Objective. This study aimed to explore the mechanism of Modified Danggui Sini Decoction in the treatment of knee osteoarthritis via a combination of network pharmacology and molecular docking. Methods. The main chemical components and corresponding targets of Modified Danggui Sini Decoction were searched and screened in TCMSP database. The disease targets of knee osteoarthritis were summarized in GeneCards, OMIM, PharmGkb, TTD, and DrugBank databases. The visual interactive network of drugs-active components-disease targets was drawn by Cytoscape 3.8.1 software. The protein-protein interaction network was constructed by STRING database. Then, GO function and KEGG pathway enrichment were analyzed by Bioconductor/R, and the pathway of the highest degree of correlation with knee osteoarthritis was selected for specific analysis. Finally, molecular docking was used to screen and verify core genes by AutoDockTools software. Results. Seventy-one main components of Modified Danggui Sini Decoction and 116 potential therapeutic targets of knee osteoarthritis were selected. The KEGG pathway and the GO function enrichment analysis showed that the targets of Modified Danggui Sini Decoction in the treatment of knee osteoarthritis were mainly concentrated on PI3K-Akt signaling pathway, TNF signaling pathway, IL-17 signaling pathway, apoptosis signaling pathway, Toll-like receptor signaling pathway, Th17 cell differentiation signaling pathway, HIF-1 signaling pathway, and NF-κB signaling pathway. It mainly involved inflammatory reaction, regulation of apoptotic signaling pathway, cellular response to regulation of inflammatory response, cellular response to oxidative stress, and other biological processes. The molecular docking results showed that ESR1-wogonin, MAPK1-quercetin, RELA-wogonin, RELA-baicalein, TP53-baicalein, TP53-quercetin, and RELA-quercetin have strong docking activities. Conclusion. Modified Danggui Sini Decoction has the hierarchical network characteristics of multicomponent, multitarget, multifunction, and multipathway in the treatment of knee osteoarthritis. It mainly regulates the proliferation and apoptosis of chondrocytes by regulating the PI3K-Akt signaling pathway and establishes cross-talk with many downstream inflammatory-related pathways to reduce the overall inflammatory response. Meanwhile, HIF-1 expression was used to ensure the normal function and metabolism of knee joint under hypoxia condition, and the above processes play a key role in the treatment of knee osteoarthritis.

Objectives: To compare the short-term outcomes of unilateral biportal endoscopic lumbar interbody fusion (BLIF) and uniportal endoscopic lumbar interbody fusion (ULIF). Methods: Sixty patients diagnosed with L4/5 spinal stenosis who underwent BLIF and ULIF were included (30 in each group). Clinical evaluation was performed preoperatively and postoperatively in the 1st week, 1st month, and 1st year. Factors such as the visual analogue score (VAS), Oswestry Disability Index (ODI), operative time, surgical complications, and radiological outcomes (fusion rate, screw loosening, and cage subsidence) were compared between the two groups. Results: All patients showed improved mean VAS and ODI at all three postoperative follow-ups, and no statistically significant differences were detected between the BLIF and ULIF groups. The mean operative time in the BLIF group was shorter than that in the ULIF group. Nerve root injury occurred in two patients in the BLIF group, while leakage of cerebrospinal fluid occurred in one patient in the ULIF group. All adverse events were treated adequately prior to discharge. The fusion rates with definite and probable grades were significantly higher in the BLIF group than that in the ULIF group. One case of cage subsidence with no screw loosening occurred in each group. Conclusion: Both BLIF and ULIF are safe and effective surgical techniques. Compared with ULIF, BLIF has the advantages of shorter operative time and a higher fusion rate. Other merits of BLIF include a wider surgical field, greater maneuverability of instruments, visibility during cage implantation, and transverse orientation of the cage.

Background: Intervertebral disc degeneration (IVDD), a prevalent spinal disorder, is closely associated with abnormal mechanical stress. The nucleus pulposus (NP), annulus fibrosus (AF), and cartilaginous endplate (CEP) collectively respond to mechanical loading. The mechanosensitive Piezo 1 ion channel senses mechanical stress changes and converts the mechanical signals into chemical signals, and serves a pivotal role in IVDD pathogenesis. Objective: This review summarizes the regional effects of Piezo 1 on mechanical stress‐induced IVDD and evaluates therapeutic strategies targeting Piezo 1 to maintain disc homeostasis. Methods: A systematic search of preclinical and clinical studies was conducted to delineate Piezo 1's phenotypic impacts, mechanistic pathways, and therapeutic potential in NP, AF, and CEP. Results: In the NP, activated Piezo 1 contributes to cellular senescence, apoptosis, ferroptosis, extracellular matrix (ECM) degradation and synthesis, oxidative stress, inflammation, and catabolic processes. Key regulatory targets involved include NLRP3, MAPK, p38, MMPs, ADAMTS, p65, Periostin, p53, p16, GRP78, CHOP, Cyt‐c, and Drp1. In the CEP, Piezo 1 mediates inflammation‐induced CEP degeneration through the CaMKII/Drp1 pathway and further participates in cellular senescence and apoptosis by activating Bax and caspase‐3 while inhibiting Bcl‐2. In the AF, Piezo 1 mediates apoptosis through the Ca ²⁺ /Calpain2/Caspase‐3 signaling pathway. Therapeutically, targeting Piezo 1 has demonstrated significant preclinical potential, including attenuating pathological alterations via pharmacological inhibition, selectively suppressing degenerative cascades through genetic/RNAi approaches, and modulating channel activity by nutritionally regulating membrane lipids. Conclusion: Piezo 1 serves as a critical mechanotransducer in IVDD, exhibiting region‐specific effects on disc pathophysiology. Targeting Piezo 1 signaling not only offers mechanistic insights but also holds translational potential as a therapeutic strategy to improve IVDD, meriting further exploration in preclinical and clinical contexts.