[Meta-analysis of traditional Chinese medicine Jianpi therapy in treatment of atopic dermatitis].

To evaluate the clinical efficacy of traditional Chinese medicine Jianpi therapy in the treatment of atopic dermatitis. CNKI, Wanfang knowledge service platform, VIP journal database, Chinese biomedical literature database (CBM), PubMed, the Cochrane Library and EMbase database from inception to December 2017 were searched for the randomized controlled trials (RCTs) on traditional Chinese medicine Jianpi therapy in the treatment of atopic dermatitis. Literature selection and information extraction was completed and screened by two independent reviewers, and then the Cochrane recommended bias risk assessment method was used to evaluate the bias risk, and Review Manager 5.3 was used for the data analysis. Totally 37 clinical RCTs were included in this study, involving 2 973 patients. Analysis results showed that as compared with the western medicine, traditional Chinese medicine Jianpi therapy had higher clinical effective rate, with statistically significant difference (OR=4.05,95%CI[3.27, 5.03],P<0.000 01); the improvement of score was more evident, including SCORAD score (WMD=-9.82,95%CI[-13.31,-6.33],P<0.000 01), EASI score (WMD=-2.80,95%CI[-3.54,-2.07],P<0.000 01), and itching VAS score (WMD=-0.79, 95%CI[-1.10,-0.47],P<0.000 01)；the improvement of serum biochemical levels was more evident,including interferon-γ (IFN-γ) (WMD=1.75,95%CI[1.14,2.35],P<0.000 01), interleukin-4 (IL-4) (WMD=-3.15,95%CI[-4.16,-2.15],P<0.000 01), and Eosinophil direct count (EOS) (WMD=-0.11,95%CI[-0.20,-0.02], P=0.02)；recurrence rate was significantly reduced (OR=0.36,95%CI[0.21,0.60],P<0.000 1); and trial-related adverse events were reported in 11 RCTs. Studies have shown that traditional Chinese medicine Jianpi therapy had significantly higher clinical efficacy than western medicine in the treatment of atopic dermatitis. However, due to the publication bias and low quality bias of included RCTs in this study, more multicenter, high quality, large-sample, randomized double-blind controlled trials are needed to further demonstrate the conclusion.

The Function of the Novel Mechanical Activated Ion Channel Piezo1 in the Human Osteosarcoma Cells.

BACKGROUND The Piezo1 protein ion channel is a novel mechanical activated ion channel which is related to mechanical signal transduction. However, the function of the mechanically activated ion channel Piezo1 had not been explored. In this study, we explored the function of the Piezo1 ion channel in human osteosarcoma (OS) cells related to apoptosis, invasion, and the cell proliferation. MATERIAL AND METHODS Reverse transcription polymerase chain reaction (RT-PCR) and western-blotting were used to detect the expression of the Piezo1 protein. CCK-8, Transwell experiments and AV-PI were used to detected cell proliferation, cell invasion and cell apoptosis. RESULTS The Piezo1 protein ion channel was highly expressed in human OS cells. The Piezo1-shRNA inhibited the expression of the Piezo1. We explored whether LV3-PIEZO1-homo-3201 could act as Piezo1-shRNA, which could then be an inhibitor of Piezo1. The expression of Piezo1 in the 2-hour stretch group were slightly higher than the 0-hour stretch group, and the difference was not statistically significant (n=3, p>0.05, one-way ANOVA). The apoptotic gene such as the Bax, BAD, caspase-3, and caspase-9 had the same characteristics as the Piezo1 expression under the stretch force. We also explored the invasion of Piezo1 in vivo using nude mice, and found that Piezo1-shRNA could inhibit the invasion of the OS cells. CONCLUSIONS The Piezo1 protein may be a novel, potential therapeutic target for OS.

Genetic Screening of Haploid Neural Stem Cells Reveals that Nfkbia and Atp2b4 are Key Regulators of Oxidative Stress in Neural Precursors.

Neurological diseases are expected to become the leading cause of death in the next decade. Although little is known about it, the interaction between oxidative stress and inflammation is harmful to the nervous system. To find an advanced tool for neural genetics, mouse haploid neural stem cells (haNSCs) from the somite of chimeric mouse embryos at E8.5 is established. The haNSCs present a haploid neural progenitor identity for long-term culture, promising to robustly differentiate into neural subtypes and being able to form cerebral organoids efficiently. Thereafter, haNSC mutants via a high-throughput approach and screened targets of oxidative stress is generated using the specific mutant library. Deletion of Nfkbia (the top hit among the insertion mutants) reduces damage from reactive oxygen species (ROS) in NSCs exposed to H2O2. Transcriptome analysis revealed that Atp2b4 is upregulated significantly in Nfkbia-null NSCs and is probably responsible for the observed resistance. Additionally, overexpression of Atp2b4 itself can increase the survival of NSCs in the presence of H2O2, suggesting that Atp2b4 is closely involved in this resistance. Herein, a powerful haploid system is presented to study functional genetics in neural lineages, shedding light on the screening of critical genes and drugs for neurological diseases.

Protocol to generate induced trophoblast stem cells from embryonic stem cells in mice.

Conversion of trophectoderm (TE)-derived trophoblast stem cells (TSCs) from inner-cell-mass-derived embryonic stem cells (ESCs) in mice is difficult to achieve naturally. Here, we introduce a reliable and repeatable protocol to generate induced TSCs (iTSCs) from ESCs via a Tet-on system in vitro. The iTSCs show typical TSC properties and have the potential to differentiate into syncytiotrophoblast cells (STCs) and trophoblast giant cells (TGCs). This cell fate transition provides a general platform to robustly investigate the mechanisms underlying TE specification. For complete details on the use and execution of this protocol, please refer to Zhang et al. (2022).1.

Effect of governor vessel moxibustion (GVM) therapy with mild to moderate psoriasis: A randomized clinical trial.

BACKGROUND: It was hypothesized that governor vessel moxibustion (GVM) therapy may improve the course of mild to moderate psoriasis (PS) in patients. METHODS: A randomized, controlled clinical trial lasting 40 days was conducted at the Shaanxi Provincial Hospital of Chinese Medicine. Investigators were blinded to patient groupings. Individuals with mild to moderate PS ranging in age from 18 to 70 years were enrolled. GVM therapy was administered one every 10 days for 40 days with 1.5 hours on the governor meridian in the GVM therapy group. The PS area and severity index (PASI) and dermatological life quality index (DLQI) scores were monitored before and after treatment. RESULTS: There was a significant reduction in the mean PASI score in the GVM therapy group of 0.76 points (2.37 [2.61]; SE, 0.39) after 40 days of treatment compared with the control group (3.12 [2.12], SE, 0.32) (P < .01). There were also significantly greater changes in the DLQI scores of the GVM therapy group (4.23 [2.25]; SE, 0.34) compared with those in the control group (8.91 [3.85]; SE, 0.59) (P < .001). CONCLUSION: GVM therapy effectively reduced both PASI and DLQI scores in patients with mild to moderate PS.

BCL2 is a major regulator of haploidy maintenance in murine embryonic stem cells.

Mammalian haploid cells are important resources for forward genetic screening and are important in genetic medicine and drug development. However, the self-diploidization of murine haploid embryonic stem cells (haESCs) during daily culture or differentiation jeopardizes their use in genetic approaches. Here, we show that overexpression (OE) of an antiapoptosis gene, BCL2, in haESCs robustly ensures their haploidy maintenance in various situations, even under strict differentiation in vivo (embryonic 10.5 chimeric fetus or 21-day teratoma). Haploid cell lines of many lineages, including epiblasts, trophectodermal lineages, and neuroectodermal lineages, can be easily derived by the differentiation of BCL2-OE haESCs in vitro. Transcriptome analysis revealed that BCL2-OE activates another regulatory gene, Has2, which is also sufficient for haploidy maintenance. Together, our findings provide an effective and secure strategy to reduce diploidization during differentiation, which will contribute to the generation of haploid cell lines of the desired lineage and related genetic screening.

Haploid-genetic screening of trophectoderm specification identifies Dyrk1a as a repressor of totipotent-like status.

Trophectoderm (TE) and the inner cell mass are the first two lineages in murine embryogenesis and cannot naturally transit to each other. The barriers between them are unclear and fascinating. Embryonic stem cells (ESCs) and trophoblast stem cells (TSCs) retain the identities of inner cell mass and TE, respectively, and, thus, are ideal platforms to investigate these lineages in vitro. Here, we develop a loss-of-function genetic screening in haploid ESCs and reveal many mutations involved in the conversion of TSCs. The disruption of either Catip or Dyrk1a (candidates) in ESCs facilitates the conversion of TSCs. According to transcriptome analysis, we find that the repression of Dyrk1a activates totipotency, which is a possible reason for TE specification. Dyrk1a-null ESCs can contribute to embryonic and extraembryonic tissues in chimeras and can efficiently form blastocyst-like structures, indicating their totipotent developmental abilities. These findings provide insights into the mechanisms underlying cell fate alternation in embryogenesis.

Genome-scale screening in a rat haploid system identifies Thop1 as a modulator of pluripotency exit.

OBJECTIVES: The rats are crucial animal models for the basic medical researches. Rat embryonic stem cells (ESCs), which are widely studied, can self-renew and exhibit pluripotency in long-term culture, but the mechanism underlying how they exit pluripotency remains obscure. To investigate the key modulators on pluripotency exiting in rat ESCs, we perform genome-wide screening using a unique rat haploid system. MATERIALS AND METHODS: Rat haploid ESCs (haESCs) enable advances in the discovery of unknown functional genes owing to their homozygous and pluripotent characteristics. REX1 is a sensitive marker for the naïve pluripotency that is often utilized to monitor pluripotency exit, thus rat haESCs carrying a Rex1-GFP reporter are used for genetic screening. Genome-wide mutations are introduced into the genomes of rat Rex1-GFP haESCs via piggyBac transposon, and differentiation-retarded mutants are obtained after random differentiation selection. The exact mutations are elucidated by high-throughput sequencing and bioinformatic analysis. The role of candidate mutation is validated in rat ESCs by knockout and overexpression experiments, and the phosphorylation of ERK1/2 (p-ERK1/2) is determined by western blotting. RESULTS: High-throughput sequencing analysis reveals numerous insertions related to various pathways affecting random differentiation. Thereafter, deletion of Thop1 (one candidate gene in the screened list) arrests the differentiation of rat ESCs by inhibiting the p-ERK1/2, whereas overexpression of Thop1 promotes rat ESCs to exit from pluripotency. CONCLUSIONS: Our findings provide an ideal tool to study functional genomics in rats: a homozygous haploid system carrying a pluripotency reporter that facilitates robust discovery of the mechanisms involved in the self-renewal or pluripotency of rat ESCs.

Genome-wide screening in the haploid system reveals Slc25a43 as a target gene of oxidative toxicity.

Reactive oxygen species (ROS) are extensively assessed in physiological and pathological studies; however, the genes and mechanisms involved in antioxidant reactions are elusive. To address this knowledge gap, we used a forward genetic approach with mouse haploid embryonic stem cells (haESCs) to generate high-throughput mutant libraries, from which numerous oxidative stress-targeting genes were screened out. We performed proof-of-concept experiments to validate the potential inserted genes. Slc25a43 (one of the candidates) knockout (KO) ESCs presented reduced damage caused by ROS and higher cell viability when exposed to H2O2. Subsequently, ROS production and mitochondrial function analysis also confirmed that Slc25a43 was a main target gene of oxidative toxicity. In addition, we identified that KO of Slc25a43 activated mitochondria-related genes including Nlrx1 to protect ESCs from oxidative damage. Overall, our findings facilitated revealing target genes of oxidative stress and shed lights on the mechanism underlying oxidative death.

Association between environmental chemicals co-exposure and peripheral blood immune-inflammatory indicators.

Chronic inflammation is closely related to chronic inflammatory diseases, autoimmune diseases and cancer. Few studies have evaluated the effects of exposure to multiple chemical combinations on immunoinflammatory related indicators and their possible molecular mechanisms. This study explored the effect of exposure to various chemicals on immune-inflammatory biomarkers and its molecular mechanism. Using data from 1,723 participants in the National Health and Nutrition Examination Survey (NHANES, 2011-2012), the aim was to determine the association between chemical mixtures and immunoinflammatory biomarkers [including White blood cell (Wbc), neutrophil (Neu), lymphocytes (Lym), and Neutrophil-to-lymphocyte ratio (NLR)] using linear regression model, weighted quantile sum regression (WQSR) model, and bayesian nuclear machine regression (BKMR) model. Meanwhile, functional enrichment analysis and protein-protein interaction network establishment were performed to explore the molecular mechanism of inflammation induced by high-weight chemicals. In the linear regression model established for each single chemical, the four immunoinflammatory biomarkers were positively correlated with polycyclic aromatic hydrocarbons (PAHs), negatively correlated with perfluoroalkyl substances (PFASs), and positively or negatively correlated with metallic and non-metallic elements. WQSR model showed that cadmium (Cd), perfluorooctane sulfonic acid (PFOS) and perfluorodecanoic acid (PFDE) had the highest weights. In BKMR analysis, the overall effect of chemical mixtures was significantly associated with Lym and showed an increasing trend. The hub genes in high-weight chemicals inflammation-related genes were interleukin-6 (IL6), tumor necrosis factor (TNF), and interleukin-1B (IL1B), etc. They were mainly enriched in inflammatory response, Cytokine-cytokine receptor interaction, Th17 cell differentiation and IL-17 signaling pathway. The above results show that exposure to environmental chemical cocktails primarily promotes an increase in Lym across the immune-inflammatory spectrum. The mechanism leading to the inflammatory response may be related to the activation of IL-6 amplifier by the co-exposure of environmental chemicals.

Ta-Xi-San Suppresses Atopic Dermatitis Involved in Multitarget Mechanism Using Experimental and Network Pharmacology Analysis.

Atopic dermatitis (AD) is a relapsing and chronic skin inflammation with a common incidence worldwide. Ta-Xi-San (TXS) is a Chinese herbal formula usually used for atopic dermatitis in clinic; however, its active compounds and mechanisms of action are still unclear. Our study was designed to reveal the pharmacological activities, the active compounds, and the pharmacological mechanisms of TXS for atopic dermatitis. Mice were induced by 2,4-dinitrocluorobenzene (DNCB) to build atopic dermatitis model. The pathological evaluation, enzyme-linked immunosorbent assay (ELISA), and hematoxylin and eosin (H&E) assay were performed. The UPLC-Q-Exactive-MSE and network pharmacology analysis were performed to explore active ingredients and therapeutic mechanisms of TXS. TXS treatment decreased levels of immunoglobulin E (IgE), interleukin-4 (IL-4), and tumor necrosis factor-α (TNF-α) in serum induced by DNCB. TXS reduced scratching behavior and alleviated inflammatory pathology of skin and ear. Meanwhile, TXS decreased the spleen index and increased spleen index. The UPLC-Q-Exactive-MSE results showed that 65 compounds of TXS were detected and 337 targets were fished. We collected 1371 AD disease targets, and the compound-target gene network reveled that the top 3 active ingredients were (-)-epigallocatechin gallate, apigenin, and esculetin, and the core target genes were PTGS2, PTGS1, and HSP90AA1. The KEGG pathway and GO analysis showed that TXS remedied atopic dermatitis via PI3K-Akt signaling pathway, mitogen-activated protein kinase (MAPK) signaling pathway, and Toll-like receptor (TLR) signaling pathway with the regulation of inflammatory response and transcription. Further, we found that the targets of PTGS2 and HSP90AA1 were both elevated in ears and skin of AD model mouse; however, TXS decreased the elevated expressions of PTGS2 and HSP90AA1. Our study revealed that TXS ameliorated AD based on (-)-epigallocatechin gallate, apigenin, and esculetin via targeting PTGS2 and HSP90AA1.

Homozygous Loss of Septin12, but not its Haploinsufficiency, Leads to Male Infertility and Fertilization Failure.

The SEPTIN12 gene has been associated with male infertility. Male Septin12 +/- chimera mice were infertile, supporting the prevailing view that SEPTIN12 haploinsufficiency causes male infertility. In this study, we identified a heterozygous mutation on SEPTIN12, c.72C>A (p.Cys24Ter) in the male partner of a patient couple, who had a previous fertilization failure (FF) after intracytoplasmic sperm injection (ICSI) and became pregnant after ICSI together with artificial oocyte activation (AOA). To investigate the role of SEPTIN12 in FF and oocyte activation, we constructed Septin12 knockout mice. Surprisingly, Septin12 -/- male mice, but not Septin12 +/- male mice, are infertile, and have reduced sperm counts and abnormal sperm morphology. Importantly, AOA treatment enhances the 2-cell embryo rate of ICSI embryos injected with Septin12 -/- sperm, indicating that FF caused by male Septin12 deficiency is overcome by AOA. Mechanistically, loss of PLCζ around the acrosome might be the reason for FF of Septin12 -/- sperm. Taken together, our data indicated that homozygous knockout of Septin12, but not Septin12 haploinsufficiency, leads to male infertility and FF.

Rif1 and Hmgn3 regulate the conversion of murine trophoblast stem cells.

The appearance of trophectoderm (TE) is a hallmark event in preimplantation development during murine embryogenesis. However, little is known about the mechanisms underlying TE specification. We find that the depletion of Rif1 breaks down the barrier to the transition from embryonic stem cells (ESCs) to trophoblast stem cells (TSCs). Rif1-null-induced TSCs show typical TE properties and the potential to differentiate into terminal trophoblast lineages. Global transcriptome analysis reveal that Rif1 deletion activates 2-cell embryo (2C)-related genes and induces a totipotent-like state. Chimeric assays further confirm that Rif1-null ESCs contribute to the functional placenta in addition to the fetus on embryonic day 12.5. Furthermore, we show overexpression of Hmgn3, one of the key upregulated gene in Rif1-null ESCs, facilitates the induction of TSCs. Therefore, we report two key genes regulating the conversion of TSCs and provide insights for investigating TE specification.

Protective Effects and Mechanisms of Recombinant Human Glutathione Peroxidase 4 on Isoproterenol-Induced Myocardial Ischemia Injury.

Ischemic heart disease (IHD) is a cardiovascular disease with high fatality rate, and its pathogenesis is closely related to oxidative stress. Reactive oxygen species (ROS) in oxidative stress can lead to myocardial ischemia (MI) injury in many ways. Therefore, the application of antioxidants may be an effective way to prevent IHD. In recent years, glutathione peroxidase 4 (GPx4) has received increasing attention due to its antioxidant effect. In a previous study, we used the new chimeric tRNAUTuT6 to express highly active recombinant human GPx4 (rhGPx4) in amber-less Escherichia coli. In this study, we established an isoproterenol- (ISO-) induced MI injury model in rats and an in vitro model to research the protective effect and mechanism of rhGPx4 on MI injury. The results showed that rhGPx4 could reduce the area of myocardial infarction and ameliorate the pathological injury of heart tissue, significantly reduce ISO-induced abnormalities on electrocardiogram (ECG) and cardiac serum biomarkers, protect mitochondrial function, and attenuate cardiac oxidative stress injury. In an in vitro model, the results also confirmed that rhGPx4 could inhibit ISO-induced oxidative stress injury and cardiomyocyte apoptosis. The mechanism of action of rhGPx4 involves not only the inhibition of lipid peroxidation by eliminating ROS but also keeping a normal level of endogenous antioxidant enzymes by eliminating ROS, thereby preventing oxidative stress injury in cardiomyocytes. Additionally, rhGPx4 could inhibit cardiomyocyte apoptosis through a mitochondria-dependent pathway. In short, rhGPx4, a recombinant antioxidant enzyme, can play an important role in the prevention of IHD and may have great potential for application.

Improvement of stability and in vivo antioxidant effect of human glutathione peroxidase mutant by PEGylation.

Human glutathione peroxidase (GPx), as an important kind of antioxidant enzyme, is often used for the removal of reactive oxygen species. Unfortunately, the application has been hindered by its limited source and poor stability. To solve these problems, human glutathione peroxidase mutant (GPxM) with high activity and yield was obtained using Escherichia coli BL21(DE3) cys auxotrophic strain and the single-protein production system in our previous work. However, the antioxidant effect of this novel recombinant protein drug in animals has not been demonstrated, and its immunogenicity and short biological half-life as a biological macromolecule may have seriously hindered its clinical application. Therefore, it is important to find an effective strategy to address the above issues. In this work, PEGylated GPxM was prepared by conjugating the corresponding mutant with monomethoxy polyethylene glycol succinimidyl succinate (SS-mPEG). We researched the structure, stability, pharmacokinetic properties, antioxidant effect in vivo and protective mechanism against adriamycin (ADR)-mediated cardiotoxicity of modified products, and compared with the above properties of GPxM. The results revealed that GPxM had an excellent antioxidant effect in vivo, and PEGylation can enhance the stability, half-life and antioxidant effect of GPxM while reducing immunogenicity. In addition, the above improvement of PEGylated GPx1M was stronger than that of monoPEGylated GPx4M. Hence, PEGylation might be an effective method to broaden the applications of GPxM as the important antioxidant drug, especially the PEGylated GPx1M with high antioxidant effect.

Rapid generation of murine haploid-induced trophoblast stem cells via a Tet-on system.

Haploid trophoblast stem cells (TSCs) are advanced in studying placental development for their placental precursor and homozygous features. Here, we describe how to generate haploid-induced TSCs (haiTSCs) from haploid embryonic stem cells with a Tet-on system. Our haiTSCs can maintain haploidy long-term and can produce genome-wide mutants combined with transposons. It is promising in high-throughput genetic screening of trophoblast-specific modulators. For complete details on the use and execution of this protocol, please refer to Peng et al. (2019).

High-throughput screening in postimplantation haploid epiblast stem cells reveals Hs3st3b1 as a modulator for reprogramming.

Epiblast stem cells (EpiSCs) derived from postimplantation epiblast are pluripotent stem cells, epigenetically distinct from embryonic stem cells (ESCs), which are widely used in reprogramming studies. Recent achieved haploid cell lines in mammalian species open a new era for high-throughput genetic screening, due to their homozygous phenotypes. Here, we report the generation of mouse haploid EpiSCs (haEpiSCs) from postimplantation chimeric embryos at embryonic day 6.5 (E6.5). These cells maintain one set of chromosomes, express EpiSC-specific genes, and have potentials to differentiate into three germ layers. We also develop a massive mutagenesis protocol with haEpiSCs, and subsequently perform reprogramming selection using this genome-wide mutation library. Multiple modules related to various pathways are implicated. The validation experiments prove that knockout of Hst3st3b1 (one of the candidates) can promote reprogramming of EpiSCs to the ground state efficiently. Our results open the feasibility of utilizing haEpiSCs to elucidate fundamental biological processes including cell fate alternations.

The milestone of genetic screening: Mammalian haploid cells.

Mammalian haploid cells provide insights into multiple genetics approaches as have been proved by advances in homozygous phenotypes and function as gametes. Recent achievements make ploidy of mammalian haploid cells stable and improve the developmental efficiency of embryos derived from mammalian haploid cells intracytoplasmic microinjection, which promise great potentials for using mammalian haploid cells in forward and reverse genetic screening. In this review, we introduce breakthroughs of mammalian haploid cells involving in mechanisms of self-diploidization, forward genetics for various targeting genes and imprinted genes related development.

Inhibition of Apoptosis Reduces Diploidization of Haploid Mouse Embryonic Stem Cells during Differentiation.

Phenotypes of haploid embryonic stem cells (haESCs) are dominant for recessive traits in mice. However, one major obstacle to their use is self-diploidization in daily culture. Although haESCs maintain haploidy well by deleting p53, whether they can sustain haploidy in differentiated status and the mechanism behind it remain unknown. To address this, we induced p53-deficient haESCs into multiple differentiated lineages maintain haploid status in vitro. Haploid cells also remained in chimeric embryos and teratomas arising from p53-null haESCs. Transcriptome analysis revealed that apoptosis genes were downregulated in p53-null haESCs compared with that in wild-type haESCs. Finally, we knocked out p73, another apoptosis-related gene, and observed stabilization of haploidy in haESCs. These results indicated that the main mechanism of diploidization was apoptosis-related gene-triggered cell death in haploid cell cultures. Thus, we can derive haploid somatic cells by manipulating the apoptosis gene, facilitating genetic screens of lineage-specific development.

Effects of moving cupping therapy for plaque psoriasis: study protocol for a randomized multicenter clinical trial.

BACKGROUND: It is difficult to achieve a balance among safety, efficacy, and cost for the clinical treatment of plaque psoriasis. The current treatment of psoriasis often involves comprehensive therapy such as topical plasters, internal medicine, and phototherapy, which are expensive, and some of the drugs have serious side effects. Moving cupping is a type of cupping that has been used clinically for thousands of years in China. It has the advantage of being inexpensive and easy to perform. Therefore, it is widely used in public hospitals in China for psoriasis treatment. However, a comprehensive evaluation of the current clinical evidence of its efficacy is lacking. In this study, we aimed to evaluate the efficacy and safety of moving cupping to treat plaque psoriasis. METHODS: A multicenter, two-arm parallel group, single-blind, randomized, controlled trial will be conducted at six hospitals in China between August 1, 2019 and December 31, 2021. A total of 122 adult patients (aged 18-65 years) who meet the inclusion criteria are being recruited. Participants will receive either basic treatment combined with moving cupping therapy or basic treatment combined with moving cupping placebo. The treatment cycle will be 4 weeks, and the efficacy of treatment will be assessed weekly by the Psoriasis Area and Severity Index during the treatment period and follow-up visits at weeks 6 and 8. The body surface area, physician's global assessment, Dermatology Life Quality Index, patient-reported quality of life, visual analog scale, Traditional Chinese Medication syndrome scoring scale, combined medication, and adverse events will also be recorded and compared to the relative baseline values. DISCUSSION: The findings of this trial may lead to better decisions regarding the treatment of plaque psoriasis. If the trial outcomes are considered favorable, this ancient Chinese medical therapy may be worthy of widespread use because of its convenience and low cost. TRIAL REGISTRATION: This study was registered on May 15,2019 at ClinicalTrials.gov with the identifier number NCT03952676.