1.Research progress in hydrogels in tissue engineering trachea
Wenxuan CHEN ; Yibo SHAN ; Fei SUN ; Zhiming SHEN ; Yi LU ; Jianwei ZHU ; Lei YUAN ; Hongcan SHI
Chinese Journal of Clinical Thoracic and Cardiovascular Surgery 2025;32(08):1195-1199
In cases where a tracheal injury exceeds half the length of the adult trachea or one-third of the length of the child trachea, it becomes difficult to perform end-to-end anastomosis after tracheal resection due to excessive tension at the anastomosis site. In such cases, tracheal replacement therapy is required. Advances in tissue engineering technology have led to the development of tissue engineering tracheal substitutes, which have promising applications. Hydrogels, which are highly hydrated and possess a good three-dimensional network structure, biocompatibility, low immunogenicity, biodegradability, and modifiability, have had wide applications in the field of tissue engineering. This article provides a review of the characteristics, advantages, disadvantages, and effects of various hydrogels commonly used in tissue engineering trachea in recent years. Additionally, the article discusses and offers prospects for the future application of hydrogels in the field of tissue engineering trachea.
2.COPB1 promotes the development and progression of esophageal squamous cell carcinoma by activating the PI3K/AKT pathway and regulating the tumor immune microenvironment
LIN Yan ; YU Shuangjian ; JIA Sifan ; LI Feiyu ; ZHAO Chenpu ; DONG Zhiming ; SHEN Supeng ; LIANG Jia ; GUO Yanli
Chinese Journal of Cancer Biotherapy 2025;32(12):1236-1246
[摘 要] 目的:探究包被蛋白复合体β1亚基(COPB1)在食管鳞状细胞癌(ESCC)中的表达,及其对ESCC细胞恶性生物学行为的影响、作用机制及临床意义。方法:采用2014~2018年间在河北医科大学第四医院生物样本库中82例ESCC组织及癌旁组织,常规培养正常食管鳞状上皮细胞HEEC和食管癌细胞KYSE-150、KYSE-170、Eca109、TE1、KYSE-30、KYSE-450,用转染试剂将pcDNA3.1-vector(空载体)、pcDNA3.1-COPB1载体,si-NC和si-COPB1转染至KYSE-150、TE1细胞中,记为NC、COPB1-OE、si-NC和si-COPB1组。用数据库数据分析COPB1 mRNA在泛癌组织中的表达及其表达与免疫细胞浸润的关系,qPCR法检测ESCC组织和细胞中COPB1、PIK3CB、CD68、CD163、CD206、ARG1、IL-10 mRNA水平表达情况,WB法检测ESCC组织和各组细胞中的COPB1、PI3K、CD68、CD163、CD206、p-AKT蛋白表达,克隆形成实验和MTS实验检测各组细胞的增殖能力,划痕愈合实验和Transwell实验检测各组细胞的迁移和侵袭能力,免疫组织化学染色(IHC)法检测ESCC组织中COPB1和CD206蛋白表达。以人单核细胞白血病细胞(THP-1)构建巨噬细胞模型,用佛波酯(PMA)和IL-3和IL-4和ESCC细胞上清液诱导巨噬细胞转型,用qPCR和WB法检测CD68和CD206m RNA和蛋白的表达。结果:COPB1在泛癌组织和ESCC组织中均呈高表达且与淋巴结转移和TNM分期有关联(均P < 0.01),COPB1高表达的ESCC患者总生存期短(P < 0.05),COPB1是潜在的ESCC的诊断标志物。COPB1在KYSE-150和TE1细胞中也呈高表达(均P < 0.05),过表达或敲减COPB1可明显抑制或促进KYSE-150和TE1细胞的增殖能力、迁移和侵袭能力(均P < 0.05)。COPB1表达变化诱导的差异表达基因主要富集于PI3K/AKT通路(均P < 0.001), COPB1可促进PI3K/AKT通路的活化(P < 0.05),COPB1高表达可导致M2型巨噬细胞浸润增加(P < 0.05),COPB1高表达促进TAM/M2极化(P < 0.05)。结论:COPB1在ESCC组织中呈高表达,其可激活PI3K/AKT通路及调控肿瘤免疫微环境促进 ESCC发生发展,COPB1有望成为ESCC诊断和预后的生物标志物及治疗靶点。
3.Traditional Chinese Medicine Regulates Signaling Pathways Related to Precancerous Lesions of Gastric Cancer: A Review
Maofu ZHANG ; Xinyu LI ; Yanyun SHEN ; Yeyuan LIU ; Jialin ZHONG ; Lulu CHEN ; Haihong ZHAO ; Zhongyang SONG ; Zhiming ZHANG
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(4):297-306
Precancerous lesions of gastric cancer (PLGC) are a group of pathological changes caused by abnormalities in the structure, morphology, and differentiation of gastric mucosal epithelial cells. Since the early symptoms are hidden and non-specific, PLGC is not easy to be diagnosed and it has often developed into intermediate or advanced gastric cancer once being diagnosed and missed the best time for treatment. Accordingly, the incidence of this disease is increasing year by year, which lifts a heavy burden on the patients. The pathogenesis of PLGC is complex, involving inflammatory microenvironment, bile reflux, glycolysis, autophagy, and apoptosis. Currently, PLGC is mainly treated with anti-inflammatory and endoscopic therapies, which are difficult to curb the development of PLGC. Therefore, seeking a safe and effective therapy is an important topic of modern research. Traditional Chinese medicine (TCM), characterized by treatment based on syndrome differentiation and a holistic view, exerts effects via multiple pathways, mechanisms, and targets. Recent studies have confirmed that TCM can regulate the phosphatidylinositol 3-kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR), Wnt/β-catenin, Sonic Hedgehog, nuclear factor-κB (NF-κB), Janus kinase/signal transducer and activator of transcription (JAK/STAT), hypoxia-inducible factor-1α (HIF-1α), neurogenic locus notch homolog protein (Notch), nuclear factor E2-related factor 2 (Nrf2) and other signaling pathways. By targeting these pathways, TCM can inhibit aerobic glycolysis, reduce oxidative stress, repair the inflammatory microenvironment, regulate cellular autophagy, and promote vascular normalization, thereby delaying or reversing PLGC. However, few researchers have systematically summarized the TCM regulation of PLGC-associated pathways. By reviewing the relevant articles at home and abroad, this paper summarized the roles of the above signaling pathways in the development of PLGC and the research progress in the regulation of signaling pathways by TCM in the treatment of PLGC, with a view to providing a new theoretical basis for the clinical research on PLGC and the drug development for this disease.
4.Research progress of traditional Chinese medicine intervention in chemotherapy renal injury
Yeyuan LIU ; Yafeng QI ; Maofu ZHANG ; Xinyu LI ; Yanyun SHEN ; Yu LIU ; Shangzu ZHANG ; Yangyang LI ; Liying ZHANG ; Zhiming ZHANG
Chinese Journal of Clinical Pharmacology and Therapeutics 2025;30(4):556-569
Renal injury is one of the common ad-verse reactions in the clinical application of chemo-therapy drugs,which is the main reason why the chemotherapy can not be carried out in the whole cycle.The pathological mechanism of chemothera-py-induced renal injury is very complicated,mainly involving oxidative stress,inflammatory response,apoptosis,mitochondrial dysfunction,and regula-tion of transporters,causing pathological damage to renal tubules or glomeruli.At present,there is no specific pharmacological intervention for the treatment of chemotherapy-induced renal injury.As a treasure of traditional Chinese medicine,tradi-tional Chinese medicine has the advantages of overall regulation,multi-targeting,small adverse re-actions and no obvious drug dependence in the prevention and treatment of chemotherapy-in-duced renal injury.In recent years,there have been more and more studies on the intervention of che-motherapy-induced renal injury by multi-compo-nent and multi-directional intervention of active components,extracts and compounds of tradition-al Chinese medicine,and some progress has been made.A large number of studies have shown that the potential mechanisms of traditional Chinese medicine in preventing and treating renal injury in-duced by chemotherapy include inhibiting oxida-tive stress,reducing inflammatory response and in-hibiting apoptosis.Although there are many stud-ies on the mechanism of action of traditional Chi-nese medicine in the treatment of chemotherapy-induced renal injury,there is still a lack of systemat-ic review.Based on this,this paper summarizes the mechanism of renal injury induced by chemothera-py and the intervention of traditional Chinese medi-cine,so as to provide theoretical support for its clinical treatment and new drug innovation.
5.Research progress of traditional Chinese medicine intervention in chemotherapy renal injury
Yeyuan LIU ; Yafeng QI ; Maofu ZHANG ; Xinyu LI ; Yanyun SHEN ; Yu LIU ; Shangzu ZHANG ; Yangyang LI ; Liying ZHANG ; Zhiming ZHANG
Chinese Journal of Clinical Pharmacology and Therapeutics 2025;30(4):556-569
Renal injury is one of the common ad-verse reactions in the clinical application of chemo-therapy drugs,which is the main reason why the chemotherapy can not be carried out in the whole cycle.The pathological mechanism of chemothera-py-induced renal injury is very complicated,mainly involving oxidative stress,inflammatory response,apoptosis,mitochondrial dysfunction,and regula-tion of transporters,causing pathological damage to renal tubules or glomeruli.At present,there is no specific pharmacological intervention for the treatment of chemotherapy-induced renal injury.As a treasure of traditional Chinese medicine,tradi-tional Chinese medicine has the advantages of overall regulation,multi-targeting,small adverse re-actions and no obvious drug dependence in the prevention and treatment of chemotherapy-in-duced renal injury.In recent years,there have been more and more studies on the intervention of che-motherapy-induced renal injury by multi-compo-nent and multi-directional intervention of active components,extracts and compounds of tradition-al Chinese medicine,and some progress has been made.A large number of studies have shown that the potential mechanisms of traditional Chinese medicine in preventing and treating renal injury in-duced by chemotherapy include inhibiting oxida-tive stress,reducing inflammatory response and in-hibiting apoptosis.Although there are many stud-ies on the mechanism of action of traditional Chi-nese medicine in the treatment of chemotherapy-induced renal injury,there is still a lack of systemat-ic review.Based on this,this paper summarizes the mechanism of renal injury induced by chemothera-py and the intervention of traditional Chinese medi-cine,so as to provide theoretical support for its clinical treatment and new drug innovation.
6.Effects of Quhan Zhufeng Mixture in Regulating NDRG2/JAK2/STAT3 Signaling Pathway on the Proliferation and Apoptosis of RA-FLS
Xiaojun SU ; Wenju ZHU ; Ying GUO ; Huan WANG ; Qian HE ; Zhiming ZHANG ; Xuemei TIAN ; Haili SHEN ; Jun MA ; Qiang BAO
Chinese Journal of Information on Traditional Chinese Medicine 2025;32(7):119-126
Objective To explore the mechanism of Quhan Zhufeng Mixture on proliferation and apoptosis of rheumatoid arthritis fibroblast-like synoviocyte(RA-FLS)based on NDRG2/JAK2/STAT3 signaling pathway.Methods RA-FLS cells were cultured in vitro,and were divided into ① blank serum group,methotrexate group,Quhan Zhufeng Mixture low-,medium-and high-dosage groups;② blank serum group,AG490 group,Quhan Zhufeng Mixture low-,medium-and high-dosage groups.Different concentrations of drug-containing serum were used to intervene cells.Cell proliferation was detected by CCK-8 method,apoptosis was detected by flow cytometry,and mRNA expressions of Bax,Bcl-2,Caspace-3,Caspace-9,N-myc downstream regulatory gene 2(NDRG2),Janus kinase 2(JAK2)and signal transduction and transcription activator 3(STAT3)were detected by RT-qPCR,Western blot was used to detect the protein expressions of Bax,Bcl-2,Caspace-3,Caspace-9,NDRG2,JAK2,STAT3,p-JAK2 and p-STAT3 in cells.Results Compared with the blank serum group,cell survival rate in methotrexate group,Quhan Zhufeng Mixture all dosage groups significantly decreased(P<0.01),the apoptosis rate significantly increased(P<0.01),the mRNA and protein expressions of Bax and Caspase-9 significantly increased(P<0.05,P<0.01),while the mRNA and protein expression of Bcl-2 significantly decreased(P<0.01),and Caspase-3 mRNA and protein expression in methotrexate group and Quhan Zhufeng Mixture medium-and high-dosage groups significantly increased(P<0.01).Compared with the blank serum group,the mRNA and protein expression of NDRG2 significantly increased in Quhan Zhufeng Mixture all dosage groups(P<0.05,P<0.01),the mRNA and protein expressions of JAK2 and STAT3 were significantly reduced in AG490 group and Quhan Zhufeng Mixture medium-and high-dosage groups(P<0.05,P<0.01),and the expressions of p-JAK2 and p-STAT3 proteins were significantly reduced(P<0.01).Conclusion Quhan Zhufeng Mixture can regulate the proliferation and apoptosis of RA-FLS by regulating the activity of NDRG2/JAK2/STAT3 signaling pathway,playing a role in treating rheumatoid arthritis.
7.Effects of Quhan Zhufeng Mixture in Regulating NDRG2/JAK2/STAT3 Signaling Pathway on the Proliferation and Apoptosis of RA-FLS
Xiaojun SU ; Wenju ZHU ; Ying GUO ; Huan WANG ; Qian HE ; Zhiming ZHANG ; Xuemei TIAN ; Haili SHEN ; Jun MA ; Qiang BAO
Chinese Journal of Information on Traditional Chinese Medicine 2025;32(7):119-126
Objective To explore the mechanism of Quhan Zhufeng Mixture on proliferation and apoptosis of rheumatoid arthritis fibroblast-like synoviocyte(RA-FLS)based on NDRG2/JAK2/STAT3 signaling pathway.Methods RA-FLS cells were cultured in vitro,and were divided into ① blank serum group,methotrexate group,Quhan Zhufeng Mixture low-,medium-and high-dosage groups;② blank serum group,AG490 group,Quhan Zhufeng Mixture low-,medium-and high-dosage groups.Different concentrations of drug-containing serum were used to intervene cells.Cell proliferation was detected by CCK-8 method,apoptosis was detected by flow cytometry,and mRNA expressions of Bax,Bcl-2,Caspace-3,Caspace-9,N-myc downstream regulatory gene 2(NDRG2),Janus kinase 2(JAK2)and signal transduction and transcription activator 3(STAT3)were detected by RT-qPCR,Western blot was used to detect the protein expressions of Bax,Bcl-2,Caspace-3,Caspace-9,NDRG2,JAK2,STAT3,p-JAK2 and p-STAT3 in cells.Results Compared with the blank serum group,cell survival rate in methotrexate group,Quhan Zhufeng Mixture all dosage groups significantly decreased(P<0.01),the apoptosis rate significantly increased(P<0.01),the mRNA and protein expressions of Bax and Caspase-9 significantly increased(P<0.05,P<0.01),while the mRNA and protein expression of Bcl-2 significantly decreased(P<0.01),and Caspase-3 mRNA and protein expression in methotrexate group and Quhan Zhufeng Mixture medium-and high-dosage groups significantly increased(P<0.01).Compared with the blank serum group,the mRNA and protein expression of NDRG2 significantly increased in Quhan Zhufeng Mixture all dosage groups(P<0.05,P<0.01),the mRNA and protein expressions of JAK2 and STAT3 were significantly reduced in AG490 group and Quhan Zhufeng Mixture medium-and high-dosage groups(P<0.05,P<0.01),and the expressions of p-JAK2 and p-STAT3 proteins were significantly reduced(P<0.01).Conclusion Quhan Zhufeng Mixture can regulate the proliferation and apoptosis of RA-FLS by regulating the activity of NDRG2/JAK2/STAT3 signaling pathway,playing a role in treating rheumatoid arthritis.
8.Erratum: Author correction to "Cascade two-stage tumor re-oxygenation and immune re-sensitization mediated by self-assembled albumin-sorafenib nanoparticles for enhanced photodynamic immunotherapy" Acta Pharm Sin B (2022) 4204-4223.
Zaigang ZHOU ; Jiashe CHEN ; Yu LIU ; Chunjuan ZHENG ; Wenjuan LUO ; Lele CHEN ; Shen ZHOU ; Zhiming LI ; Jianliang SHEN
Acta Pharmaceutica Sinica B 2024;14(2):900-903
[This corrects the article DOI: 10.1016/j.apsb.2022.07.023.].
9.A bibliometric analysis of nanoparticles in the treatment of non-small cell lung cancer
Xiangyu XU ; Lei YUAN ; Fei SUN ; Zhiming SHEN ; Yibo SHAN ; Yi LU ; Jianwei ZHU ; Wenxuan CHEN ; Hongcan SHI
Chinese Journal of Clinical Thoracic and Cardiovascular Surgery 2024;31(08):1139-1147
Objective To analyze the current research application status and hotspots of nanoparticles in the treatment of non-small cell lung cancer (NSCLC) and predict the future development trend. Methods The Web of Science database was searched for literatures on nanoparticles use in the treatment of NSCLC from inception to November 2022. CiteSpace, VOSviewer and literature measurement analysis online platform (https://bibliometric.com/) were used for the visual analysis of the number of documents, source journals, authors, organizations, countries and keywords. Results A total of 742 English literatures were included. The results showed that the number of published literatures increased year by year from 2011 and reached the peak in 2020. Researches on nanoparticles and NSCLC treatment were mainly concentrated in China, the United States, India and Japan. China is a major research country in this field, but it lacked cooperation with other countries and related institutions. Among numerous research institutions, the Chinese Academy of Sciences was the authoritative and backbone force in this research field, with the number of published literatures ranking first and the research achievements outstanding. The keyword analysis found that "poly lactic-co-glycolic acid nanoparticles (PLGA NPs)" and "photothermal therapy" had become the latest breakout words since 2018. Moreover, the occurrence frequency of related keywords such as "drug delivery" increased significantly, indicating that the application of PLGA NPs in photothermal therapy might be the current research hotspot and future development trend of NSCLC treatment. Conclusion Currently, the domestic research on the treatment of nanoparticles and NSCLC is in a leading position in the world. The organic combination of nanoparticles with different materials and other NSCLC therapies is expected to improve the prognosis of NSCLC patients. In the future, attempts to develop nanoparticles with different sources and structures and combined with photothermal therapy for the treatment of NSCLC may become a research hotspot of nanoparticles in the treatment of NSCLC.
10.Mechanism of Bone Destruction in Rheumatoid Arthritis Based on the Theory of Kidney Deficiency and Essence Deficiency
Wenju ZHU ; Xiaojun SU ; Qian HE ; Huan WANG ; Zhiming ZHANG ; Haili SHEN ; Xiaotao YE
Journal of Traditional Chinese Medicine 2024;65(19):2045-2049
Rheumatoid arthritis is a common clinical autoimmune disease characterized by persistent synovitis and pannus formation. In late stage, irreversible destruction and deformation of bone and joint may occur. In this paper, the authors believe that kidney deficiency and essence deficiency is the core mechanism of rheumatoid arthritis bone destruction, and its disease evolution law is summarized as "marrow reduction, flesh flaccid, collaterals blocked". On the basis of modern medical understanding of bone destruction in rheumatoid arthritis, it is considered that the mechanism in Chinese medicine of "marrow reduction, flesh flaccid, collaterals blocked" ultimately leads to bone destruction, is similar to that in the western medicine of abnormal differentiation of osteoclasts, high expression of nuclear factor-κB receptor activator of ligand, and abnormal expression of inflammatory factors. This point of view may provide a more comprehensive and scientific understanding of the key pathogenic mechanism of bone destruction in rheumatoid arthritis.

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