Background The quality of occupational health technical services is directly linked to the protection of workers' health rights and the efficacy of occupational disease prevention and control. However, the industry still faces critical challenges: sporadic instances of institutional non-compliance and persistent irregularities in professional practice continue to undermine overall service performance. Objective To assess the current quality status of occupational health technical services in Zhejiang Province and propose countermeasures for quality improvement, providing a scientific basis for policy optimization and service delivery quality enhancement. Methods A total of 69 occupational health technical service institutions in Zhejiang Province that obtained formal accreditation as of April 30, 2024, were sampled, including 3 public institutions and 66 private institutions (comprising 3 formerly Class-A, 28 formerly Class-B, 11 formerly Class-C, and 24 newly certified institutions). Following the Technical Protocol for Quality Monitoring of Occupational Health Technical Service in Zhejiang Province and the Technical Protocol for Proficiency Testing of Occupational Health Detection in Zhejiang Province, a quality assessment task force comprising national and provincial experts was established. Evaluation was conducted across four dimensions: qualification maintenance and compliance, standardization of technical services, authenticity of technical services, and proficiency testing, utilizing a combination of document review, on-site inspections, and technical skill assessments. Results The occupational health technical service institutions in Zhejiang Province were predominantly private entities (82.5%), with significant disparities in overall service quality. The pass rates for qualification maintenance and compliance, technical service standardization, technical service authenticity, and the excellence rate for laboratory proficiency testing were 81.5%, 80.7%, 97.3%, and 90.4%, respectively. Regarding qualification maintenance, the pass rates for "environmental conditions" (49.8%, 56.7%) and "instrumentation and equipment" (58.2%、65.6%) were significantly lower for formerly Class-C and newly certified institutions compared to other categories. In terms of technical standardization, "standardized on-site inspections" recorded the lowest pass rate (67.4%), with newly certified institutions at only 48.0%. Regarding technical service authenticity, formerly Class-C institutions exhibited issues such as missing raw chromatograms for blank samples (85.7% pass rate). In laboratory proficiency testing, public and formerly Class-A institutions achieved 100% excellence rates, but the performance of formerly Class-C and newly certified institutions was comparatively weak; specifically, the failure rate for organic analysis in formerly Class-C institutions reached 20%; the failure rate for dust testing items in newly certified institutions was 10.3%. Conclusion The overall quality of occupational health technical services in Zhejiang Province still requires significant improvement, particularly in basic institutional conditions, the standardization of on-site inspections, and laboratory proficiency in organic and dust analysis. Formerly Class-C and newly certified institutions should be the primary focus of quality management efforts. Differentiated regulatory strategies are recommended, alongside strengthening interim and ex-post supervision to gradually enhance the quality of occupational health technical services across all institutions.

ObjectiveTo investigate the inhibitory effects of curcumol （Cur） on the proliferation and metastasis of non-small cell lung cancer （NSCLC） cells and to explore the underlying mechanisms. MethodsIn vivo， a subcutaneous tumor xenograft model was established to evaluate the antiproliferative effect of Cur. In vitro， the cell counting kit-8 （CCK-8） assay was used to assess the effects of Cur at concentrations of 0， 60， 120， 240， 360， 480， 600， 720， 840， 960 μmol·L^-1 on the viability of NCI-A549 and NCI-H23 cells， and to evaluate its inhibitory effect on the proliferation of human bronchial epithelial BEAS-2B cells. Wound healing and Transwell migration assays were conducted to assess changes in cell migratory capacity following Cur treatment. Immunohistochemistry （IHC-P） was used to investigate the regulatory effect of Cur on the Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathway in tumor tissues. Western blot was performed to determine the protein expression levels of phosphorylated JAK2 （p-JAK2）， phosphorylated STAT3 （p-STAT3）， proliferating cell nuclear antigen （PCNA）， matrix metalloproteinase-2 （MMP-2）， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA） in tumor tissues and cells. To further verify the role of the JAK2/STAT3 signaling pathway in the pharmacological effects of Cur， rescue experiments were performed using the pathway agonist colivelin. ResultsIn vivo experiments showed that， compared with the model group， the tumor volumes of subcutaneous xenografts in nude mice in both low- and high-dose Cur groups were significantly reduced （P<0.05）， and the tumor inhibition rates were significantly increased （P<0.05）. The inhibitory effect in the high-dose group was comparable to that of the cisplatin group， and the body weight of mice in the Cur groups remained stable throughout the experiment. In vitro， compared with the control group， Cur at concentrations of 120 and 240 μmol·L^-1 inhibited the proliferation of NCI-A549 and NCI-H23 cells in a concentration-dependent manner （P<0.05）， with a significant inhibitory effect observed at 360 μmol·L^-1 （P<0.01）， while no significant effect on the viability of BEAS-2B cells was observed. Migration assays demonstrated that， compared with the control group， Cur treatment significantly reduced the migration rates of both cell lines in a concentration-dependent manner （P<0.05）， with an inhibitory effect at 360 μmol·L^-1 comparable to that of the cisplatin group. Mechanistic validation showed that， compared with the control group， the protein expression levels of p-JAK2 and p-STAT3 in tumor tissues and cells were significantly downregulated in the Cur groups （P<0.01）， and the expression levels of downstream proteins PCNA， MMP-2， MMP-9， and VEGFA were also significantly decreased with increasing Cur concentration （P<0.05）. In the rescue experiments， compared with the control group， colivelin pretreatment increased cell proliferation and migration rates （P<0.05） and upregulated the expression of related proteins （P<0.05）. Compared with the Cur group， the colivelin+Cur group showed significantly increased proliferation and migration rates （P<0.05）， along with significantly upregulated protein expression levels （P<0.05）. ConclusionCur can significantly inhibit the proliferation and metastasis of NSCLC both in vivo and in vitro， and its mechanism of action is closely associated with the inhibition of JAK2/STAT3 signaling pathway activation.

ObjectiveTo investigate the mechanisms by which oxyresveratrol （OXY） inhibits epithelial-mesenchymal transition （EMT） in non-small cell lung cancer （NSCLC） through the phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway. MethodsCell counting kit-8 （CCK-8） assays were used to determine the survival rates of A549 and H1299 cells treated with different concentrations of OXY， and appropriate concentrations （0， 30， 60， 90 μmol·L^-1） were selected. The effects of OXY on the proliferation of A549 and H1299 cells were evaluated using 5-ethynyl-2′-deoxyuridine （EdU） assays and colony formation assays. Wound healing assays and Transwell invasion assays were performed to assess the effects of OXY on cell migration and invasion. Western blot （WB） was used to detect the expression levels of Snail， E-cadherin， N-cadherin， and Vimentin in A549 and H1299 cells. Network pharmacology and molecular docking were applied to predict the mechanism of action of OXY， and WB was used to evaluate the effects of OXY on proteins in the PI3K/Akt signaling pathway. Rescue experiments were conducted using the PI3K/Akt signaling pathway agonist 740Y-P. Under activation of the PI3K/Akt pathway， the effect of OXY on proliferation， migration， and invasion phenotypes， as well as on the expression levels of PI3K/Akt pathway-related proteins and EMT markers （Snail， E-cadherin， N-cadherin， and Vimentin）， were examined. ResultsIn the forward experiments， CCK-8 assay results showed that， compared with the control group， the survival rates of NSCLC cells in the OXY-treated groups （20-120 μmol·L^-1） were significantly decreased （P<0.05）. The half-maximal inhibitory concentration （IC₅₀） values of A549 and H1299 cells after 48 h of OXY treatment were 113.6 μmol·L^-1 and 92.53 μmol·L^-1， respectively. Therefore， concentrations of 0， 30， 60， 90 μmol·L^-1 were selected as the gradient for subsequent phenotypic and mechanistic studies. Compared with the control group， the proliferation rate， colony number， migration rate， and invasion number of NSCLC cells in the OXY groups （30， 60， and 90 μmol·L^-1） were significantly decreased （P<0.01， P<0.05）. WB results showed that， compared with the control group， the protein expression levels of Snail， N-cadherin， and Vimentin in NSCLC cells of the OXY groups were significantly decreased （P<0.05）， whereas E-cadherin expression was significantly increased （P<0.01）. Network pharmacology and molecular docking results indicated that OXY could act on the PI3K/Akt signaling pathway and exhibited good binding affinity with PI3K and Akt proteins. Further WB results showed that， compared with the control group， there were no statistically significant differences in the expression levels of PI3K and Akt proteins in NSCLC cells of the OXY groups， whereas the expression levels of phosphorylated PI3K （p-PI3K） and phosphorylated Akt （p-Akt） were significantly decreased （P<0.05）. In the rescue experiments， compared with the control group， the proliferation rate， colony number， migration rate， and invasion number of NSCLC cells in the 740Y-P group （15 μmol·L^-1） were significantly increased （P<0.01）. Compared with the control + OXY group （90 μmol·L^-1）， these indices in the 740Y-P + OXY group （15 μmol·L^-1 + 90 μmol·L^-1） were also significantly increased （P<0.01）. WB results showed that， compared with the control group， there were no statistically significant differences in the expression levels of PI3K and Akt proteins in the 740Y-P group. However， the expression levels of p-PI3K， p-Akt， Snail， N-cadherin， and Vimentin were significantly increased （P<0.05）， while E-cadherin expression was significantly decreased （P<0.01）. Compared with the control + OXY group， there were no statistically significant differences in PI3K and Akt protein expression in the 740Y-P + OXY group. However， the expression levels of p-PI3K， p-Akt， Snail， N-cadherin， and Vimentin were significantly increased （P<0.05）， while E-cadherin expression was significantly decreased （P<0.05）. ConclusionOXY inhibits the PI3K/Akt signaling pathway and suppresses the EMT process， thereby exerting anti-metastatic effects in NSCLC.

Lung cancer， particularly non-small cell lung cancer （NSCLC）， is the malignant tumor with the highest incidence and mortality in China and worldwide. In 2022， the global number of deaths reached 1.8 million， accounting for 18.7% of all cancer-related deaths， seriously threatening human health and life， and posing a severe challenge for prevention and treatment. Although treatment strategies for lung cancer have been continuously enriched in recent years， and progress has been made in targeted therapy and immunotherapy， long-term survival benefits remain limited due to primary or acquired drug resistance， low immune responsiveness， and chemotherapy-related toxicities. Therefore， there is an urgent need to explore safe and effective adjunctive therapeutic strategies. Traditional Chinese medicine （TCM）， with its advantages of holistic regulation and individualized syndrome differentiation， has played an increasingly prominent role in comprehensive cancer treatment. TCM holds that "Yang deficiency leads to accumulation" is a key pathogenesis of tumors. Based on the theory that "Yang transforms Qi， while Yin forms substance"， deficiency of Yang Qi results in impaired warming and transformation functions， leading to internal accumulation of Yin-cold. This is closely related to dysregulation of the immune microenvironment， "cold tumor" characteristics， and dysfunction of the neuroendocrine system in modern medicine. Accordingly， the therapeutic strategy of "warming Yang， supporting healthy Qi， and combating cancer" has gained increasing attention. In recent years， commonly used Yang-warming Chinese herbs， including Aconiti Lateralis Radix Praeparata， Zingiberis Rhizoma， Cinnamomi Cortex， Epimedii Folium， and Psoraleae Fructus， as well as their active constituents， have achieved notable progress in anti-lung cancer research by regulating multiple signaling pathways， inducing apoptosis， inhibiting metastasis， and reversing drug resistance. In addition， Yang-warming formulae such as Sini Tang and Yanghe Tang have shown promising effects in alleviating myelosuppression， improving cancer-related fatigue， managing malignant pleural effusion， and relieving cancer pain. These therapies exhibit toxicity-reducing and efficacy-enhancing effects， significantly improving patients' quality of life and survival benefits. To systematically summarize the roles and mechanisms of Yang-warming Chinese herbal medicines and compound formulae in lung cancer， this paper provides a comprehensive review of recent advances， aiming to offer insights for the clinical practice of TCM in the prevention and treatment of lung cancer.

ObjectiveTo investigate the inhibitory effects of curcumol （Cur） on the proliferation and metastasis of non-small cell lung cancer （NSCLC） cells and to explore the underlying mechanisms. MethodsIn vivo， a subcutaneous tumor xenograft model was established to evaluate the antiproliferative effect of Cur. In vitro， the cell counting kit-8 （CCK-8） assay was used to assess the effects of Cur at concentrations of 0， 60， 120， 240， 360， 480， 600， 720， 840， 960 μmol·L^-1 on the viability of NCI-A549 and NCI-H23 cells， and to evaluate its inhibitory effect on the proliferation of human bronchial epithelial BEAS-2B cells. Wound healing and Transwell migration assays were conducted to assess changes in cell migratory capacity following Cur treatment. Immunohistochemistry （IHC-P） was used to investigate the regulatory effect of Cur on the Janus kinase 2/signal transducer and activator of transcription 3 （JAK2/STAT3） signaling pathway in tumor tissues. Western blot was performed to determine the protein expression levels of phosphorylated JAK2 （p-JAK2）， phosphorylated STAT3 （p-STAT3）， proliferating cell nuclear antigen （PCNA）， matrix metalloproteinase-2 （MMP-2）， matrix metalloproteinase-9 （MMP-9）， and vascular endothelial growth factor A （VEGFA） in tumor tissues and cells. To further verify the role of the JAK2/STAT3 signaling pathway in the pharmacological effects of Cur， rescue experiments were performed using the pathway agonist colivelin. ResultsIn vivo experiments showed that， compared with the model group， the tumor volumes of subcutaneous xenografts in nude mice in both low- and high-dose Cur groups were significantly reduced （P<0.05）， and the tumor inhibition rates were significantly increased （P<0.05）. The inhibitory effect in the high-dose group was comparable to that of the cisplatin group， and the body weight of mice in the Cur groups remained stable throughout the experiment. In vitro， compared with the control group， Cur at concentrations of 120 and 240 μmol·L^-1 inhibited the proliferation of NCI-A549 and NCI-H23 cells in a concentration-dependent manner （P<0.05）， with a significant inhibitory effect observed at 360 μmol·L^-1 （P<0.01）， while no significant effect on the viability of BEAS-2B cells was observed. Migration assays demonstrated that， compared with the control group， Cur treatment significantly reduced the migration rates of both cell lines in a concentration-dependent manner （P<0.05）， with an inhibitory effect at 360 μmol·L^-1 comparable to that of the cisplatin group. Mechanistic validation showed that， compared with the control group， the protein expression levels of p-JAK2 and p-STAT3 in tumor tissues and cells were significantly downregulated in the Cur groups （P<0.01）， and the expression levels of downstream proteins PCNA， MMP-2， MMP-9， and VEGFA were also significantly decreased with increasing Cur concentration （P<0.05）. In the rescue experiments， compared with the control group， colivelin pretreatment increased cell proliferation and migration rates （P<0.05） and upregulated the expression of related proteins （P<0.05）. Compared with the Cur group， the colivelin+Cur group showed significantly increased proliferation and migration rates （P<0.05）， along with significantly upregulated protein expression levels （P<0.05）. ConclusionCur can significantly inhibit the proliferation and metastasis of NSCLC both in vivo and in vitro， and its mechanism of action is closely associated with the inhibition of JAK2/STAT3 signaling pathway activation.

ObjectiveTo investigate the mechanisms by which oxyresveratrol （OXY） inhibits epithelial-mesenchymal transition （EMT） in non-small cell lung cancer （NSCLC） through the phosphatidylinositol 3-kinase/protein kinase B （PI3K/Akt） signaling pathway. MethodsCell counting kit-8 （CCK-8） assays were used to determine the survival rates of A549 and H1299 cells treated with different concentrations of OXY， and appropriate concentrations （0， 30， 60， 90 μmol·L^-1） were selected. The effects of OXY on the proliferation of A549 and H1299 cells were evaluated using 5-ethynyl-2′-deoxyuridine （EdU） assays and colony formation assays. Wound healing assays and Transwell invasion assays were performed to assess the effects of OXY on cell migration and invasion. Western blot （WB） was used to detect the expression levels of Snail， E-cadherin， N-cadherin， and Vimentin in A549 and H1299 cells. Network pharmacology and molecular docking were applied to predict the mechanism of action of OXY， and WB was used to evaluate the effects of OXY on proteins in the PI3K/Akt signaling pathway. Rescue experiments were conducted using the PI3K/Akt signaling pathway agonist 740Y-P. Under activation of the PI3K/Akt pathway， the effect of OXY on proliferation， migration， and invasion phenotypes， as well as on the expression levels of PI3K/Akt pathway-related proteins and EMT markers （Snail， E-cadherin， N-cadherin， and Vimentin）， were examined. ResultsIn the forward experiments， CCK-8 assay results showed that， compared with the control group， the survival rates of NSCLC cells in the OXY-treated groups （20-120 μmol·L^-1） were significantly decreased （P<0.05）. The half-maximal inhibitory concentration （IC₅₀） values of A549 and H1299 cells after 48 h of OXY treatment were 113.6 μmol·L^-1 and 92.53 μmol·L^-1， respectively. Therefore， concentrations of 0， 30， 60， 90 μmol·L^-1 were selected as the gradient for subsequent phenotypic and mechanistic studies. Compared with the control group， the proliferation rate， colony number， migration rate， and invasion number of NSCLC cells in the OXY groups （30， 60， and 90 μmol·L^-1） were significantly decreased （P<0.01， P<0.05）. WB results showed that， compared with the control group， the protein expression levels of Snail， N-cadherin， and Vimentin in NSCLC cells of the OXY groups were significantly decreased （P<0.05）， whereas E-cadherin expression was significantly increased （P<0.01）. Network pharmacology and molecular docking results indicated that OXY could act on the PI3K/Akt signaling pathway and exhibited good binding affinity with PI3K and Akt proteins. Further WB results showed that， compared with the control group， there were no statistically significant differences in the expression levels of PI3K and Akt proteins in NSCLC cells of the OXY groups， whereas the expression levels of phosphorylated PI3K （p-PI3K） and phosphorylated Akt （p-Akt） were significantly decreased （P<0.05）. In the rescue experiments， compared with the control group， the proliferation rate， colony number， migration rate， and invasion number of NSCLC cells in the 740Y-P group （15 μmol·L^-1） were significantly increased （P<0.01）. Compared with the control + OXY group （90 μmol·L^-1）， these indices in the 740Y-P + OXY group （15 μmol·L^-1 + 90 μmol·L^-1） were also significantly increased （P<0.01）. WB results showed that， compared with the control group， there were no statistically significant differences in the expression levels of PI3K and Akt proteins in the 740Y-P group. However， the expression levels of p-PI3K， p-Akt， Snail， N-cadherin， and Vimentin were significantly increased （P<0.05）， while E-cadherin expression was significantly decreased （P<0.01）. Compared with the control + OXY group， there were no statistically significant differences in PI3K and Akt protein expression in the 740Y-P + OXY group. However， the expression levels of p-PI3K， p-Akt， Snail， N-cadherin， and Vimentin were significantly increased （P<0.05）， while E-cadherin expression was significantly decreased （P<0.05）. ConclusionOXY inhibits the PI3K/Akt signaling pathway and suppresses the EMT process， thereby exerting anti-metastatic effects in NSCLC.

Lung cancer， particularly non-small cell lung cancer （NSCLC）， is the malignant tumor with the highest incidence and mortality in China and worldwide. In 2022， the global number of deaths reached 1.8 million， accounting for 18.7% of all cancer-related deaths， seriously threatening human health and life， and posing a severe challenge for prevention and treatment. Although treatment strategies for lung cancer have been continuously enriched in recent years， and progress has been made in targeted therapy and immunotherapy， long-term survival benefits remain limited due to primary or acquired drug resistance， low immune responsiveness， and chemotherapy-related toxicities. Therefore， there is an urgent need to explore safe and effective adjunctive therapeutic strategies. Traditional Chinese medicine （TCM）， with its advantages of holistic regulation and individualized syndrome differentiation， has played an increasingly prominent role in comprehensive cancer treatment. TCM holds that "Yang deficiency leads to accumulation" is a key pathogenesis of tumors. Based on the theory that "Yang transforms Qi， while Yin forms substance"， deficiency of Yang Qi results in impaired warming and transformation functions， leading to internal accumulation of Yin-cold. This is closely related to dysregulation of the immune microenvironment， "cold tumor" characteristics， and dysfunction of the neuroendocrine system in modern medicine. Accordingly， the therapeutic strategy of "warming Yang， supporting healthy Qi， and combating cancer" has gained increasing attention. In recent years， commonly used Yang-warming Chinese herbs， including Aconiti Lateralis Radix Praeparata， Zingiberis Rhizoma， Cinnamomi Cortex， Epimedii Folium， and Psoraleae Fructus， as well as their active constituents， have achieved notable progress in anti-lung cancer research by regulating multiple signaling pathways， inducing apoptosis， inhibiting metastasis， and reversing drug resistance. In addition， Yang-warming formulae such as Sini Tang and Yanghe Tang have shown promising effects in alleviating myelosuppression， improving cancer-related fatigue， managing malignant pleural effusion， and relieving cancer pain. These therapies exhibit toxicity-reducing and efficacy-enhancing effects， significantly improving patients' quality of life and survival benefits. To systematically summarize the roles and mechanisms of Yang-warming Chinese herbal medicines and compound formulae in lung cancer， this paper provides a comprehensive review of recent advances， aiming to offer insights for the clinical practice of TCM in the prevention and treatment of lung cancer.

OBJECTIVE To evaluate the efficacy of Compound glutamine enteric-coated capsules in the treatment and prevention of radiotherapy- and chemotherapy-related intestinal dysfunction in patients with malignant tumors. METHODS PubMed， Embase， CNKI， and Wanfang data were searched to collect randomized controlled trial （RCT） and cohort studies comparing Compound glutamine enteric-coated capsules （experimental group） with or without other treatments versus other treatments or blank control （control group）. The search period was from the establishment of each database to November 19， 2025. After literature screening， data extraction， and quality assessment， a meta-analysis was performed using RevMan 5.4 software. RESULTS A total of 23 studies were included， involving 2 014 patients. Meta-analysis results showed that the effective rate in the experimental group was significantly higher than that in the control group， the overall incidence and moderate-to-severe incidence of radiotherapy- and chemotherapy-related intestinal dysfunction， quality of life scores， and interleukin-6 levels in the experimental group were significantly lower than those in the control group （ P ＜0.05）. However， no statistically significant differences were observed between the two groups in terms of Karnofsky Performance Status score improvement rate and tumor necrosis factor-α levels （ P ＞0.05）. The results of subgroup analysis based on different medications in the control group showed that， when used for treatment， regardless of whether patients in the control group received blank control or positive control， the efficacy in the experimental group was significantly higher than that in the control group （ P ＜0.05）. When used for prevention， compared with patients who received blank control in the control group， the overall incidence and the incidence of moderate-to-severe radiotherapy- and chemotherapy-related intestinal dysfunction in the experimental group were significantly reduced （ P ＜0.05）. No statistically significant difference was found in the overall incidence or incidences of moderate-to-severe radiotherapy- and chemotherapy-related intestinal dysfunction with positive control between the two groups （ P ＞0.05）. CONCLUSIONS Compound glutamine enteric-coated capsules can effectively treat and prevent radiotherapy- and chemotherapy-related intestinal dysfunction in patients with malignant tumors， improve patients’ quality of life， and alleviate inflammatory responses.

As a patented characteristic medicine of Yi ethnic minority， Pingxuan capsules have the effects of nourishing the liver and kidney， pacifying the liver， and subduing Yang. With the main indications of dizziness， headache， palpitations， tinnitus， insomnia， dreaminess， waist and knee soreness caused by liver-kidney deficiency and liver Yang upward disturbance， Pingxuan capsules are widely used in the treatment of posterior circulation ischemic vertigo， vestibular migraine， benign paroxysmal positional vertigo. However， the current knowledge is limited regarding the efficacy， syndrome differentiation， and safety of this medicine. On the basis of summarizing the experience of clinicians and the existing evidence， this study invites clinical experts of traditional Chinese and Western medicine， pharmaceutical experts， and methodological experts from relevant fields across China to conduct evidence-based evaluation of Pingxuan capsules. The evaluation follows the Specifications for the Development of Clinical Expert Consensus on Chinese Patent Medicines issued by the Standardization Office of the China Association of Chinese Medicine， and reaches 5 recommendations and 16 consensus suggestions. The consensus clarifies the clinical applications， efficacy， dose， course of treatment， combination of medicines， precautions， and contraindications of Pingxuan capsules in the treatment of vertigo and explains the safety of clinical application. This consensus is applicable to clinicians （traditional Chinese medicine， Western medicine， and integrated traditional Chinese and Western medicine） and pharmacists in tertiary hospitals， secondary hospitals， and community-level medical and health institutions across China， providing a reference for the rational use of Pingxuan capsules in the treatment of vertigo. It is hoped that the promotion of this consensus can facilitate the rational use of drugs in clinical practice， reduce the risk of drug use， and give full play to the advantages of Pingxuan capsules in the treatment of vertigo diseases. This consensus has been reviewed and published by the China Association of Chinese Medicine， with the number GS/CACM330-2023.

BACKGROUND:Neuregulin 1 has been shown to be characterized in cell proliferation,differentiation,and vascular growth.Human amniotic mesenchymal stem cells are important seed cells in the field of tissue engineering,and have been shown to be involved in tissue repair and regeneration. OBJECTIVE:To construct human amniotic mesenchymal stem cells overexpressing neuregulin 1 and investigate their proliferation and migration abilities,as well as their effects on wound healing. METHODS:(1)Human amniotic mesenchymal stem cells were in vitro isolated and cultured and identified.(2)A lentivirus overexpressing neuregulin 1 was constructed.Human amniotic mesenchymal stem cells were divided into empty group,neuregulin 1 group,and control group,and transfected with empty lentivirus and lentivirus overexpressing neuregulin 1,or not transfected,respectively.(3)Edu assay was used to detect the proliferation ability of the cells of each group,and Transwell assay was used to detect the migration ability of the cells.(4)The C57 BL/6 mouse trauma models were constructed and randomly divided into control group,empty group,neuregulin 1 group,with 8 mice in each group.Human amniotic mesenchymal stem cells transfected with empty lentivirus or lentivirus overexpressing neuregulin-1 were uniformly injected with 1 mL at multiple local wound sites.The control group was injected with an equal amount of saline.(5)The healing of the trauma was observed at 1,7,and 14 days after model establishment.Histological changes of the healing of the trauma were observed by hematoxylin-eosin staining.The expression of CD31 on the trauma was observed by immunohistochemistry. RESULTS AND CONCLUSION:(1)Human amniotic mesenchymal stem cells overexpressing neuregulin-1 were successfully constructed.The mRNA and protein expression of intracellular neuregulin 1 was significantly up-regulated compared with the empty group(P<0.05).(2)The overexpression of neuregulin 1 promoted the migratory ability(P<0.01)and proliferative ability of human amniotic mesenchymal stem cells(P<0.05).(3)Human amniotic mesenchymal stem cells overexpressing neuregulin 1 promoted wound healing in mice(P<0.05)and wound angiogenesis(P<0.05).The results showed that overexpression of neuregulin 1 resulted in an increase in the proliferative and migratory capacities of human amniotic mesenchymal stem cells,significantly promoting wound healing and angiogenesis.