Skeletal muscle HSF1 prevents insulin resistance by improving glucose utilization.

The regulation of muscle glucose utilization has significant potential for the treatment of type 2 diabetes mellitus (T2DM) and obesity. Heat shock factor 1 (HSF1) is involved in cellular metabolism and regulation of muscle metabolism. However, it is unclear how HSF1 regulates muscle glucose metabolism. In the present study, the development of obesity in mice was associated with HSF1 downregulation. Serum samples and muscle biopsies were obtained from obese and healthy humans. Fasting glucose and insulin levels and the homeostasis model assessment of insulin resistance value showed that obesity was associated with insulin resistance. The skeletal muscle level of HSF1 was decreased in obese and ob/ob mice. HSF1 was selectively over-expressed in the skeletal muscles of high fat diet (HFD)-fed mice. Muscle HSF1 over-expression successfully triggered glycolytic-to-oxidative myofiber switch and increased fatty acid metabolism and insulin sensitivity in the skeletal muscles of HFD-fed mice. Moreover, HSF1 improved energy expenditure and blocked muscle accumulation of triglycerides in HFD-fed mice. Consequently, muscle HSF1 mitigated the impaired muscle insulin signaling and insulin resistance in HFD-fed mice. In conclusion, T2DM and obesity in HFD-fed mice may be treated with selective HSF1-directed programming of exercise-like effects in skeletal muscle. These findings may aid the development of a new therapeutic approach for obesity and T2DM.

Exposure to Nitro-PAHs interfere with germination and early growth of Hordeum vulgare via oxidative stress.

Nitrated polycyclic aromatic hydrocarbons (Nitro-PAHs) as important organic pollutants are ubiquitous in the atmospheric environment, agricultural soils and aquatic environments to pose a severe polluting risk. However, little is known about the mechanism of Nitro-PAHs genotoxicity in plants. We analyzed seeds germination, seedlings growth, and toxicity mechanism following 1-Nitropyrene treatment in Hordeum vulgare. Our results reveal that 1-NP treatment could be an inhibited agent on seeds germination and growth of roots and shoots. Additionally, the reduction of mitotic index and the increasing frequency of micronucleus suggest that 1-NP may pose a potential risk of genotoxicity in the plant. We further clarify that O2- and H2O2 radicals contribute to 1-NP stimulation induced oxidative damage. Our study provides insights into the role of Nitro-PAHs exposure on growth processing toxicity and genotoxicity in plant and provided a useful reference for the surveillance and risk management of Nitro-PAHs in environments.

Up-regulation of Siah1 by ethanol triggers apoptosis in neural crest cells through p38 MAPK-mediated activation of p53 signaling pathway.

Seven in absentia homolog 1 (Siah1) is one of the E3 ubiquitin ligases and plays a key role in regulating target protein degradation. This study was designed to test the hypothesis that Siah1 mediates ethanol-induced apoptosis in NCCs through p38 MAPK-mediated activation of the p53 signaling pathway. We found that exposure of NCCs to ethanol resulted in the increases in the total protein levels of p53 and the phosphorylation of p53 at serine 15. Ethanol exposure also resulted in a significant increase in the phosphorylation of p38 MAPK. Knock-down of Siah1 dramatically reduced the ethanol-induced increase in the phosphorylation of p38 MAPK. Knock-down of Siah1 by siRNA or down-regulation of p38 MAPK by either siRNA or inhibitor significantly diminished ethanol-induced accumulations of p53 and the phosphorylation of p53. In addition, ethanol exposure resulted in a significant increase in the expression of p53 downstream targets and apoptosis in NCCs, which can be significantly diminished by down-regulation of Siah1 with siRNA. Knock-down of p38 MAPK by siRNA also dramatically reduced the ethanol-induced apoptosis. These results demonstrate that Siah1 plays a crucial role in ethanol-induced apoptosis in NCCs, and that the up-regulation of Siah1 by ethanol can trigger apoptosis through p38 MAPK-mediated activation of the p53 signaling pathway.

[Understanding and Thinking on America Clinical Evaluation of Medical Devices].

This paper introduces the risk classification and listing way of medical devices in the United States, and according to the contents in various situations, FDA provides the requirements for clinical evaluation. At the same time, through the comparative study on the similarities and differences between USA and our country of the clinical evaluation, the paper puts forward some suggestions.

[Quality control research of cold light source of endoscope].

This paper introduced the significance parameters of the quality control of cold light source of endoscope, expounded the importance and necessity of quality control of cold light source; it investigated several manufacturers, analyzed and discussed the main causes of the cold light source uneven, in order to realized the standard management and effective supervision on the cold light source, at the end, the next step quality control work was brought out, which provide technical support for quality supervision of cold light source.

Hsa_circ_0092856 Promoted the Proliferation, Migration, and Invasion of NSCLC Cells by Up-Regulating the Expression of eIF3a.

Circular RNA (circRNA) plays a very important regulatory role in a variety of human malignancies such as non-small-cell lung cancer (NSCLC). In the current study, we explored the role of hsa_circ_0092856 in the progression of NSCLC. We screened CircRNA from the eIF3a gene in the Circbase database. The biological functions of hsa_circ_0092856 in NSCLC were analyzed via qRT-PCR, a CCK-8 assay, a plate cloning experiment, scratch testing, a transwell chamber experiment, an RNA nuclear mass separation experiment, an RIP experiment, and a Western blot test. The results showed that hsa_circ_0092856 was highly expressed in NSCLC cells, and the knockdown of hsa_circ_0092856 could inhibit the proliferation, migration, and invasion of NSCLC cells. The overexpression of hsa_circ_0092856 has the opposite effect. The expression of eIF3a also changed with the change in hsa_circ_0092856. These results suggest that hsa_circ_0092856 may play a key role in the progression of NSCLC by regulating the expression of eIF3a.

Farnesoid X receptor activation protects against renal fibrosis via modulation of ß-catenin signaling.

OBJECTIVE: Activation of farnesoid X receptor (FXR), a bile acid nuclear receptor, may be implicated in the pathophysiology of diabetic nephropathy. We explored a possible role for FXR activation in preventing renal fibrosis in high fat diet (HFD)-fed mice. METHODS: We investigated the effects of HFD on mouse kidney and renal tubular epithelial cells both in vivo and in vitro, and observed the changes of FXR and ß-catenin pathway. FXR agonist was also used to alleviate this HFD-induced effect, and the interaction between FXR and ß-catenin was further verified. RESULTS: Mice were fed by a 60% kcal fat diet for 20 weeks developed the typical traits of metabolic syndrome with subsequent renal lipid accumulation and renal injury. Treatment with the FXR agonist CDCA or GW4064 decreased body weight, renal lipid accumulation, as well as renal injury. Moreover, renal ß-catenin signaling was activated and improved with FXR-agonist treatment in HFD-fed mice. To examine whether FXR affected ß-catenin signaling, and was involved in tubulo-interstitial fibrosis, we explored the FXR expression and function in ox-LDL induced-renal tubular injury. In rat proximal tubular epithelial cells (NRK-52E) stimulated by ox-LDL, FXR protein was decreased compared to control group, and phosphorylated (Ser675) ß-catenin was activated by ox-LDL in a dose- and time-dependent manner. Ox-LDL enhanced α-SMA and fibronectin expressions and reduced E-cadherin levels, whereas FXR agonism or FXR overexpression inhibited fibronectin and α-SMA expressions and restored E-cadherin. Moreover, FXR agonist treatment also decreased phosphorylated (Ser675) ß-catenin, nuclear translocation and ß-catenin-mediated transcription induced by ox-LDL in NRK-52E cells. We showed that FXR could bind with ß-catenin via the AF1 domain, and disrupt the assembly of the core ß-catenin/TCF4 complex. CONCLUSION: These experimental data suggest that FXR activation, via modulating ß-catenin signaling, may contribute to attenuating the development of lipid-mediated tubulo-interstitial fibrosis.

Proteomic profiling of expression of proteasomal subunits from livers of mice treated with diethylnitrosamine.

The liver plays a central role in transforming and clearing chemicals and is susceptible to the toxicity from these agents. Diethylnitrosamine is metabolized primarily in the liver by cytochrome P-450 and can cause DNA damage. The 26S proteasome is a large proteolytic complex that degrades ubiquitinated proteins, and regulates many physiological processes. We used proteomics-based approaches to examine expressional differences of liver proteasomal subunits from diethylnitrosamine-treated mice. The expression of most proteasomal subunits was observed to be upregulated in the analysis of 2DE and MALDI-TOF MS/MS. Some of these differentially expressed proteasomal subunits were further confirmed by Western blot, RT-PCR, and immunohistochemistry. Our results provided useful information on the relationship between the proteasomal complex and related diseases.

Application of Virtual Reality Technology in Post-Stroke Depression.

Post-stroke depression (PSD) is one of the most common complications of emotional disorders after stroke, and the recovery effect of clinical intervention using conventional means is limited. As an emerging technology, virtual reality technology provides a new idea for the clinical rehabilitation of patients with post-stroke depression. Through literature retrieval and review of domestic and foreign studies, this paper summarizes the development of virtual reality technology in psychotherapy. This paper expounds the application value of virtual reality technology in post-stroke depression, summarizes the common types of virtual reality technology combined with conventional intervention to treat post-stroke depression, and analyzes the influence of virtual reality technology on physical and mental rehabilitation of patients with post-stroke depression combined with empirical data. At the same time, the positive significance of virtual reality technology popularization and application is discussed. Finally, it is concluded that virtual reality technology can make up for the shortcomings of traditional treatment in the application of post-stroke depression, and can effectively improve the physical and mental state of patients. The application prospect is broad, but there is still room for development and improvement.

Silencing of long noncoding RNA X-inactive specific transcript alleviates Aß1-42-induced microglia-mediated neurotoxicity by shifting microglial M1/M2 polarization.

OBJECTIVES: This experimental study aims to investigate the role of long noncoding RNA X-inactive specific transcript (lncRNA XIST) in the microglial polarization and microglia-mediated neurotoxicity in Alzheimer's disease (AD). METHODS: The levels of XIST and microRNA-107 (miR-107) were detected by quantitative real-time polymerase chain reaction. The spatial learning and memory capability of APPswe/PS1dE9 (APP/PS1) mice were evaluated by the Morris water maze test. The morphology of mouse hippocampus cells was evaluated by hematoxylin and eosin staining. The Iba1-positive microglia were labeled by immunohistochemistry staining. The protein levels were determined by western blot and enzyme-linked immunosorbent assay. Neurotoxicity was evaluated by the terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling, caspase-3 activity, and Cell Counting Kit-8 assay. The XIST, miR-107, and AD targets were predicted by bioinformatics analysis. RESULTS: The level of XIST was increased in APP/PS1 mice, and XIST silencing ameliorated AD progression. XIST silencing suppressed microglia activation, microglial M1 polarization, and proinflammatory factor levels, but promoted microglial M2 polarization in APP/PS1 mice and Aß1-42-treated BV-2 cells. XIST knockdown reduced Aß1-42-induced microglia-mediated apoptosis and enhanced cell viability in HT22 cells. XIST silencing down-regulated miR-107 level and attenuated Aß1-42-caused suppression of the phosphatidylinositol 3-kinase (PI3K)/Akt signaling. Those effects of XIST silencing were attenuated by miR-107 inhibitor or LY294002. CONCLUSION: Downregulation of XIST lessened Aß1-42-induced microglia-mediated neurotoxicity by modulating microglial M1/M2 polarization, which may be mediated by the miR-107/PI3K/Akt pathway.

Ethanol exposure disrupted the formation of radial glial processes and impaired the generation and migration of outer radial glial cells in forebrain organoids derived from human embryonic stem cells.

Radial glial cells (RGCs) play a pivotal role in cerebral cortical development by functioning as a source of new neurons and by supporting the migration of newborn neurons. These functions are primarily dependent on the apical-basolateral structures of radial glial processes. This study aims to investigate the effects of ethanol exposure on the development of radial glial processes and the generation, migration, and transformation of outer radial glial cells (oRGCs). For this purpose, forebrain organoids were developed from human embryonic stem cells. These forebrain organoids contain abundant neural progenitor cells (SOX2+), express high levels of neural epithelial markers ß-catenin and PKCλ, and dorsal forebrain marker PAX6, and display well-organized cortical architectures containing abundant apical and basal RGCs, intermediate progenitors (IPCs), and neurons. Exposure of forebrain organoids to ethanol resulted in a significant increase in apoptosis in Nestin-positive radial glial cells. Ethanol exposure also remarkably decreased the levels of radial glial process-associated proteins, including Nestin, GFAP, and Vimentin, in radial glial cells and distinctly impaired the integrity and morphologies of radial glial processes. In addition, the ethanol-induced impairment of the radial glial processes is associated with decreased migration and proliferation of radial glial cells, reduction in the generation of HOPX+ oRGCs, and the accelerated transformation of oRGCs into astrocytes. These results demonstrate that ethanol exposure can disrupt cerebral cortex development by impairing the formation of radial glial processes and the generation, migration, and transformation of oRGCs.

Up-regulation of microRNA-34a mediates ethanol-induced impairment of neural crest cell migration in vitro and in zebrafish embryos through modulating epithelial-mesenchymal transition by targeting Snail1.

Prenatal ethanol exposure can impair neural crest cell (NCC) development, including NCC survival, differentiation and migration, contributing to the craniofacial dysmorphology in Fetal Alcohol Spectrum Disorders (FASD). Epithelial-mesenchymal transition (EMT) plays an important role in regulating the migration of NCCs. The objective of this study is to determine whether ethanol exposure can suppress NCC migration through inhibiting EMT and whether microRNA-34a (miR-34a) is involved in the ethanol-induced impairment of EMT in NCCs. We found that exposure to 100 mM ethanol significantly inhibited the migration of NCCs. qRT-PCR and Western Blot analysis revealed that exposure to ethanol robustly reduced the mRNA and protein expression of Snail1, a critical transcriptional factor that has a pivotal role in the regulation of EMT. Ethanol exposure also significantly increased the mRNA expression of the Snail1 target gene E-cadherin1 and inhibited EMT in NCCs. We also found that exposure to ethanol significantly elevated the expression of miR-34a that targets Snail1 in NCCs. In addition, down-regulation of miR-34a prevented ethanol-induced repression of Snail1 and diminished ethanol-induced upregulation of Snail1 target gene E-cadherin1 in NCCs. Inhibition of miR-34a restored EMT and prevented ethanol-induced inhibition of NCC migration in vitro and in zebrafish embryos in vivo. These results demonstrate that ethanol-induced upregulation of miR-34a contributes to the impairment of NCC migration through suppressing EMT by targeting Snail1.

Effectiveness and safety of music therapy for insomnia disorder patients: A protocol for systematic review and meta-analysis.

BACKGROUND: Music therapy has been widely used clinically to relieve insomnia disorder patients. However, the efficacy of music therapy in the treatment of insomnia disorder patients is uncertain. The purpose of this study is to determine the effectiveness and safety of music therapy in the treatment of insomnia disorder patients. METHODS: Search PubMed, Cochrane Library, Embase, China National Knowledge Infrastructure Database, Wanfang Database, China Science and Technology Journal Database, China Biomedical Literature Database, and search-related randomized controlled trials. Two reviewers will independently select studies, collect data, and evaluate methodological quality through the Cochrane Deviation Risk Tool. Revman V.5.3 will be used for meta-analysis. RESULTS: This study will evaluate the current status of music therapy treatment for insomnia disorder patients, aiming to illustrate the effectiveness and safety of music therapy treatment. CONCLUSION: This study will provide a basis for judging whether music therapy is effective in treating insomnia disorder patients. INPLASY REGISTRATION NUMBER: INPLASY202150087.

Effectiveness and safety of music-supported therapy on mood in post-stroke rehabilitation patients: A protocol for systematic review and meta-analysis.

BACKGROUND: Music-supported therapy has been widely used clinically to relieve post-stroke rehabilitation. However, the efficacy of Music-supported therapy in the treatment of Mood in post-stroke rehabilitation Patients is uncertain. The purpose of this study is to determine the effectiveness and safety of Music-supported therapy in the treatment of Mood in post-stroke rehabilitation Patients. METHODS: Search PubMed, Cochrane Library, Embase, China National Knowledge Infrastructure Database, Wanfang Database, China Science and Technology Journal Database, China Biomedical Literature Database, and search related randomized controlled trials. Two reviewers will independently select studies, collect data, and evaluate methodological quality through the Cochrane Deviation Risk Tool. Revman V.5.3 will be used for meta-analysis. RESULTS: This study will evaluate the current status of Music-supported therapy treatment for mood in post-stroke rehabilitation Patients, aiming to illustrate the effectiveness and safety of Music-supported therapy treatment. CONCLUSION: This study will provide a basis for judging whether Music-supported therapy is effective in treating mood in post-stroke rehabilitation Patients. INPLASY REGISTRATION NUMBER: INPLASY202120011.

Sulforaphane Protects Against Ethanol-Induced Apoptosis in Human Neural Crest Cells Through Diminishing Ethanol-Induced Hypermethylation at the Promoters of the Genes Encoding the Inhibitor of Apoptosis Proteins.

The neural crest cell (NCC) is a multipotent progenitor cell population that is sensitive to ethanol and is implicated in the Fetal Alcohol Spectrum Disorders (FASD). Studies have shown that sulforaphane (SFN) can prevent ethanol-induced apoptosis in NCCs. This study aims to investigate whether ethanol exposure can induce apoptosis in human NCCs (hNCCs) through epigenetically suppressing the expression of anti-apoptotic genes and whether SFN can restore the expression of anti-apoptotic genes and prevent apoptosis in ethanol-exposed hNCCs. We found that ethanol exposure resulted in a significant increase in the expression of DNMT3a and the activity of DNMTs. SFN treatment diminished the ethanol-induced upregulation of DNMT3a and dramatically reduced the activity of DNMTs in ethanol-exposed hNCCs. We also found that ethanol exposure induced hypermethylation at the promoter regions of two inhibitor of apoptosis proteins (IAP), NAIP and XIAP, in hNCCs, which were prevented by co-treatment with SFN. SFN treatment also significantly diminished ethanol-induced downregulation of NAIP and XIAP in hNCCs. The knockdown of DNMT3a significantly enhanced the effects of SFN on preventing the ethanol-induced repression of NAIP and XIAP and apoptosis in hNCCs. These results demonstrate that SFN can prevent ethanol-induced apoptosis in hNCCs by preventing ethanol-induced hypermethylation at the promoter regions of the genes encoding the IAP proteins and diminishing ethanol-induced repression of NAIP and XIAP through modulating DNMT3a expression and DNMT activity.

DCBLD2 Affects the Development of Colorectal Cancer via EMT and Angiogenesis and Modulates 5-FU Drug Resistance.

Background: DCBLD2 is highly expressed in various cancers, including colorectal cancer. DCBLD2 overexpression promotes tumor occurrence, development, and metastasis. However, DCBLD2 sensitivity to chemotherapy drugs and its mechanism on tumor development are unknown. Methods: DCBLD2 expression differences in cancer and normal tissues were obtained from GEO and TCGA databases. DCBLD2 influence on prognosis was also compared, and the database analysis results were verified via the analysis of clinical samples. GDSC database was used to analyze the effect of DCBLD2 expression difference on 5-FU drug sensitivity on tumor cells. CCK-8, clone formation, scratch, Transwell invasion and migration assays were used to assess DCBLD2 effects on the proliferation, metastasis, and 5-FU drug sensitivity on HCT116 and Caco-2 colorectal cancer cells. Angiogenesis and Matrigel plug assays were used to study the effect of DCBLD2 on angiogenesis. Q-RCR and Western Blot were used to analyze DCBLD2 impact on the EMT signaling pathway, and TAP-MS assay with Co-IP verification was used to identify the downstream target proteins binding to DCBLD2. Results: Both database and clinical sample validation results showed that the expression of DCBLD2 in colorectal cancer tissues was significantly higher than that in normal tissues, leading to poor prognosis of patients. GDSC database analysis showed that DCBLD2 overexpression caused tumor cell resistance to 5-FU. The results of in vitro and in vivo experiments showed that the inhibition of DCBLD2 reduced the proliferation, migration and invasion of colorectal cancer cells, inhibited the angiogenesis of endothelial cells, and enhanced the drug sensitivity to 5-FU. The results of q-RCR and Western Blot experiments showed that the inhibition of DCBLD2 can suppress the EMT signal. The results of TAP-MS assay showed that the proteins bound to DCBLD2 were enriched to the Focal adhesion pathway. The results of Co-IP assay show that DCBLD2 can combine with ITGB1, the key factor of Focal adhesion pathway. Conclusion: DCBLD2 may affect the development of colorectal cancer by regulating cell proliferation and motility, and modulate 5-FU resistance. Down-regulation of DCBLD2 can inhibit EMT signal and angiogenesis. DCBLD2 can combine with ITGB1, the key signal factor of the Focal adhesion pathway.

Silver nanoparticles crossing through and distribution in the blood-brain barrier in vitro.

Silver nanoparticles (SNPs) translocate to the brain through the blood stream after they are implanted in vivo. The aim of this study was to investigate the distribution of SNPs that crossed through the blood-brain barrier (BBB). An in vitro BBB model established by co-cultures of rat brain microvessel vascular endothelial cells (BMVECs) with astrocytes (ACs) was cultured with cell culture medium containing 100 microg/mL of either SNPs or silver microparticles (SMPs). After 4 hours of culture, the ultrastructure and its silver content of BBB was evaluated with transmission electronic microscopy (TEM) and inductively-coupled plasma mass spectrometry (ICP-MS) respectively. Results demonstrated that SNPs crossed the BBB and accumulated inside BMVECs, while the SMPs did not. The data indicated a special distribution of SNPs in the BBB and suggested that SNPs pass the BBB mainly by transcytosis of capillary endothelial cells. Further study would be necessary to evaluate the actual biological effects of SNPs on the brain.

Effectiveness and safety of traditional Chinese medicines for non-alcoholic fatty liver disease: Protocol for systematic review and meta-analysis.

BACKGROUND: Previous reviews indicate that the effect of Traditional Chinese medicines (TCM) on non-alcoholic fatty liver disease (NAFLD) remains uncertainty. The study results published in the past 8 years may change this situation, but there is no updated systematic review. Therefore, we designed this study to systematically evaluate the effectiveness and safety of TCM in the treatment of NAFLD. METHODS AND ANALYSIS: We will search nine online databases from inception to October 01 2019, and the language will not be restricted on included trials. Randomized controlled trials that included patients with NAFLD receiving TCM therapy versus a control group will be included. Two researcher will perform independently the selection of studies, risk of bias assessment and data extraction. We will use the RevMan V.5.2 software with fixed effects model or random effects model according to the heterogeneity test to conduct the data synthesis. We will present the dichotomous data and the continuous data with risk ratios with 95% CIs and weighted mean differences or standardized mean differences with 95% CIs. The Grading of Recommendations Assessment, Development and Evaluation (GRADE) system will be used to evaluate the evidence quality with low risk, unclear risk, and high risk. RESULTS: This study will demonstrate an evidence-based review of TCM for NAFLD. CONCLUSION: The study will provide clear evidence to assess the effectiveness and side effects of TCM for NAFLD.

Effectiveness and safety of massage in the treatment of the congenital muscular torticollis: A systematic review and meta-analysis protocol.

BACKGROUND: Massage has been widely used in the treatment of muscular torticollis in children, but there is no objective and systematic evaluation of the efficacy of various literature, and the efficacy of massage in the treatment of congenital muscular torticollis (CMT) is not clear. The purpose of this study is to evaluate the clinical efficacy and safety of massage in the treatment of muscular torticollis in children. METHODS: Relevant randomized controlled trials (RCTs) will be searched from the databases of PubMed, the Cochrane Library, Embase, the China National Knowledge Infrastructure, Wanfang Database, Chinese Science and Technology Periodical Database, and Chinese Biomedical Literature Database from their inception to May 2020. Two reviewers will independently select studies, collect data, and assess the methodology quality by the Cochrane risk of bias tool. The RevMan V.5.3 will be used for meta-analysis. RESULTS: This study will provide an assessment of the current state of Chinese massage therapy for the congenital muscular torticollis, aiming to show the efficacy and safety of massage treatment. CONCLUSION: This study will provide evidence to judge whether massage is an effective intervention for the third lumbar vertebrae transverse process syndrome. INPLASY REGISTRATION NUMBER: INPLASY202070086.

Acupotomy for third lumbar vertebrae transverse process syndrome: A protocol for systematic review.

BACKGROUND: Acupotomy has been widely used clinically to relieve low back pain. However, the efficacy of acupotomy for the third lumbar vertebrae transverse process syndrome is still uncertain. The aim of this study is to determine the effectiveness and safety of acupotomy therapy for the third lumbar vertebrae transverse process syndrome. METHODS: Relevant randomized controlled trials will be searched from the databases of PubMed, the Cochrane Library, Embase, the China National Knowledge Infrastructure, Wanfang Database, Chinese Science and Technology Periodical Database, and Chinese Biomedical Literature Database from their inception to May 2020. Two reviewers will independently select studies, collect data, and assess the methodology quality by the Cochrane risk of bias tool. The RevMan V.5.3 will be used for meta-analysis. RESULTS: This study will provide an assessment of the current state of acupotomy for the third lumbar vertebrae transverse process syndrome, aiming to show the efficacy and safety of acupotomy treatment. CONCLUSION: This study will provide evidence to judge whether acupotomy is an effective intervention for the third lumbar vertebrae transverse process syndrome. PROSPERO REGISTRATION NUMBER: CRD42019134945.