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International Journal of Oral Science 2015年第4期7卷 232-241页

作者： Hui Xu Ding Bai L-Bruno Ruest Jian Q Feng Yong-Wen Guo Ye Tian Yan Jing Yao He Xiang-Long Han State Key Laboratory of Oral Diseases Department of OrthodonticsWest China Hospital of StomatologySichuan University Department of Biomedical Sciences Baylor College of DentistryTexas A&M University

α-smooth muscle actin （α-SMA） and tenascin-C are stress-induced phenotypic features of myofibroblasts. The expression levels of these two proteins closely correlate with the extracellular mechanical microenvironment. We investigated how the expression of α-SMA and tenascin-C was altered in the periodontal ligament （PDL） under orthodontic loading to indirectly reveal the intrinsic mechanical microenvironment in the PDL. In this study, we demonstrated the synergistic effects of transforming growth factor-β1 （TGF-β1） and mechanical tensile or compressive stress on myofibroblast differentiation from human periodontal ligament cells （hPDLCs）. The hPDLCs under higher tensile or compressive stress significantly increased their levels of α-SMA and tenascin-C compared with those under lower tensile or compressive stress. A similar trend was observed in the tension and compression areas of the PDL under continuous light or heavy orthodontic load in rats. During the time-course analysis of expression, we observed that an increase in α-SMA levels was matched by an increase in tenascin-C levels in the PDL under orthodontic load in vivo. The time-dependent variation of α-SMA and tenascin-C expression in the PDL may indicate the time-dependent variation of intrinsic stress under constant extrinsic loading.

关键词： α-smooth muscle actin mechanical load myofibroblast periodontal ligament tenascin-C transforming growthfactor-β1

Emodin protects rat liver from CCl_4-induced fibrogenesis via inhibition of hepatic stellate cells activation

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World Journal of Gastroenterology 2009年第38期15卷 4753-4762页

作者： Miao-Xian Dong Yan Jia Ying-Bo Zhang Cheng-Chong Li Yu-Tao Geng Li Zhou Xue-Yan Li Ji-Cheng Liu Ying-Cai Niu The Institute of Medicine Qiqihar Medical University Qiqihar161042 Heilongjiang Province China Department of Pathophysiology Heilongjiang University of Chinese Medicine Harbin 150040 Heilongjiang Province China

AIM： To investigate the role of emodin in protecting the liver against fibrogenesis caused by carbon tetrachloride （CCh） in rats and to further explore the underlying mechanisms. METHODS： Rat models of experimental hepatic fibrosis were established by injection with CCh; the treated rats received emodin via oral administration at a dosage of 20 mg/kg twice a week at the same time. Rats injected with olive oil served as a normal group. Histopathological changes were observed by hematoxylin and eosin staining. The activities of alanine aminotransferase （ALT） and aspartate aminotransferase （AST） in serum and hepatic hydroxyproline content were assayed by biochemical analyses. The mRNA and protein relevant to hepatic stellate cell （HSC） activation in the liver were assessed using real-time reverse transcription-polymerase chain reaction （RT-PCR）, immunohistochernistry, western blotting and enzymelinked immunosorbent ***： The degree of hepatic fibrosis increased markedly in the CCh group compared to the normal group （P 〈 0.01）, and decreased markedly in the emodin group compared to the CCI4 group according to METAVIR scale （P 〈 0.01） compared with those in the normal control group （51.02 ± 10.64 IU/L and 132.28 ± 18.14 IU/L）. The activities of serum ALT and AST were significantly higher in rats injected with CCh （289.25 ± 68.84 IU/L and 423.89 ± 35.67 IU/L, both P 〈 0.05）. The activities of serum ALT and AST were significantly reduced by administration of emodin （176.34 ± 47.29 IU/L and 226.1 ± 44.52 IU/L, both P 〈 0.05）. Compared with the normal controls （54.53 ± 13.46 mg/g）, hepatic hydroxyproline content was significantly higher in rats injected with CCI4 （120.27 ± 28.47 mg/g, P 〈 0.05）. Hepatic hydroxyproline content was significantly reduced in the rats treated with emodin at 20 mg/kg （71.25 ± 17.02 mg/g, P 〈 0.05）. Emodin significantly protected the liver from injury by reducing serum AST and ALT activities and reducing hepatic hydroxyproline content. The

关键词： Emodin Hepatic fibrosis Transforming growth factor-β1 Smad4 Hepatic stellate cell α-smooth muscle actin

The ROCK pathway inhibitor Y-27632 mitigates hypoxia and oxidative stress-induced injury to retinal Müller cells

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Neural Regeneration Research 2018年第3期13卷 549-555页

作者： Xiao-hui Zhang Zhao-hui Feng Xiao-yu Wang Department of Ophthalmology Second Affiliated Hospital of Xi'an Jiaotong University Medical College Xi'an Shaanxi Province China

Rho kinase （ROCK） was the first downstream Rho effector found to mediate RhoA-induced actin cytoskeletal changes through effects on myosin light chain phosphorylation. There is abundant evidence that the ROCK pathway participates in the pathogenesis of retinal endothelial injury and proliferative epiretinal membrane traction. In this study, we investigated the effect of the ROCK pathway inhibitor Y-27632 on retinal Müller cells subjected to hypoxia or oxidative stress. Müller cells were subjected to hypoxia or oxidative stress by exposure to CoCl2 or H2O2. After a 24-hour treatment with Y-27632, the 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyl tetrazolium bromide assay was used to assess the survival of Müller cells. Hoechst 33258 was used to detect apoptosis, while 2′,7′-dichlorodihydrofluorescein diacetate was used to measure reactive oxygen species generation. A transwell chamber system was used to examine the migration ability of Müller cells. Western blot assay was used to detect the expression levels of α-smooth muscle actin, glutamine synthetase and vimentin. After treatment with Y-27632, Müller cells subjected to hypoxia or oxidative stress exhibited a morphology similar to control cells. Y-27632 reduced apoptosis, α-smooth muscle actin expression and reactive oxygen species generation under oxidative stress, and it reduced cell migration under hypoxia. Y-27632 also upregulated glutamine synthetase expression under hypoxia but did not impact vimentin expression. These findings suggest that Y-27632 protects Müller cells against cellular injury caused by oxidative stress and hypoxia by inhibiting the ROCK pathway.

关键词： nerve regeneration diabetic retinopathy Rho kinases Müller cells reactive oxygen species glutamine synthetase α-smooth muscle actin CoCl2 H2O2 hypoxia oxidative stress neural regeneration

Effects of pharmacological serum from normal and liver fibrotic rats on HSCs

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World Journal of Gastroenterology 2005年第16期11卷 2444-2449页

作者： Xi-XianYao TaoLv HebeiInstituteofGastroenterology DepartmentofDigestiveDiseaseTheSecondHospitalofHebeiMedicalUniversityShijiazhuang050000HebeiProvinceChina

AIM: To make drug sera of Salvia miltiorrhiza and Yigankang, both of which are Chinese herbs that activate bleeding and eliminate stasis, in normal rats and those with liver fibrosis, respectively. To investigate and compare the effects of the two different drug sera on the proliferation and activation of hepatic stellate cells (HSCs). METHODS: Some rats were induced with liver fibrosis: 40% carbon tetrachloride (CCI4) subcutaneous injection, twice a week for 9 wk. Salvia miltiorrhiza, Yigankang, colchicines and normal saline were administered into the stomachs of normal rats and those with liver fibrosis. Drug sera were extracted 5 d later. HSCs in vitro were cultivated in different drug sera for 24 h. The rates of proliferation and expression of a-smooth muscle actin (α-SMA) were detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) and immunocyt-ochemistry stain, respectively. RESULTS: The drug sera from normal and liver fibrotic rats could be used to cultivate HSCs and to observe the effects of the corresponding components of herbs on HSCs. Salvia miltiorrhiza and Yigankang had better inhibitory effects on HSCs than colchicines (MTT: normal drug serum: Salvia miltiorrhiza 0.42 ±0.08, Yigankang 0.32±0.10 vs colchicines 0.45±0.12 pathological drug serum: Salvia miltiorrhiza 0.33±0.02, Yigankang 0.26±0.01 vs colchicines 0.41±0.09. P<0.05). The drug sera of Salvia miltiorrhiza, Yigankang from liver fibrotic rats had a stronger inhibitory effect than the same ones from normal rats (MTT: Salvia miltiorrhiza: normal drug serum 0.42±0.08 vs pathological drug serum 0.33±0.02. Yigankang: normal drug serum 0.32±0.10 vs pathological drug serum 0.26±0.01. P<0.05) CONCLUSION: Salvia miltiorrhiza and Yigankang could inhibit the expression of a-SMA and the proliferation of HSCs. The drug sera from normal and liver fibrotic rats had different effects on HSCs, probably due to different metabolic processes, effective components and different quantities of

关键词： Seropharmocological method Hepatic stellate cell α-smooth muscle actin Salvia Yigankang

Gardenia jasminoides attenuates hepatocellular injury and fibrosis in bile duct-ligated rats and human hepatic stellate cells

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World Journal of Gastroenterology 2012年第48期18卷 7158-7165页

作者： Ying-Hua Chen Tian Lan Jing Li Chun-Hui Qiu Teng Wu Hong-Ju Gou Min-Qiang Lu The First Affiliated Hospital of Sun Yat-sen University Institute of Vascular Biology Guangdong Pharmaceutical University Guangzhou PTDS Biotechnology Science and Technology Co.Ltd. Department of Hepatology The Third Affiliated Hospital of Sun Yat-sen University

AIM:To investigate the anti-hepatofibrotic effects of Gardenia jasminoides in liver ***:Male Sprague-Dawley rats underwent common bile duct ligation(BDL) for 14 d and were treated with Gardenia jasminoides by *** ef-fects of Gardenia jasminoides on liver fibrosis and the detailed molecular mechanisms were also assessed in human hepatic stellate cells(LX-2) in ***:Treatment with Gardenia jasminoides decreased serum alanine aminotransferase(BDL vs BDL + 100 mg/kg Gardenia jasminoides,146.6 ± 15 U/L vs 77 ± 6.5 U/L,P = 0.0007) and aspartate aminotransferase(BDL vs BDL + 100 mg/kg Gardenia jasminoides,188 ± 35.2 U/L vs 128 ± 19 U/L,P = 0.005) as well as hydroxyproline(BDL vs BDL + 100 mg/kg Gardenia jasminoides,438 ± 40.2 μg/g vs 228 ± 10.3 μg/g liver tissue,P = 0.004) after ***,Gardenia jasminoides significantly reduced liver mRNA and/or protein expression of transforming growth factor β1(TGF-β1),collagen type?Ⅰ?(Col?Ⅰ) and α-smooth muscle actin(α-SMA).Gardenia jasminoides significantly suppressed the upregulation of TGF-β1,Col?Ⅰand α-SMA in LX-2 exposed to recombinant TGF-β***,Gardenia jasminoides inhibited TGF-β1-induced Smad2 phosphorylation in LX-2 ***:Gardenia jasminoides exerts antifibrotic effects in the liver fibrosis and may represent a novel antifibrotic agent.

关键词： Gardenia jasminoides Liver fibrosis Collagen typeⅠ Transforming growth factor-β1/Smad2 pathway α-smooth muscle actin

Effects of interleukin-10 on activation and apoptosis of hepatic stellate cells in fibrotic rat liver

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World Journal of Gastroenterology 2006年第12期12卷 1918-1923页

作者： Li-Juan Zhana Wei-Da Zheng Mei-Na Shi Department of Gastroenterology Union Hospital of Fujian Medical University.Fuzhou 350001.Fujian Province.China

AIM： TO study the effects of interleukin-10 （IL-10） on the expression of o-smooth muscle actin （α-SMA）, nuclear factor-κB（NF-κB） and Fas/Fas ligand （FasL） in hepatic stellate cells of experimental rats with hepatic fibrosis. METHODS： Sixty clean SD rats were randomly divided into control group （group N）, liver fibrotic group （group C） and IL-10 treatment group （group I）. Control group received intraperitoneal injection of saline （2ml·kg^-1）, twice a week. Fibrotic group was injected intraperitoneally with 50% carbon tetrachloride （CCh）（2 ml·kg^-1）, twice a week. IL-10 treatment group was given IL-10 at a dose of 4 pg·kg^-1 20 minutes before CCl4 administration from the third week. Hepatic stellate cells （HSCs） were isolated from these rats at the seventh and eleventh weeks during the course of liver fibrosis, respectively. The expression of α-SMA and NF-κB in HSCs was measured by S-P immunohistochemistry. The expression of Fas and FasL mRNA was measured by RT-PCR. Furthermore, liver tissues were harvested from three groups at the same time. RESULTS： The CCh- induced experimental rat hepatic fibrosis model was established successfully. The purity of extracted hepatic stellate cells was about 95% and the yield of hepatic stellate cells was 1.2-2.3×10^6/g liver tissue averagely. The positive expression of α-SMA and NF-κB was 36.5% and 28.5% respectively in group N. The positive levels of α-SMA and NF-κB were increased significantly in group C compared to group N （P〈0.01）. The positive signals decreased significantly （P〈0.05） in group I. In the 11^th week, the HSCs of group I became round with visible pyknotic nuclei. The expression of NF-κB in group C was significantly increased in a timedependentmanner （P〈0.01）, but there was no difference in the α-SMA expression （P〉0.05）. The mRNA of Fas and FasL in group C was significantly increased in a timedependent manner compared to that in control group. After treated with IL-10, the expression level of Fas and FasL was h

关键词： Liver fibrosis Hepatic stellate cell Znterleuldn-10 α-smooth muscle actin Nuclear factor-κB Rat

Preventive approach against drug-induced pulmonary fibrosis through the suppression of epithelial-mesenchymal transition

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BIOCELL 2022年第8期46卷 1861-1865页

作者： MASASHI KAWAMI RYOKO YUMOTO MIKIHISA TAKANO Graduate School of Biomedical and Health Sciences Hiroshima UniversityHiroshima7348553Japan

A number of drugs induce pulmonary injury and subsequently lead to serious lung diseases such as pulmonary fibrosis as the adverse drug ***,an effective preventive approach against drug-induced pulmonary fibrosis has not been established due to poor understanding of common preventive targets in a variety of drugs showing pulmonary ***-mesenchymal transition(EMT),a cellular phenotypic change of the epithelial to mesenchymal state,contributes to the development of pulmonary fibrosis through the conversion of damaged alveolar epithelium into *** several drugs with pulmonary toxicity have been reported to induce EMT,EMT serves as a bridge between the drugs and pulmonary *** evidence supports the potential of EMT as a preventive target against drug-induced pulmonary ***,since there are mechanistic differences between the main pharmacological effect and EMT induced by the drug,prevention based on EMT suppression would be possible and would contribute to continuous clinical treatment with the drug to avoid EMT-mediated serious pulmonary ***,targeting EMT seems to be adequate for exerting a preventive effect since EMT in damaged alveolar epithelial cells occurs prior to the development of the pathophysiological state of the whole lung in a bleomycin-induced lung injury rat *** viewpoint deals with the benefits and perspectives of preventive approaches against druginduced pulmonary fibrosis through the suppression of EMT,which has rarely been addressed.

关键词： Drug-induced lung injury Epithelial-mesenchymal transition Pulmonary fibrosis α-smooth muscle actin

Effect of NF-κB p65 antisense oligodeoxynucleotide on transdifferentiation of normal human lens epithelial cells induced by transforming growth factor-β2

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International Journal of Ophthalmology(English edition) 2016年第1期9卷 29-32页

作者： Chao Liu Xao-Li Wu Xin-Yi Wu Zhen-Hua Zhang Xiao-Hua Liu Department of Ophthalmology Qilu Hospital Shandong University Jinan 250012 Shandong Province China Department of Ophthalmology Central Hospital of QingdaoQingdao 266042 Shandong Province China Department of Ophthalmology Rongjun Hospital of Shandong Jinan 250013 Shandong Province China Department of Stomatology Central Hospital of QingdaoQingdao 266042 Shandong Province China

AIM：To study the inhibition of nuclear factor kappa-B p65（NF-κB p65）antisense oligodeoxynucleotide（ASODN）on transdifferentiation of normal human lens epithelial cells induced by transforming growth factor-β2（TGF-β2）.·M ETHODS：NF-κBp65ASODNand NF-κBp65missense oligodeoxynucleotide（MSODN）were designed and *** lens epithelial cell line（HLE B-3）cells were prepared for study and divided into 7 *** group was HLE B-3 cells cultured in dulbecco’s modified eagle medium（DMEM）.T1,T2,and T3 group were HLE B-3 cells cultured in DMEM with 10 ng/m L TGF-β2 for 6h,12h,24h respectively.A＋T group was HLE B-3 cells cultured with 10 ng/m L TGF-β2for 24h after transfected by NF-κB p65 ASODN for 24h.M＋T group was HLE B-3 cells cultured with 10 ng/m L TGF-β2 for 24h after transfected by NF-κB p65 MSODN for *** negative control group was HLE B-3 cells cultured with 10 ng/m L TGF-β2 for 24h after cultured with transfer agent（Hi Per Fect）for *** morphology was observed at different time points using an inverted *** expression of NF-κB p65 m RNA was detected with reverse transcription-polymerase chain reaction（RT-PCR）,and the expression ofα-smooth muscle actin（α-SMA）protein was assayed with ELISA.·RESULTS：With the TGF-β2 stimulation prolongation,the expression of NF-κB p65 m RNA and a-SMA protein increased in T1,T2,T3 groups compared with the control group,and the difference was statistically significant（〈0.05）.NF-κB p65 ASODN lowered the expression of NF-κB p65 m RNA andα-SMA protein induced by TGF-β***-κB p65 MSODN and Hi Per Fect did not lower the expression of NF-κB p65 m RNA andα-SMA protein induced by TGF-β*** difference between control group and A＋T group was not statistically significant（〉0.05）,but the difference among A＋T group and other groups was statistically significant（〈0.05）.·CONCLUSION：NF-κB p65 ASODN could lower the expression of NF-κB p65 m RNA andα-SMA protein induced by TGF-β2,and antagonized TGF-β2-induced transdifferentiati

关键词： nuclear factor kappa-B p65 antisenseoligodeoxynucleotide transforming growth factor-β2 α-smooth muscle actin lens epithelial cells

Depressant effect and mechanism of atorvastatin on the chronic rejection of aortic allograft in rats

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China Medical Abstracts 2008年第2期17卷 160-162,165页

作者：左克强钱振宇黄道景龚凯汤敬东 Department of Vascular Surgery Tongji HospitalTongji University

Objective To investigate the depressant effect and mechanism of atorvastatin on the chronic rejection of aortic allograft in rats. Methods： The models of abdominal aorta transplantation were made with micro-surgery in rats. The recipients were divided into three groups： allograft control group, atorvastatin-treated group and isograft control group. Vascular intimal thickness in all of the groups were observed by histological examination. The expression of PCNA and α-SMA were determined by immunohistochemistry. The content of nitric oxide was determined by nitrate reductase chromatometry. Results： The vascular intimal thickness in rats of atorvastatin-treated group （11.60% ± 2.40% ） were lower than those in allograft control group （34.60 % ± 6.40 % ; P 〈 0.05） and higher than those in isograft control group （1.15 % ± 0.65 %; P〈 0.05 ）. The expression level of PCNA was decreased in atorvastatin-treated group （4.80% ± 0.80% ） than allograft control group （18.40% ± 1.80% ; P〈0.05） and higher than isograft group （1.20% ± 0.40% ; P〈0.05）. Conclusion： The expression of PCNA in the transplant aorta could be suppressed by atorvastatin, which resalted in relief of chronic rejection of aortic allograft.

关键词： Atorvastatin Transplant Chronic rejection Proliferation cell nuclear antigen α-smooth muscle actin Nitric oxide

Effects and mechanisms of total saponins of panax notoginseng on the transdifferentiation of human renal tubular epithelial cells mduced by aristolochic acid Ⅰ

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Effects and mechanisms of total saponins of panax notoginsen...