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.

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.

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.

Magnolol, a compound extracted from Magnolia officinalis, demonstrates potential efficacy in addressing metabolic dysfunction and cardiovascular diseases. Its biological activities encompass anti-inflammatory, antioxidant, anticoagulant, and anti-diabetic effects. Growth/differentiation factor-15 (GDF-15), a member of the transforming growth factor β superfamily, is considered a potential therapeutic target for metabolic disorders. This study investigated the impact of magnolol on GDF-15 production and its underlying mechanism. The research examined the pharmacological effect of magnolol on GDF-15 expression in vitro and in vivo, and determined the involvement of endoplasmic reticulum (ER) stress signaling in this process. Luciferase reporter assays, chromatin immunoprecipitation, and in vitro DNA binding assays were employed to examine the regulation of GDF-15 by activating transcription factor 4 (ATF4), CCAAT enhancer binding protein γ (CEBPG), and CCCTC-binding factor (CTCF). The study also investigated the effect of magnolol and ATF4 on the activity of a putative enhancer located in the intron of the GDF-15 gene, as well as the influence of single nucleotide polymorphisms (SNPs) on magnolol and ATF4-induced transcription activity. Results demonstrated that magnolol triggers GDF-15 production in endothelial cells (ECs), hepatoma cell line G2 (HepG2) and hepatoma cell line 3B (Hep3B) cell lines, and primary mouse hepatocytes. The cooperative binding of ATF4 and CEBPG upstream of the GDF-15 gene or the E1944285 enhancer located in the intron led to full-power transcription of the GDF-15 gene. SNP alleles were found to impact the magnolol and ATF4-induced transcription activity of GDF-15. In high-fat diet ApoE^-/- mice, administration of magnolol induced GDF-15 production and partially suppressed appetite through GDF-15. These findings suggest that magnolol regulates GDF-15 expression through priming of promoter and enhancer activity, indicating its potential as a drug for the treatment of metabolic disorders.
Lignans/pharmacology* ; Growth Differentiation Factor 15/metabolism* ; Animals ; Biphenyl Compounds/pharmacology* ; Endoplasmic Reticulum Stress/drug effects* ; Activating Transcription Factor 4/genetics* ; Mice ; Humans ; Male ; Magnolia/chemistry* ; CCAAT-Enhancer-Binding Proteins/genetics* ; Mice, Inbred C57BL

Objective To investigate the therapeutic effects and mechanisms of Yishen Shengyang formula in allergic rhinitis(AR)by regulating the transcription factor BTB and CNC homology 2(Bach2)to promote regulatory T cell(Treg cell)differentiation.Methods AR mouse models were established via ovalbumin(OVA)sensitization and randomly divided into control group,AR model group(AR group),Yishen Shengyang formula group and dexamethasone group.Nasal symptoms were evaluated using behavioral scores;Histopathological changes in nasal mucosa were observed via hematoxylin-eosin and periodic acid Schiff stain;Serum levels of OVA-specific immunoglobulin E(sIgE),interleukin-4(IL-4),and transforming growth factor-β(TGF-β)were measured by enzyme linked immunosorbent assay;Splenic Treg proportions were analyzed via flow cytometry;Bach2 protein expression was assessed by Western blot.Results Compared with control group,AR group mice showed significantly increased behavioral scores(P<0.05),goblet cell hyperplasia,inflammatory infiltration,elevated OVA-sIgE and IL-4 levels(P<0.05),reduced TGF-β(P<0.05),and decreased splenic Treg proportions and Bach2 expression(P<0.05).Yishen Shengyang formula treatment alleviated nasal symptoms(P<0.05),mitigated mucosal damage,decreased OVA-sIgE and IL-4,increased TGF-β(P<0.05),and upregulated Treg proportions and Bach2 expression(P<0.05),with efficacy comparable to dexamethasone.Conclusion Yishen Shengyang formula demonstrates potential therapeutic effects on allergic rhinitis by upregulating Bach2 expression and promoting Treg cell differentiation.This study provides a novel strategy and experimental basis for the traditional Chinese medicine treatment of AR.

Objective:To investigate the management of cancer pain and the clinical practices of hospice care across 11 cities in Zhejiang Province.Methods:From May 22 to 29, 2023, the Zhejiang Provincial Health Commission conducted a survey to assess the current status of hospice care practitioners regarding cancer pain management, the practices employed by medical staff in managing cancer pain, and the understanding of medical personnel concerning self-controlled analgesia for cancer pain treatment in Zhejiang Province.Results:A total of 505 questionnaires were collected from 198 hospitals across 11 cities in the province.Among the medical staff in secondary and tertiary medical institutions, 85.71%(198 out of 231)participated in the management of cancer pain in patients.Oral analgesics emerged as the most commonly used treatment for pain outbreaks, accounting for 38.53%(89 out of 231)of cases.Additionally, 37.66%(87 out of 231)of medical personnel were involved in the development of self-controlled analgesia devices within their institutions.Conclusions:In the management of cancer pain within hospice care, it is essential to enhance the theoretical training of medical staff, ensure the availability of basic analgesic medications, and establish standardized management protocols for the entire process as promptly as possible.

Objective:To evaluate the optimization effects of ciprofol-based intravenous anesthesia in elderly patients undergoing retroperitoneal laparoscopic radical nephrectomy.Methods:This study was a prospective randomized controlled study. Eighty elderly patients scheduled for elective retroperitoneal laparoscopic radical nephrectomy were randomized to receive either ciprofol-based (group C) or propofol-based intravenous anesthesia (P group), with 40 patients in each group. Anesthesia was induced by intravenous injection of ciprofol 0.4 mg/kg and maintained by intravenous infusion of ciprofol and remifentanil during operation in group C. In group P, anesthesia was induced by intravenous injection of propofol 1.5 mg/kg and maintained by intravenous infusion of propofol and remifentanil during operation. The onset time of sedative effect following anesthesia induction, hypotension and injection pain during induction and intraoperative hypotension were recorded.Results:Compared to P group, the incidence of hypotension and injection pain during induction was significantly decreased (28% vs 10%, 60% vs 18%, P<0.05); although the difference in the incidence of intraoperative hypotension was not statistically significant (25% vs 15%, P>0.05), the RR was 0.6; no significant change was found in the onset time of sedative effect following anesthesia induction in C group ( P>0.05). Conclusions:Compared to propofol-based intravenous anesthesia, ciprofol-based intravenous anesthesia has certain optimization effects in elderly patients undergoing retroperitoneal laparoscopic radical nephrectomy.

Chronic wounds, defined as persistent failure to heal due to specific etiological factors, remain a major clinical challenge. Current standard interventions such as negative pressure wound therapy are limited by complications like hypergranulation and poor patient compliance, while emerging stem cell-based therapies carry potential tumorigenic risks. Consequently, identifying strategies to safely and effectively accelerate wound healing continues to be a critical focus in contemporary clinical research. Platelet-rich plasma derived extracellular vesicles (PRP-EVs) are extracellular vesicles released by platelets after activation. They have the characteristics of autologous origin, higher safety, and more mild and convenient clinical application. Studies have shown that PRP-EVs are rich in bioactive molecules such as lipids, proteins and RNA, which have outstanding performance in regulating wound inflammation, promoting angiogenesis, enhancing cell migration and proliferation, and are expected to become an effective tool for the treatment of chronic wounds. This review discusses the methods, mechanisms of action, and challenges associated with the use of PRP-EVs in chronic wound management, providing a foundation for future research and clinical applications in this field.

BACKGROUND:Gait dysfunction is one of the significant reasons for patient dissatisfaction following total knee arthroplasty.Clinical studies have identified a relationship between the preoperative strength of the quadriceps and hamstring muscles and postoperative gait dysfunction,but the exact nature of this correlation is not yet fully understood.OBJECTIVE:To investigate the correlation between the preoperative strength of the quadriceps and hamstring muscles and postoperative gait dysfunction in total knee arthroplasty.METHODS:A retrospective analysis was conducted on longitudinal data from 70 patients who underwent unilateral primary total knee arthroplasty.Preoperative measurements included peak torque of the extensor and flexor muscles,peak torque/body weight,and total work.Six months postoperatively,the Timed Up and Go Test and gait speed were measured.Ridge regression analysis was used to identify factors influencing postoperative gait function.RESULTS AND CONCLUSION:(1)Preoperative peak torque,peak torque/body weight,and total work of the extensor muscles,as well as the peak torque and total work of the flexor muscles,showed a very strong positive correlation with postoperative gait speed(P＜0.001).The preoperative flexor muscle peak torque/body weight had a strong positive correlation with postoperative gait speed(P＜0.001).Preoperative extensor and flexor muscle peak torques,peak torque/body weight,and total work showed a very strong negative correlation with results from postoperative Timed Up and Go Test(P＜0.001).(2)Ridge regression analysis indicated a 94.2％likelihood that preoperative extensor muscle peak torque,peak torque/body weight,and total work,along with flexor muscle peak torque and total work,had a positive impact on gait speed after total knee arthroplasty(P＜0.001).The preoperative flexor muscle peak torque/body weight had a negative impact on postoperative gait speed(P＜0.001).There was an 87.7％likelihood that preoperative extensor and flexor muscle peak torques,peak torque/body weight,and total work,along with flexor muscle peak torque and total work,had a negative impact on postoperative Timed Up and Go Test(P＜0.05),while the flexor muscle peak torque/body weight had no impact on the Timed Up and Go Test(P＞0.05).(3)It is indicated that the strength of the quadriceps and hamstring muscles prior to total knee arthroplasty correlates with postoperative gait speed and Timed Up and Go Test,and can predict the outcomes of postoperative gait function.Enhancing preoperative knee muscle exercises may be a way to reduce the incidence of gait dysfunction following total knee arthroplasty.