐7‐oxozeaenol. Chronic kidney disease (CKD) was induced in mice by 5/6 nephrectomy, followed by PDS treatment. The therapeutic effects of SBD III and Apigenin were evaluated. CKD mice exhibited reduced body weight and kidney weight indices, along with elevated blood urea nitrogen, urinary creatinine, and urinary protein levels. Fibrosis was observed in the kidneys and peritoneum. PDS treatment also significantly alleviated these effects. Notably, therapeutic effects were further augmented when SBD III and Apigenin were administered. Conclusion: SBD III and Apigenin ameliorated PDS‐induced peritoneal fibrosis by inhibiting epithelial–mesenchymal transition via the TAK1/p38MAPK/NF‐κB pathway, indicating promising pharmaceutical candidates for CKD.