Research hotspots and trends on acupuncture treatment for headache: a bibliometric analysis from 2003 to 2023.

Background: While acupuncture treatment has gained extensive usage in addressing headaches, there remains a notable gap in the literature analysis for this field. Therefore, this study aims to conduct a literature review using Citespace, VOSviewer, and Bibliometrix, aiming to examine the current status, strengths, and potential future directions in the utilization of acupuncture for headache treatment. Methods: Relevant literature on acupuncture treatment for headaches between 2003 and 2023 was retrieved from the Web of Science (WoS) core database. Utilizing CiteSpace 6.1.R6, VOSviewer 1.6.18, and Bibliometrix 4.1.4, we conducted bibliometric analyses across various categories, including countries/regions, institutions, authors, journals, references, and keywords. Results: A total of 808 research reports were included. China and the United States have significantly contributed to this field. Chengdu University of Chinese Medicine holds the record for the highest number of published papers. Liu Lu has the highest publication output, while Linde K has the highest citation rate. MEDICINE leads in publication frequency, while CEPHALALGIA holds the highest citation rate. The Long-term Effect of Acupuncture for Migraine Prophylaxis a Randomized Clinical Trial is the most cited reference. Migraine was the most researched type. Filiform needle acupuncture was the most widely used stimulation method. The safety and efficacy of acupuncture have received significant attention. Modern mechanism research shows that depression, brain functional connectivity, and neuroimaging technology have become research hotspots in the acupuncture treatment of headaches. Conclusion: Acupuncture treatment for headaches has established a stable trend with a promising developmental trajectory. Research in this field mainly focuses on different acupuncture prevention and treatment for various types of headaches, the safety and efficacy of acupuncture, etc. Research on the mechanism of action mainly focuses on interpreting bidirectional and holistic regulation between pain and emotion by acupuncture and the regulation of brain function connection and neuroimaging technology by acupuncture. Future research should expand on the advantages and indications of acupuncture treatment for different headaches and their modern mechanisms.

Multiple intra-articular injections of autologous stromal vascular fractions for the treatment of multicompartmental osteoarthritis in both the tibiofemoral and patellofemoral joint: a single-blind randomized controlled study.

BACKGROUND: Multicompartmental osteoarthritis (MOA) in both tibiofemoral and patellofemoral joints is a more commonly occurring, but neglected, clinical condition, and we examined the short-term safety and efficacy of autologous stromal vascular fractions (SVFs) for MOA using a single-blind, prospective, randomized, placebo-controlled trial. METHODS: Seventy MOA patients were recruited and randomly assigned to the SVF group and hyaluronic acid (HA) group (control group). The scores of visual analog scale, the Western Ontario and McMaster University Osteoarthritis Index, and the Samsung Medical Center patellofemoral scoring system were assessed and compared between the two groups 3, 6 and 12 months after treatment. RESULTS: The SVF group had significantly better visual analog scale scores than the HA group at 6 and 12 months after treatment and had better Western Ontario and McMaster University Osteoarthritis Index scores than the HA group only at 6 months after treatment. For Samsung Medical Center patellofemoral scoring system of the patellofemoral joint, the SVF group had significantly better scores than the control group at all postoperative time points. The proportion of patients whose visual analog scale and Western Ontario and McMaster University Osteoarthritis Index scores were above the minimal clinically important improvement was higher in the SVF group than in the HA group in the majority of assessments. The improvement of bone marrow by SVF treatment was significantly better than that of the HA group as observed by pre- and postoperative Magnetic resonance imaging (MRI). CONCLUSIONS: Multiple intra-articular injection of autologous SVF reduces pain and improves function in the short term in patients with early or midstage MOA. However, there was heterogeneity in the improvement of overall knee and isolated patellofemoral joint after treatment.

Protective effects of Shensuitongzhi formula on intervertebral disc degeneration via downregulation of NF-κB signaling pathway and inflammatory response.

Low back pain (LBP) is a common orthopedic disease over the world. Lumbar intervertebral disc degeneration (IDD) is regarded as an important cause of LBP. Shensuitongzhi formula (SSTZF) is a drug used in clinical treatment for orthopedic diseases. It has been found that SSTZF can have a good treatment for IDD. But the exact mechanism has not been clarified. The results showed that SSTZF protects against LSI-induced degeneration of cartilage endplates and intervertebral discs. Meanwhile, SSTZF treatment dramatically reduces the expression of inflammatory factor as well as the expression of catabolism protein and upregulates the expression of anabolism protein in LSI-induced mice. In addition, SSTZF delayed the progression of LSI-induced IDD via downregulation the level of NF-κB signaling key gene RELA and phosphorylation of key protein P65 in endplate chondrocytes. Our study has illustrated the treatment as well as the latent mechanism of SSTZF in IDD.

Warm acupuncture therapy alleviates neuronal apoptosis after spinal cord injury via inhibition of the ERK signaling pathway.

PURPOSE: Warm acupuncture (WA) therapy has been applied to treat spinal cord injury (SCI), but the underlying mechanism is unclear. The current study attempted to explore the WA therapy on neuronal apoptosis of SCI and the relationship with the extracellular signal-regulated kinase (ERK) signaling pathway. METHODS: The rat SCI models were established by the impact method. SCI rat models were subjected to WA treatment at Dazhui (GV14) and Jiaji points (T10), Yaoyangguan (GV3), Zusanli (ST36), and Ciliao (BL32). The rat SCI models were established by the impact method. WA and U0126 treatments were performed on the SCI rats. Motor function and neuronal apoptosis were detected. The relative mRNA of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and interleukin-6 (IL-6), the phosphorylation level of ERK 1/2 and levels of B-cell lymphoma-2 (Bcl-2), BCL2-Associated X (Bax), and caspase-3 in spinal cord tissue were tested. RESULTS: After WA treatment, the Basso, Beattie & Bresnahan locomotor rating scale (BBB scale) of SCI rats in the WA treatment was significantly raised from 7 to 14 days after SCI. WA and U0126 treatment significantly diminished apoptotic cells and preserved the neurons in the injured spinal cord. WA and U0126 treatment alleviated the production of inflammatory cytokines in the spinal cord. The distinct increase of p-ERK 1/2 induced by SCI was reversed in WA and U0126 treatment groups. WA and U0126 treatment augmented the level of Bcl-2 and reversed the elevated cleaved caspase-3 protein level after SCI. CONCLUSION: Our study demonstrated that WA might be associated with the downregulation of the ERK signaling pathway. In summary, our findings indicated that WA promotes the recovery of SCI via the protection of nerve cells and the prevention of apoptosis. Meanwhile, the anti-apoptotic effect of WA might be associated with the downregulation of the ERK signaling pathway, which could be one of the mechanisms of WA in the treatment of SCI.

Glycyrrhizic acid alters the hyperoxidative stress-induced differentiation commitment of MSCs by activating the Wnt/ß-catenin pathway to prevent SONFH.

This study aimed to examine the in vivo and in vitro therapeutic effects of glycyrrhizic acid (GA) on steroid-induced osteonecrosis of the femoral head (SONFH), which is caused by the overuse of glucocorticoids (GCs). Clinically, we identified elevated oxidative stress (OS) levels and an imbalance in osteolipogenic homeostasis in SONFH patients compared to femoral neck fracture (FNF) patients. In vivo, we established experimental SONFH in rats via lipopolysaccharides (LPSs) combined with methylprednisolone (MPS). We showed that GA and Wnt agonist-S8320 alleviated SONFH, as evidenced by the reduced microstructural and histopathological alterations in the subchondral bone of the femoral head and the decreased levels of OS in rat models. In vitro, GA reduced dexamethasone (Dex)-induced excessive NOX4 and OS levels by activating the Wnt/ß-catenin pathway, thereby promoting the osteogenic differentiation of mesenchymal stem cells (MSCs) and inhibiting lipogenic differentiation. In addition, GA regulated the expression levels of the key transcription factors downstream of this pathway, Runx2 and PPARγ, thus maintaining osteolipogenic homeostasis. In summary, we demonstrated for the first time that GA modulates the osteolipogenic differentiation commitment of MSCs induced by excessive OS through activating the Wnt/ß-catenin pathway, thereby ameliorating SONFH.

Elucidation of the Underlying Mechanism of Gujian Oral Liquid Acting on Osteoarthritis through Network Pharmacology, Molecular Docking, and Experiment.

Gujian oral liquid (GJ), a traditional herbal formula in China, has been widely used to treat patients with osteoarthritis (OA). Nevertheless, the active component and potential mechanism of GJ are not fully elucidated. Thus, we investigate the effect of GJ and explore its underlying mechanism on OA through network pharmacology and experimental validation. First, a total of 175 bioactive compounds were identified, and 134 overlapping targets were acquired after comparing the targets of the GJ with those of OA. 8 hub targets, including IL6 and AKT1, were obtained in PPI network analysis. Then, we built up GJ-target-OA network and protein-protein interaction (PPI) network, followed by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses. The results underlined inflammatory tumor necrosis factor (TNF) as a promising signaling pathway of GJ for OA treatment. Moreover, molecular docking also verified the top two active compounds had direct bindings with the top three target genes. Finally, we verified the effect of GJ on OA in vivo and in vitro. In vivo experiments validated that GJ not only significantly attenuated OA phenotypes including articular cartilage degeneration and subchondral bone sclerosis but also reduced the expressions of tumor necrosis factor-α (TNF-α) and p-p65 in articular chondrocytes. Besides, GJ serum also had a protective effect on chondrocytes against inflammation caused by TNF-α in vitro. Hence, our study predicted and verified that GJ could exert anti-inflammation and anticatabolism effects partially via regulating TNF-α/NF-kappa B (NF-κB) signaling.

Col9a2 gene deletion accelerates the degeneration of intervertebral discs.

As an essential component of the extracellular matrix (ECM) in cartilage, the α2 chain of type IX collagen (Col9a2), has been implicated in human intervertebral disc degeneration (IVDD). However, the precise role of the Col9a2 gene in the pathogenesis of IVDD has remained elusive. In the present study, the spines of Col9a2-deficient (Col9a2-/-) mice were systematically analyzed and compared with wild-type control mice using micro-CT (µCT), histomorphology, immunofluorescence, immunohistochemistry and reverse transcription-quantitative PCR (RT-qPCR). µCT analysis revealed that endplate (EP) osteochondral remodeling in the Col9a2-/- group was accompanied by a significant increase in EP porosity. Likewise, histopathological staining at 12 weeks revealed that the Col9a2-/- mice exhibited a marked early-stage IVDD phenotype, including EP sclerosis, calcification and annulus fibrosus rupture. The immunofluorescence results indicated that Col9a2 was extensively expressed in the IVDs, whereas it was barely detectable in Col9a2-/- mice. Immunohistochemical and RT-qPCR analyses demonstrated that the expression levels of Col2a1 and Aggrecan in the IVDs of Col9a2-/- mice were significantly decreased. In addition, the levels of Mmp13, ADAM metallopeptidase with thrombospondin type 1 motif 5, Col10a1 and Runx family transcription factor 2 were significantly elevated. These results suggested that deletion of the Col9a2 gene led to osteochondral remodeling of cartilage EP and suppressed ECM synthesis, accelerating matrix degradation and chondrocyte hypertrophy in the IVD tissue.

Acupuncture combined with moxibustion promote the recovery of spinal cord injury in correlation with Shh/Gli-1 signaling pathway.

Objective: Acupuncture combined with moxibustion (AM) therapy has been applied to treat spinal cord injury (SCI), but the underlying mechanism is unclear. The present study aimed to confirm the effect and mechanism of AM treatment on the recovery of SCI.Design: Male Sprague-Dawley rats were used to establish the SCI model by impact method. SCI rat models were subjected to AM treatment at Dazhui (GV14) and Jiaji points (T7-T12), Yaoyangguan (GV3), Zusanli (ST36) and Ciliao (BL32).Outcome measures: Motor function and cell apoptosis in rats after SCI. The mRNA and protein expression levels of Shh and Gli-1 were determined by real-time quantitative polymerase chain reaction, western blot and immunohistochemistry.Results: After AM treatment, the hindlimb motor function of SCI rats was significantly increased than the SCI group at 7, 9, 11, 14 days (P < 0.05). AM treatment 7 d and 14 d significantly preserved the nissl-stained positive neurons and significantly decreased number of apoptotic cells, compared to that of SCI 7 and 14 d groups (P < 0.05). AM treatment improved the mRNA protein levels of Shh and Gli-1 after 7 and 14 days treatment compared to the SCI group (P < 0.05).Conclusion: AM could improve the expression of Shh and Gli-1 in injured spinal cord of rats. That could be part of underlying mechanisms of AM treatment including recover motor function and preserve the neuron cells and alleviate the apoptosis of nerve cells in rats after SCI.

Osteoking Decelerates Cartilage Degeneration in DMM-Induced Osteoarthritic Mice Model Through TGF-ß/smad-dependent Manner.

Osteoarthritis (OA) is a common disease characterized by cartilage degeneration. In recent years much attention has been paid to Traditional Chinese Medicine (TCM) since its treatments have shown efficacy for ameliorating cartilage degradation with mild side effects. Osteoking is a TCM prescription that has long been used in OA treatment. However, the exact mechanism of Osteoking are not fully elucidated. In the current study, destabilization of the medial meniscus (DMM)-induced OA mice was introduced as a wild type animal model. After 8 weeks of administration of Osteoking, histomorphometry, OARSI scoring, gait analysis, micro-CT, and immunohistochemical staining for Col2, MMP-13, TGFßRII and pSmad-2 were conducted to evaluate the chondroprotective effects of Osteoking in vivo. Further in vitro experiments were then performed to detect the effect of Osteoking on chondrocytes. TGFßRIICol2ER transgenic mice were constructed and introduced in the current study to validate whether Osteoking exerts its anti-OA effects via the TGF-ß signaling pathway. Results demonstrated that in wild type DMM mice, Osteoking ameliorated OA-phenotype including cartilage degradation, subchondral bone sclerosis, and gait abnormality. Col2, TGFßRII, and pSmad-2 expressions were also found to be up-regulated after Osteoking treatment, while MMP-13 was down-regulated. In vitro, the mRNA expression of MMP-13 and ADAMTS5 decreased and the mRNA expression of Aggrecan, COL2, and TGFßRII were up-regulated after the treatment of Osteoking in IL-1ß treated chondrocytes. The additional treatment of SB505124 counteracted the positive impact of Osteoking on primary chondrocytes. In TGFßRIICol2ER mice, spontaneous OA-liked phenotype was observed and treatment of Osteoking failed to reverse the OA spontaneous progression. In conclusion, Osteoking ameliorates OA progression by decelerating cartilage degradation and alleviating subchondral bone sclerosis partly via the TGF-ß signaling pathway.

Valproic Acid: A Potential Therapeutic for Spinal Cord Injury.

The lack of an effective pharmaceutical agent for spinal cord injury (SCI) is a current problematic situation for clinicians, as the rate of motor vehicle accidents among young adults is on the rise. SCI contributes to the high disability rate. Presently, evidences detailing the precise pathological mechanisms in SCI are limited, compounding to the unavailability of an effective treatment method. Surgery, though not a complete curative method, is useful in managing some of the associated symptoms of secondary SCI. Autophagy and inflammation are contributive factors to both exacerbation and improvement of SCI. The mammalian target of rapamycin (mTOR) signaling pathway is a key player in the regulation of inflammatory response and autophagy. Valproic acid (VPA), a clinically used antiepileptic drug, has been suggested to improve neurological conditions, including SCI. This report reviewed the correlation between mTOR and autophagy, as well as autophagy's role and the therapeutic effects of VPA in SCI. VPA regulates autophagy by potentially inhibiting mTORC1, a complex of mTOR, while also hindering inflammatory response. Conclusively, an effective treatment for SCI could lie in the timely regulation of mTOR signaling pathway, and VPA could be the potential drug that improves SCI owing to its propensity to regulate the mTOR signaling pathway.

Efficacy and safety of massage in the treatment of post-stroke insomnia: A protocol for systematic review and meta-analysis.

BACKGROUND: : Post-stroke insomnia (PSI) is a serious problem which has significant adverse effects on the subsequent recovery of patients and the quality of their daily life. Massage is effective in improving the quality of sleep for stroke patients displaying no significant adverse reactions. Up to now, however, there are still no systematic studies conducted to provide compelling evidence for its effectiveness in treating PSI. Allowing for this, this project is purposed to make a thorough summary of the efficacy of massage therapy in treating PSI and the safety of this practice. METHODS: : Without considering the status of publication and language, a meticulous search will be conducted, covering the Web of Science, the Cochrane Library search, PubMed, EMBASE, Chinese biomedical literature database, Chongqing VIP Database for Chinese Technical Periodicals, China National Knowledge Infrastructure, and Wanfang. All randomized controlled trials of PSI will be retrieved. The deadline is set as October 23, 2020. The team will be comprised of 2 experienced researchers who will apply RevMan V.5.3 software to conduct literature selection, data collection, data analysis, and data synthesis, respectively. In addition, the Cochrane risk Assessment tool will be taken as the top choice to evaluate the quality of the trials involved in this study. RESULTS: : The effectiveness and safety of massage therapy intended for PSI will be subject to a systematic evaluation under this program. CONCLUSION: : It will be substantiated in this review whether massage therapy is a reliable intervention for PSI by examining the evidence collected.

Effectiveness and safety of massage in the treatment of restless legs syndrome: A protocol for systematic review and meta analysis.

BACKGROUND: Restless legs syndrome (RLS), known as a kind of neurological disease, is prevalent but easy to be ignored. Studies have demonstrated that massage therapy can effectively reduce the symptoms of patients with RLS and improve their quality of life. However, the efficacy of massage therapy for RLS is still controversial. Therefore, this protocol aims to evaluate the reliability of massage therapy in treating RLS in a thorough way. METHODS: We will search relevant randomized controlled trials from Chinese Biomedical Literature Database, Chongqing VIP, CNKI, Wanfang, Web of Science, Cochrane Library, PubMed, and EMBASE, when publication status and language are not considered and the time limit ends with September 6, 2020. Two experienced researchers will use RevMan V.5.3 software to perform the selection of literature, data collection, data analysis and synthesis separately. Besides, the quality of trials involved in this study will be measured with the Cochrane bias risk assessment tool. RESULTS: This protocol will be applied to carry out a systematic evaluation of the massage therapy purposed to treat RLS for its effectiveness and safety. CONCLUSION: The review will provide a credible evidence suggesting whether massage therapy is a reliable intervention for RLS. INPLASY REGISTRATION NUMBER: INPLASY202090038.

Amygdalin Promotes Fracture Healing through TGF-ß/Smad Signaling in Mesenchymal Stem Cells.

Chondrogenesis and subsequent osteogenesis of mesenchymal stem cells (MSCs) and angiogenesis at injured sites are crucial for bone fracture healing. Amygdalin, a cyanogenic glycoside compound derived from bitter apricot kernel, has been reported to inhibit IL-1ß-induced chondrocyte degeneration and to stimulate blood circulation, suggesting a promising role of amygdalin in fracture healing. In this study, tibial fractures in C57BL/6 mice were treated with amygdalin. Fracture calluses were then harvested and subjected to radiographic, histological, and biomechanical testing, as well as angiography and gene expression analyses to evaluate fracture healing. The results showed that amygdalin treatment promoted bone fracture healing. Further experiments using MSC-specific transforming growth factor- (TGF-) ß receptor 2 conditional knockout (KO) mice (Tgfbr2Gli1-Cre ) and C3H10 T1/2 murine mesenchymal progenitor cells showed that this effect was mediated through TGF-ß/Smad signaling. We conclude that amygdalin could be used as an alternative treatment for bone fractures.

Bushenhuoxue formula accelerates fracture healing via upregulation of TGF-ß/Smad2 signaling in mesenchymal progenitor cells.

BACKGROUND: Although Bushenhuoxue formula (BSHXF) is successfully used as a non-traumatic therapy in treating bone fracture in China, the molecular mechanism underlying its effects remains poorly understood. PURPOSE: The present study aims to explore the therapeutic effects of BSHXF on fracture healing in mice and the underlying mechanism. METHODS: We performed unilateral open transverse tibial fracture procedure in C57BL/6 mice which were treated with or without BSHXF. Fracture callus tissues were collected and analyzed by X-ray, micro-CT, biomechanical testing, histopathology and quantitative gene expression analysis. Tibial fracture procedure was also performed in Cre-negative and Gli1-CreER; Tgfbr2flox/flox conditional knockout (KO) mice (Tgfbr2Gli1ER) to determine if BSHXF enhances fracture healing in a TGF-ß-dependent manner. In addition, scratch-wound assay and cell counting kit-8 (CCK-8) assay were used to evaluate the effect of BSHXF on cell migration and cell proliferation in C3H10T1/2 mesenchymal stem cells, respectively. RESULTS: BSHXF promoted endochondral ossification and enhanced bone strength in wild-type (WT) or Cre- control mice. In contrast, BSHXF failed to promote bone fracture healing in Tgfbr2Gli1ER conditional KO mice. In the mice receiving BSHXF treatment, TGF-ß/Smad2 signaling was significantly activated. Moreover, BSHXF enhanced cell migration and cell proliferation in C3H10T1/2 cells, which was strongly attenuated by the small molecule inhibitor SB525334 against TGF-ß type I receptor. CONCLUSION: These data demonstrated that BSHXF promotes fracture healing by activating TGF-ß/Smad2 signaling. BSHXF may be used as a type of alternative medicine for the treatment of bone fracture healing.

Saikosaponin D: A potential therapeutic drug for osteoarthritis.

Osteoarthritis is a degenerative joint disease. Currently, no effective therapeutic exists for osteoarthritis in the clinic setting. Inflammatory response and autophagy are key players in the occurrence and prognosis of osteoarthritis. In recent years, the regulation of inflammation and autophagy signal pathway has been touted as a potential treatment course for osteoarthritis. Saikosaponin D has anti-inflammatory and induces autophagy effects via inhibiting the nuclear transcription factor-κB, mTOR signaling pathways. Here in the report, we analyze and summarize recent evidences pertaining to the relationship between Saikosaponin and osteoarthritis. Published studies were scoured for in research databases, such as PubMed and Scopus with the keywords Saikosaponin and osteoarthritis. Phosphatidylinositol 3-kinase (PI3k)/Akt/mTOR signaling pathway is an important autophagy modulator, and can regulate chondrocytic autophagy, inflammation, and apoptosis. Saikosaponin D alleviates inflammation and regulates autophagy by inhibiting the PI3k/Akt/mTOR signaling pathway. Saikosaponin D could be a potential therapeutic drug for osteoarthritis.

Genome-wide microRNA screening reveals miR-582-5p as a mesenchymal stem cell-specific microRNA in subchondral bone of the human knee joint.

Emerging evidence suggests that microRNAs (miRNAs) may be pathologically involved in osteoarthritis (OA). Subchondral bone (SCB) sclerosis is accounted for the knee osteoarthritis (KOA) development and progression. In this study, we aimed to screen the miRNA biomarkers of KOA and investigated whether these miRNAs regulate the differentiation potential of mesenchymal stem cells (MSCs) and thus contributing to SCB. We identified 48 miRNAs in the blood samples in KOA patients (n = 5) through microarray expression profiling detection. After validation with larger sample number, we confirmed hsa-miR-582-5p and hsa-miR-424-5p were associated with the pathology of SCB sclerosis. Target genes prediction and pathway analysis were implemented with online databases, indicating these two candidate miRNAs were closely related to the pathways of pluripotency of stem cells and pathology of OA. Surprisingly, mmu-miR-582-5p (homology of hsa-miR-582-5p) was downregulated in osteogenic differentiation and upregulated in adipogenic differentiation of mesenchymal progenitor C3H10T1/2 cells, whereas mmu-mir-322-5p (homology of hsa-miR-424-5p) showed no change through the in vitro study. Supplementing mmu-miR-582-5p mimics blocked osteogenic and induced adipogenic differentiation of C3H10T1/2 cells, whereas silencing of the endogenous mmu-miR-582-5p enhanced osteogenic and repressed adipogenic differentiation. Further mechanism studies showed that mmu-miR-582-5p was directly targeted to Runx2. Mutation of putative mmu-miR-582-5p binding sites in Runx2 3' untranslated region (3'UTR) could abolish the response of the 3'UTR-luciferase construct to mmu-miR-582-5p supplementation. Generally speaking, our data suggest that miR-582-5p is an important biomarker of KOA and is able to regulate osteogenic and adipogenic differentiation of MSCs via targeting Runx2. The study also suggests that miR-582-5p may play a crucial role in SCB sclerosis of human KOA.

Bushenhuoxue Formula Facilitates Articular Cartilage Repair and Attenuates Matrix Degradation by Activation of TGF-ß Signaling Pathway.

OBJECTIVE: To investigate the effect and underlying mechanism of Bushenhuoxue (BSHX) formula on articular cartilage repair. METHODS: Twenty-four full-thickness cartilage defect rats were divided into two groups: model group and BSHX group (treated with BSHX formula). Macroscopic observation and histopathological study were conducted after 4- and 8-week treatment. Additionally, we also evaluated chondrocyte proliferation, extracellular matrix (ECM) deposition, cartilage degradation, and chondrocyte hypertrophy-related genes expression in chondrogenic ATDC5 cells cultured in BSHX formula-mediated serum. Moreover, we assessed aforementioned genes expression and pSMAD2/3 protein level in Tgfßr2 siRNA transfected chondrogenic ATDC5 cells in order to address whether BSHX formula exerts cartilage repairing effect through TGF-ß signaling. RESULTS: Neocartilage regeneration promotion effect was observed in cartilage defect rats after BSHX formula treatment, with increases in Col2 and pSMAD2 and decreases in Mmp13 and Runx2. Moreover, cell proliferation, the elevated Col2a1, Aggrecan and pSMAD2/3, reduced Mmp13, Adamts5, Col10a1, and Runx2 expression were also observed in chondrogenic ATDC5 cells cultured in BSHX formula-mediated serum. Besides, the expression alteration of ECM deposition, cartilage degradation, chondrocyte hypertrophy-related genes, and pSMAD2/3 protein levels presented in Tgfßr2 downregulated chondrogenic ATDC5 cells couldn't be adjusted by BSHX formula treatment. CONCLUSION: By activation of TGF-ß signaling, BSHX formula can promote articular cartilage repair by accelerating chondrocyte proliferation and maintaining chondrocyte phenotype, upregulate ECM accumulation, and inhibit matrix degradation.

Effect of Auricular Point Acupressure on Axial Neck Pain After Anterior Cervical Discectomy and Fusion: A Randomized Controlled Trial.

Objectives: To evaluate the effect of auricular point acupressure (APA) on axial neck pain after anterior cervical discectomy and fusion (ACDF) surgery. Design: A prospective randomized controlled trial was performed. Subjects and setting: Twenty-nine participants were randomly divided into two groups, real or sham APA. Participants were enrolled from Shaoxing Hospital of Traditional Chinese Medicine, affiliated with Zhejiang Chinese Medical University. Methods: Eligible participants received a four-week real or sham APA treatment according to their assigned groups. The clinical outcomes were assessed by the criteria of Hosono et al., the Brief Pain Inventory Short Form (BPI), and the 36-item Short Form Health Survey (SF-36). In addition, plasma interleukin (IL)-1ß, IL-6, and tumor necrosis factor (TNF)-α were analyzed. Results: Patients with severe or moderate axial neck pain accounted for 28.6% and 35.7% in the real APA group at the end of treatment and one-month follow-up. BPI scores were decreased in the real APA group at the end of treatment and one-month follow-up. The total mean score of SF-36 was improved in the real APA group and significantly higher than in the sham APA group. Additional, the levels of IL-1ß, IL-6, and TNF-α were decreased in the real APA group. Conclusions: The findings supported the therapeutic effect of APA treatment on axial neck pain after ACDF surgery, and they exert the possible therapeutic effect on downregulating the levels of plasma IL-1ß, IL-6, and TNF-α.

[HE Xingwei's exploration and experience in the pathogenesis and treatment of motor impairment of the trunk after stroke].

In the paper, it is introduced professor HE Xingwei's recognition on the pathogenesis and professor HE's experience in the treatment of the motor impairment of the trunk after stroke. Professor He believes that the motor impairment of the trunk after stroke is the essential factor affecting the rehabilitation in stroke. The motor impairment of the trunk after stroke results from brain marrow damage and spiritual impairment. Hence, regaining the consciousness and promoting the circulation of the governor vessel are the basic principles of the treatment, named regulating the mind and controlling qi, benefiting qi and warming yang, tonifying the kidney and filling up the essence, and promoting the circulation of the governor vessel. Those four therapeutic methods are equally important. Acupuncture, moxibusiton and herbal medicine are applied in combination in the treatment. Additionally, the psychotherapy and rehabilitation are the accessory therapies.

Osteoarthritis pathogenesis: a review of molecular mechanisms.

Osteoarthritis (OA), the most prevalent chronic joint disease, increases in prevalence with age, and affects majority of individuals over the age of 65 and is a leading musculoskeletal cause of impaired mobility in the elderly. Because the precise molecular mechanisms which are involved in the degradation of cartilage matrix and development of OA are poorly understood and there are currently no effective interventions to decelerate the progression of OA or retard the irreversible degradation of cartilage except for total joint replacement surgery. In this paper, the important molecular mechanisms related to OA pathogenesis will be summarized and new insights into potential molecular targets for the prevention and treatment of OA will be provided.