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Yangfei Kongliu Formula, a compound Chinese herbal medicine, combined with cisplatin, inhibits growth of lung cancer cells through transforming growth factor-β1 signaling pathway

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Journal of Integrative Medicine 2017年第3期15卷 242-251页

作者： Shui-jie Shen Yong-hong Zhang Xiao-xia Gu Shui-ju Jiang Ling-jun Xu The First Clinical Medical College Nanjing University of Chinese Medicine Department of Oncology Nantong Hospital of Traditional Chinese MedicineNanjing University of Chinese Medicine Department of Respiratory Medicine Nantong Third People's Hospital

OBJECTIVE： To investigate the tumor inhibition effect of Yangfei Kongliu Formula （YKF）, a compound Chinese herbal medicine, combined with cisplatin （DDP） and its action mechanisms. METHODS： C57BL/6 mice with Lewis lung carcinoma were divided into six groups： control group （C）, DDP group （2 mg/kg, DDP）, low-dose YKF group （2.43 g/kg, L）, high-dose YKF group （24.3 g/kg, H）, low- dose YKF combined with DDP group （L ＋ DDP） and high-dose YKF combined with DDP group （H ＋ DDP）. transforming growth factor-β1 （TGF-β1）, mothers against decapentaplegic homolog 3 （Smad3） and Smad7 levels were measured with quantitative real-time polymerase chain reaction （qPCR）, Western blotting and immunohistochemistry. An enzyme-linked immunosorbent assay was used to analyze the expressions of interleukin-2 （IL-2） and tumor necrosis factor-α （TNF-α）. RESULTS： YKF combined with DDP significantly inhibited the growth and metastasis of tumors relative to the control group, and YKF groups （P 〈 0.05）. There was no significant difference between high-dose YKF group and low-dose YKF group （P 〉 0.05）. We also found that the expression levels of TGF-β1 and Smad3 were both significantly decreased by YKF relative to the control group （P 〈 0.05）. Furthermore, after treatment with YKF combined with DDP, the expression levels of TGF-β1 and Smad3 were decreased but the expression level of Smad7 was increased relative to the DDP group （P 〈 0.05）. Compared to the DDP group, the combination of YKF and DDP enhanced the effect of tumor inhibition （P 〈 0.05）, showing obvious synergy between YKF and DDP. Treatment with DDP or YKF decreased serum levels of IL-2 and TNF-α relative to the control group （P 〈 0.05）. Furthermore, the expression levels of IL-2 and TNF-α were significantly decreased when treated with YKF in combination with DDP. Co-treatment with YKF and DDP significantly inhibited tumor growth, decreased the expressions of TGF-β1, Smad3, IL-2 and TNF-α and increased the expression of Smad7; these differences were significant relative to both YKF group

关键词： cisplatin transforming growth factor-β1 Smad3 Smad7 lung cancer drugs, Chinese herbal

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transforming growth factor-β1 phage model peptides isolated from a phage display 7-mer peptide library can inhibit the activity of keloid fibroblasts

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Chinese Medical Journal 2011年第3期124卷 429-435页

作者： ZONG Xian-lei JIANG Du-yin WANG Ji-chang LIU Jun-li LIU Zhen-zhong CAI Jing-long Institute of Tissue Engineering the Second Hospital Shandong University Jinan Shandong 250033 China Department of Plastic and Burn Surgery the Second Hospital Shandong University Jinan Shandong 250033 China Plastic Surgery Hospital Chinese Academy of Medical SciencesBeijing 100144 China Institute of Tissue Engineering the Second Hospital Shandong University Jinan Shandong 250033 China Department of Plastic and Burn Surgery the Second Hospital Shandong University Jinan Shandong 250033 China Department of Plastic and Burn Surgery the Second Hospital Shandong University Jinan Shandong 250033 China Lab of Clinical Molecular Biology the Second Hospital Shandong University Jinan Shandong 250033 China Plastic Surgery Hospital Chinese Academy of Medical SciencesBeijing 100144 China

Background transforming growth factor-β1 （TGF-β1） is known to have a role in keloid formation through the activation of fibroblasts and the acceleration of collagen deposition. The objective of this current study was to isolate TGF-β1 phage model peptides from a phage display 7-mer peptide library to evaluate their therapeutic effect on inhibiting the activity of keloid fibroblasts.Methods A phage display 7-mer peptide library was screened using monoclonal anti-human TGF-β1 as the target to obtain specific phages containing ectogenous model peptides similar to TGF-β1. Enzyme-linked immunosorbent assay （ELISA） was performed to select monoclonal phages with good binding activity, which underwent DNA sequencing. MTT assay and apoptosis assessment were used to evaluate the biological effects of the phage model peptides on keloid fibroblasts. Immunofluorescence assay was employed to show the binding affinity of the model peptides on phages causing keloid fibroblasts. Quantitative real-time PCR analysis was carried out to detect the expressions of nuclear factor κB （NF-κB） mRNA, connective tissue growth factor （CTGF） mRNA and TGF-β receptor Ⅱ （TβRII） mRNA in keloid fibroblasts.Results Specific phages with good results of ELISA were beneficiated. Four phage model peptides were obtained. The data of MTT showed that TGF-β1 and one phage model peptide （No. 4） could promote keloid fibroblasts proliferation,however, three phage model peptides （No. 1-3） could inhibit keloid fibroblasts proliferation. The results of apoptosis assessment showed that the three phage model peptides could slightly induce the apoptosis in keloid fibroblasts. The data of immunofluorescence assay revealed that the model peptides on phages rather than phages could bind to keloid fibroblasts. The findings of quantitative real-time PCR analysis suggested that the expressions of NF-κB mRNA and CTGF mRNA in the three phage model peptide groups decreased, while the expression of TβRII mRNA slightly increased.Conclusions Three phage model peptides isolated

关键词： keloid transforming growth factor-β1 phage display peptide library fibroblast proliferation inhibitor apoptosis

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Construction of recombinant adenovirus co-expression vector carrying the human transforming growth factor-β1 and vascular endothelial growth factor genes and its effect on anterior cruciate ligament fibroblasts

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Chinese Medical Journal 2008年第15期121卷 1426-1432页

作者： WEI Xue-lei LIN Lin HOU Yu FU Xin ZHANG Ji-ying MAO Ze-bin YU Chang-long Institute of Sports Medicine Peking University Third Hospital Beijing 100083 China Department of Biochemistry and Molecular Biology Peking University School of Basic Medical Sciences Beijing 100083 China

Background Remodeling of the anterior cruciate ligament （ACL） graft usually takes longer than expected. Gene therapy offers a radical different approach to remodeling of the graft. In this study, the internal ribosome entry site （IRES） sequence was used to construct a new recombinant adenovirus which permits co-expression of transforming growth factor-β1 （TGFβ1） and vascular endothelial growth factor 165 （VEGF165） genes （named Ad-VEGF165-IRES-TGFβ1）. We investigated the effects of the new adenovirus on the migration of and matrix synthesis by ACL fibroblasts. Methods Adenoviral vector containing TGFβ1 and VEGF165 genes was constructed. ACL fibroblasts were obtained from New Zealand white rabbits. After ACL fibroblasts were exposed to Ad-VEGF165-IRES-TGFβ1, the expression of VEGF165 and TGFβ1 proteins were assessed by enzyme-linked immunosorbent assay （ELISA） and Western blotting analysis. Bioassay of VEGF165 and TGFβ1 proteins were assessed by Western blotting analysis. Proliferation and migration of ACL fibroblasts were assessed by in vitro wound closure assay. Gene expression of collagen type Ⅰ, collagen type Ⅲ, and fibronectin mRNA among matrix markers were assessed by real-time PCR. Results The results showed the successful construction of a recombinant co-expression adenovirus vector containing TGFβ1 and VEGF165 genes. Co-expression of TGFβ1 and VEGF165 can induce relatively rapid and continuous proliferation of ACL fibroblasts and high gene expression of collagen type Ⅰ, collagen type Ⅲ, and fibronectin mRNA among matrix markers. Conclusion Co-expression of TGFβ1 and VEGF165 genes has more powerful and efficient effects on the migration of and matrix synthesis by ACL fibroblasts.

关键词： adenovirus fibroblasts transforming growth factor-β1 vascular endothelial growth factor 165

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transforming growth factor-β1 Induces Transdifferentiation of Fibroblasts into Myofibroblasts in Hyp0Xic Pulmonary Vascular Remodeling

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Acta Biochimica et Biophysica Sinica 2006年第1期38卷 29-36页

作者： Yong-Liang JIANG Ai-Guo DAI Qi-Fang LI Rui-Cheng HU Department of Respiratory Medicine,Hunan Institute of Gerontology,Hunan Province Geriatric Hospital,Changsha 410001,China Department of Respiratory Medicine Hunan Institute of Gerontology Hunan Province Geriatric Hospital Changsha 410001 China

The muscularization of non-muscular pulmonary arterioles is an important pathological featureof hypoxic pulmonary vascular remodeling.However,the origin of the cells involved in this process is stillnot well understood.The present study was undertaken to test the hypothesis that transforming growthfactor-β1 (TGF-β1) can induce transdifferentiation of fibroblasts into myofibroblasts,which might play akey role in the muscularization of non-muscular pulmonary arterioles.It was found that mean pulmonaryarterial pressure increased significantly after 7 d of hypoxia.Pulmonary artery remodeling index and rightventricular hypertrophy became evident after 14 d of hypoxia.The distribution of nonmuscular,partiallymuscular,and muscular vessels was significantly different after 7 d of hypoxia.Immunocytochemistryresults demonstrated that the expression of co-smooth muscle actin was increased in intra-acinar pulmonaryarteries with increasing hypoxic time.TGF-β1 mRNA expression in pulmonary arterial walls was increasedsignificantly after 14 d of hypoxia,but showed no obvious changes after 3 or 7 d of hypoxia.In pulmonarytunica adventitia and tunica media,TGF-β1 protein staining was poorly positive in control rats,but wasmarkedly enhanced after 3 d of hypoxia,reaching its peak after 7 d Of hypoxia.The myofibroblast phenotypewas confirmed by electron microscopy,which revealed microfilaments and a well-developed rough endo-plasmic reticulum.Taken together,our results suggested that TGF-β1 induces transdifferentiation of fibro-blasts into myofibroblasts,which is important in hypoxic pulmonary vascular remodeling.

关键词： transforming growth factor-β1 fibroblast myofibroblast hypertension lung

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Hypoxia Induces transforming growth factor-β1 Gene Expression in the Pulmonary Artery of Rats via Hypoxia-inducible factor-1α

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Acta Biochimica et Biophysica Sinica 2007年第1期39卷 73-80页

作者： Yongliang JIANG Aiguo DAI Qifang LI and Ruicheng HU Depoptment of Respiratory Medicine,Hunan Institute of Gerontology,Hunan Province Geriatric Hospital,Changsha 410001,China Department of Respiratory Medicine Hunan Institute of Gerontology Hunan Province Geriatric HospitalChangsha 410001 China

The present study was undertaken to investigate the dynamic expression of hypoxia induciblefactor-1 α (HIF-1α) and transforming growth factor-β1 (TGF-β1) in hypoxia-induced pulmonary hypertensionof rats.It was found that mean pulmonary arterial pressure (mPAP) increased significantly after 7 d ofhypoxia.Pulmonary artery remodeling index and right ventricular hypertrophy became evident after 14 d ofhypoxia.HIF-1α mRNA staining was less positive in the control,hypoxia for 3 d and hypoxia for 7 d,butbegan to enhance significantly after 14 d of hypoxia,then remained stable.Expression of HIF-1 α protein inthe control was less positive,but was up-regulated in pulmonary arterial tunica intima of all hypoxic rats.TGF-β1 mRNA expression in pulmonary arterial walls was increased significantly after 14 d of hypoxia, butshowed no obvious changes after 3 or 7 d of hypoxia.In pulmonary tunica adventitia and tunica media,TGF-β1 protein staining was less positive in control rats,but was markedly enhanced after 3 d of hypoxia,reaching its peak after 7 d of hypoxia,and then weakening after 14 and 21 d of hypoxia.Western blottingshowed that HIF- 1α protein levels increased significantly after 7 d of hypoxia and then remained at a highlevel. TGF-β1 protein level was markedly enhanced after 3 d of hypoxia,reaching its peak after 7 d ofhypoxia,and then decreasing after 14 and 21 d of hypoxia.Linear correlation analysis showed that HIF-1αmRNA, TGF-β1 mRNA, TGF-β1 protein were positively correlated with mPAP,vessel morphometry andright ventricular hypertrophy index.TGF-β1 protein (tunica adventitia) was negatively correlated withHIF-lα mRNA.Taken together,our results suggest that changes in HIF-lα and TGF-β1 expression afterhypoxia play an important role in hypoxia-induced pulmonary hypertension of rats.

关键词： hypoxia inducible factor-1α transforming growth factor-β1 hypertension lung hypoxia

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Histone deacetylase inhibitor suberoylanilide hydroxamic acid alleviates liver fibrosis by suppressing the transforming growth factor-β1 signal pathway

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Hepatobiliary & Pancreatic Diseases International 2018年第5期17卷 423-429页

作者： Yao Wang Lei Zhao Fang-Zhou Jiao Wen-Bin Zhang Qian Chen Zuo-Jiong Gong Department of Infectious Diseases Renmin Hospital of Wuhan University Department of Infectious Diseases Union Hospital Tongji Medical College Huazhong University of Science and Technology

Background: Histone deacetylases(HDACs) inhibitors are new anti-fibrotic drugs that inhibit the activity of hepatic stellate cells. The present study focused on the anti-fibrotic function of HDAC inhibitor suberoylanilide hydroxamic acid(SAHA) by suppressing transforming growth factor-β1(TGF-β1) signaling. Methods: Male Sprague-Dawley rats were used to induce liver fibrosis with carbon tetrachloride(CCl 4) and LX2 cell(human hepatic stellate cell line) was stimulated by TGF-β1. Both animals and cells were treated with SAHA. The Smad7 and connective tissue growth factor(CTGF) mRNA levels were detected by real-time polymerase chain reaction(PCR). Western blotting was used to examine the protein levels of CTGF, Histone H3(H3), Smad7, Smad2/3, Acetyl-Histone H3(AH3), HDAC2, α-smooth muscle actin( α-SMA), HDAC6, p-Smad2/3 and HDAC8. In addition, the TGF-β1 and liver enzyme levels from rat serum were detected. Histopathological changes were examined by hematoxylin and eosin(HE), Sirius red and Masson trichrome staining. The α-SMA expression was detected by immumohistochemical staining. Results: Compared with control group, the TGF-β1 and liver enzyme levels from rat serum, together with the mRNA levels of CTGF and protein levels of CTGF, HDAC2, α-SMA, HDAC6, p-Smad2/3 and HDAC8 were elevated in fibrotic rats( P < 0.01). But the Smad7 mRNA and AH3 protein levels were notably suppressed in the fibrotic rats( P < 0.01). Pathological examination showed the typical changes of liver fibrosis in the fibrotic rats. After the treatment with SAHA, the levels of liver enzymes, TGF-β1, CTGF, HDAC2, α-SMA, HDAC6, p-Smad2/3 and HDAC8 were reduced( P < 0.01) and Smad7 and AH3 protein contents were elevated in liver fibrotic rats( P < 0.01). Moreover, immumohistochemistry showed that SAHA significantly suppressed the α-SMA protein content in fibrotic liver( P < 0.01). Conclusion: The HDAC inhibitor SAHA alleviated liver fibrosis by suppressing the TGF-β1 signaling.

关键词： Acetylation transforming growth factor-β1 Liver fibrosis Suberoylanilide hydroxamic acid

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transforming growth factor-β1 gene polymorphisms associated with chronic obstructive pulmonary disease in Chinese population

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Acta Pharmacologica Sinica 2005年第6期26卷 714-720页

作者： Zhi-guang SU~2, Fu-qiang WEN, Yu-lin FENG, Min XIAO, Xiao-ling WU Laboratory of Pulmonary Medicine, West China Hospital, Sichuan University Key Laboratory of Biotherapy of Human Disease, Ministry of Education, Chengdu 610041, China Laboratory of Pulmonary Medicine West China Hospital Sichuan University Key Laboratory of Biotherapy of Human Disease Ministry of Education Chengdu China

Aim: To determine the frequencies of polymorphism and haplotype in the transforming growth factor-beta 1 (TGF-1) gene promoter in the Chinese population and to investigate the susceptibility of this population to chronic obstructive pulmonary disease (COPD). Methods: The target fragments of the TGF-1 gene promoter were amplified and analyzed by polymerase chain reaction-restriction fragment length polymorphism technique in 84 COPD patients and 97 age- and sex-matched healthy controls. The test for Hardy-Weinberg equilibrium was performed using HWE program of the LINKUTIL package and statistical analysis was carried out with the SPSS statistical package. An expectation maximization algorithm was used for the pairwise linkage disequilibrium test and haplotype analysis. Results: More carriers of the -800A allele, or fewer carriers of the -509T allele, were detected in the COPD patients compared with the non-symptomatic control subjects [for the -800A allele, 29.8% vs 14.4%, respectively, x~2=6.257, degrees of freedom (df)=l, P=0.012; for the -509T allele, 27.3% vs 44.3%, respectively,x~2=5.582, df=l, P=0.018]. The prevalence of the -800A allele was significantly higher in the COPD patients than in control subjects OP=0.009), whereas the frequency of the -509T allele was significantly higher in control subjects than in the COPD patients (P=0.008). In addition, this distribution tendency for the -800A or -509T allele was similar in heavy smokers (smoking history 鈮?0 pack years); (number of packs of cigarettes per day multiplied by the number of years of smoking) X~2=7.235, P=0.007, and X~2=5.636, P=0.018, respectively). The linkage disequilibrium was found between -800 G鈫扐 and -509 C鈫扵 (D>0.60,P<0.0001), and the frequency of the AC haplotype, consisting of the least common base at -800 and the most common base at -509, was significantly higher in patients with COPD than in controls (0.056 vs 0.021, P<0.05). Conclusions: The single nucleotide polymorphism (SNP) in the TGF-1 gene promoter might be associated with COPD,

关键词： chronic obstructive pulmonary disease transforming growth factor-β1 single nucleotide polymorphisms haplotypes

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Distribution of intracellular and extracellular expression of transforming growth factor—β1（TGF—β1） in human testis and their association with spermatogenesis

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Asian Journal of Andrology 2002年第2期4卷 105-109页

作者： MaskiDobashi MasatoFujisawa 等 DivisionofUrolgy DepartmentofOrgansTherapeuticsGraduateSchoolofMedicineKobeUniversityJapan

OBJECTIVE:Spermatogenic dysfunction may result from thickening of seminiferous tubular basement membrane (BM) with tubular sclerosis. transforming growth factor beta1 (TGF-beta1) plays an important role in fibrogenesis. The intracellular and extracellular expression of TGF-beta1 in the testis were immunohistochemically determined, using LC antibody (LC) for intracellular TGF-beta1 and CC antibody (CC) for extracellular TGF-beta1.;METHODS:Twenty-three testicular biopsy specimens were obtained from varicocele and five from Sertoli-cell-only (SCO) patients, and five from normal volunteers. The relative area involved by the expression of TGF-beta1 for CC or LC (TGF-beta1 index for CC or LC) was examined, and semen parameters and serum hormonal levels and TGF-beta1 were analyzed. The Johnson score (JS), the BM thickness, and the tubular diameter were also determined.;RESULTS:Immunoreactivity for CC was hardly detected. That for LC was detected in the Sertoli and germ cells. The TGF-beta1 index for LC was significantly higher in the varicoceles than in the normal testes. Interestingly, that for LC was significantly higher in the varicoceles than in the SCO. The level of serum TGF-beta1 was significantly higher in varicoceles than in the normal testes.;CONCLUSIONS:The distribution of the intracellular and extracellular expression of TGF-beta1 in human testis was demonstrated. It suggests that TGF-beta1 is related to fibrosis of seminiferous tubules and may lead to spermatogenic disruption.

关键词： Fibrosis Spermatogenesis Testis transforming growth factor-β1

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Effects of transforming growth factor beta 1 on the growth of rhabdomyosarcoma cell line RD

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Chinese Medical Journal 2005年第8期118卷 678-686页

作者： YELü ZHANGHong-ying WANGHua YANGGuang-hua BUHong ZHANGLi WANGShou-li DepartmentofPathology WestChinaHospitalSichuanUniversityChengdu610041China LabofTransplantEngineeringandImmunology WestChinaHospitalSichuanUniversityChina

Backgroud transforming growth factor-β (TGF-β) can inhibit the growth of most epithelial and endothelial cells. The growth regulative role of TGF-β on soft tissue sarcoma was seldom reported. Here we examined TGF-β1 effects on the growth of human rhabdomyosarcoma cell RD and searched the relative molecular mechanism. Methods The viability of RD was examined by [ 3H]-thymidine incorporation and [3-(4,5-dimethylthiazol-z-yl)-2,5-diphenyltetraz olium bromide] (MTT) assay. RD cell cycle was analysed by flow cytometry. The protein and mRNA of cell cycle regulative factors in RD were detected by Western blot and reverse transcription-polymerase chain reation (RT-PCR), respectively. The kinase activity of cdk2 or cdk4 was examined by immunoprecipitation and kinase assay. Immunofluorescent staining was used to detect the location of cell cycle regulative factors in RD by laser scanning confocal microscope.Results TGF-β1 inhibits RD proliferation by G1-arrest in cell cycle progression. TGF-β1 can prominently up-regulate P27 of RD, then augment P27 to bind cyclinE-cdk2 complexes, which effectively suppress cdk2 kinase activity. P21 increased and c-myc decreased in RD due to TGF-β1. Both P15 and cdk4 have not been involved in the growth inhibitory event. TGF-β1 treatment induced P27 to congregate around nucleus. P21 pervaded from nucleus to both nucleus and cytoplasm by TGF-β1 treatment.Conclusion TGF-β1 inhibits the proliferation of human rhabdomyosarcoma cell line RD and induces RD G1-arrest. This course is accomplished by TGF-β1 up-regulating P27 to suppress cdk2 kinase activity. The induction of P21 and down-regulation of C-myc might participate in the growth-arrest event.

关键词： transforming growth factor-β1 Rhabdomyosarcoma cell cycle cyclin dependent kinase

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Association of Chinese Medicine Constitution Susceptibility to Diabetic Nephropathy and transforming growth factor-β1(T869C)Gene Polymorphism

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Chinese Journal of Integrative Medicine 2011年第9期17卷 680-684页

作者：牟新刘文洪周旦阳刘颖慧胡永宾马国玲寿成珉陈家炜赵进喜 Department of Endocrinology of Hangzhou Red Cross Hospital Zhejiang University of Chinese Medicine Dongzhimen Hospital Affiliated to Beijing University of Chinese Medicine

Objective：To explore the association of Chinese medicine constitution susceptibility to diabetic nephropathy（DN） and transforming growth factor（TGF）-β1（T869C） gene polymorphism.Methods：TGF-β1 gene polymorphism detected with polymerase chain reaction-restriction fragment length polymorphism（PCRRFLP） was screened for 180 DN cases and 180 type 2 diabetic mellitus（T2DM） cases without combined DN. Patients with DN were surveyed epidemiologically with constitution in the Chinese medicine questionnaire （CCMQ）.Binary logistic regression analysis was utilized to study the correlation between nine types of Chinese medicine constitution and TGF-β1（T869C） gene polymorphisms.Results：The DN group has a higher frequency of TGF-β1（T869C） gene polymorphism than the T2DM group,and CC/CT genotypes than the T2DM group[CC,CT,TT（DN group）：88,87,5（cases） versus（T2DM group） 71,73,36（cases）,P0.05].The phlegm-dampness constitution,damp-heat constitution,and blood stasis constitution have correlations with TGF-β1 （T869C） gene polymorphism.Conclusion：Chinese medicine constitutions were associated with TGF-β1（T869C） gene polymorphism,a potential predictor of susceptibility to DN in T2DM patients.

关键词： diabetic nephropathy gene polymorphism transforming growth factor-β1 Chinese medicine constitution

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