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Electroacupuncture attenuates chronic salpingitis via transforming growth factor-β1/p38 mitogen-activated protein kinase signaling pathway

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Journal of Traditional Chinese Medicine 2022年第5期42卷 781-787页

作者： HU Xijiao CHENG Yinglong KANG Huanan LI Shuoxi WANG Yawen LIU Jinzhe SUN Yiming LIU Li Department of obstetrics and gynecology the Second Affiliated Hospital of Heilongjiang University of Chinese MedicineHeilongjiang 150001China Deapartment of Hysteroscopy chamber the First Affiliated Hospital of Heilongjiang University of Chinese MedicineHarbin 150040China College of pharmacy Heilongjiang University of Chinese MedicineHarbin 150040China Midwifery Teaching and Research Section Heilongjiang University of Chinese Medicine Jiamusi CollegeHarbin 150040China The department of obstetrics and gynecology the First Affiliated Hospital of Henan University of Chinese MedicineHenan 450000China Department of Chinese Pharmacy School of PharmacyGuizhou University of Chinese MedicineGuizhou 550000China Andrology department Heilongjiang Academy of Traditional Chinese Medicine Harbin 150036China Endoscopy room the First Affiliated Hospital of Heilongjiang University of Traditional Chinese MedicineHysteroscopy DepartmentHarbin 150040China

OBJECTIVE:To explore the effect of electroacupuncture(EA)on rats with chronic fallopian tube inflammation and its potential mechanisms.METHODS:Thirty-six female Sprague-Dawley rats were divided into Control,Model and EA groups.The pathological morphology of the fallopian tubes was observed by hematoxylin-eosin(HE)and Masson staining.The results of transforming growth factor-β1(TGF-β1),P38 mitogen-activated protein kinase(MAPK),phosphorylation(p)-p38MAPK in rat oviduct tissues were detected by immunohistochemistry.Results of P38MAPK,p-P38MAPK and TGF-β1 in rat oviduct tissues were detected by immunofluorescence.The expression level of p38MAPK,p-P38MAPK,TGF-β1 protein in rats was detected by Western blot.Quantitative real-time polymerase chain reaction(RT-q PCR)was used to detect m RNA expression levels of TGF-β1.RESULTS:It found that collagen fibers counts decreased significantly in EA group compared to Model group.The phosphorylation of P38MAPK in EA group was significantly reduced compared to Model group.The serum TGF-β1 expressions in EA group increased decreased significantly.CONCLUSION:Electroacupuncture was able to attenuate chronic salpingitis through down-regulating TGF-β1/MAPK signaling pathway.

关键词： electroacupuncture salpingitis transforming growth factor beta1 mitogen-activated protein kinase

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Buyang Huanwu Tang(补阳还五汤) protects H_(2)O_(2)-induced RGC-5 cell against oxidative stress and apoptosis via reactive oxygen species-mitogen-activated protein kinase signaling pathway

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Journal of Traditional Chinese Medicine 2022年第6期42卷 885-891页

作者： ZHENG Wei WANG Mingxing LIU Shanxue LUAN Chao ZHANG Yanqiu XU Duoduo WANG Jian Department of Ophthalmology First Affiliated HospitalChangchun University of Chinese MedicineChangchun 130021China Department of Experimental Center First Affiliated HospitalChangchun University of Chinese MedicineChangchun 130021China Changchun University of Chinese Medicine Changchun 130117China Pharmaceutical Department First Affiliated HospitalChangchun University of Chinese MedicineChangchun 130021China College of Pharmacy Changchun University of Chinese MedicineChangchun 130117China Department of Encephalopathy Center First Affiliated HospitalChangchun University of Chinese MedicineChangchun 130021China

OBJECTIVE: To study the molecular mechanism of Buyang Huanwu Tang( 补阳还五汤)(BHT) protecting retinal ganglion cells(RGCs) from oxygen induced oxidative stress and apoptosis after anterior ischemia. METHODS: In this study, the Chinese herbs of BHT were extracted by first boiling in water, then were filtered, concentrated, and freeze-dried. The chemical profile of BHT extract was determined by liquid chromatography mass spectrometry(LC-MS). H2O2-induced RGC-5 cells were used as a cell model to investigate the protective effect and mechanism of BHT on RGCs. RESULTS: The survival rate of damaged RGC-5 by BHT was significantly increased by the 3-(4,5)-dimethylthiahiazo(-z-y1)-3,5-di-phenytetrazolium-romid method. Fluorescence activating cell sorter(FACS analysis) showed that BHT could significantly reduce apoptosis induced by oxidative stress via the reactive oxygen species(ROS)-mitogen-activated protein kinase(MAPK)-Caspase-3 signal pathway. CONCLUSION: BHT possesses a high antioxidant capacity and could significantly reduce ROS levels of RGC-5 cells damaged by H2O2.Therefore, the present study has provided possible alternative strategies for the prevention and treatment of ischemic optic disease by using traditional Chinese herbal formulas.

关键词： optic neuropathy ischemic oxidative stress apoptosis reactive oxygen species mitogen-activated protein kinase caspase 3 Buyang Huanwu Tang

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Induction of Protection against Paraquat-induced Oxidative Damage by Abscisic Acid in Maize Leaves is Mediated through mitogen-activated protein kinase

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Journal of Integrative Plant Biology 2009年第10期51卷 961-972页

作者： Hai-Dong Ding Xiao-Hua Zhang Shu-Cheng XU Li-Li Sun Ming-Yi Jiang A-Ying Zhang Yin-Gen Jin College of Life Sciences Nanjing Agricultural University Nanjing 210095 China College of Biosciences and Biotechnology Yangzhou University Yangzhou 225009 China College of Life Sciences Fuyang Teachers College Fuyang 236032 China National Key Laboratory of Crop Genetics and Germplasm Enhancement Nanjing Agricultural University Nanjing 210095 China

mitogen-activated protein kinase （MAPK） cascade has been shown to be important components in stress signal transduction pathway. In the present study, protection of maize seedlings （Zea mays L.） against paraquat-generated oxidative toxicity by abscisic acid （ABA）, its association with MAPK and ZmMPK5, a candidate for MAPK were investigated. Treatment of maize leaves with exogenous ABA led to significant decreases in the content of malondialdehyde, the percentage of ion leakage and the level of protein oxidation （in terms of carbonyl groups） under paraquat （PQ） stress. However, such decreases were blocked by the pretreatment with two MAPK kinase inhibitors PD98059 and U0126. The damage caused by PQ was further aggravated by inhibitors. Two inhibitors also suppressed the total activities of the antioxidant enzymes superoxide dismutase （SOD, EC 1.***.1.1）, catalase （CAT, EC 1.***.1.6）, ascorbate peroxidase （APX, EC 1.***.1.tl）, and glutathione reductase （GR, EC 1.***.4.2）. Besides, treatment with PQ stimulated the activation of a 46 kDa MAPK, which was identified as ZmMPK5 by in-gel kinase assay with immunoprecipitation. These results reveal that ABA-induced protection against PQ-generated oxidative damage is mediated through MAPK cascade in maize leaves, in which ZmMPK5, a candidate for MAPK, is demonstrated to be involved.

关键词： abscisic acid mitogen-activated protein kinase oxidative damage paraquat Zea mays

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Follistatin-Like 1 Promotes Bleomycin-lnduced Pulmonary Fibrosis through the Transforming Growth Factor Beta 1/mitogen-activated protein kinase Signaling Pathway

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Chinese Medical Journal 2018年第16期131卷 1917-1925页

作者： Yan-Kun Jin Xiao-He Li Wang Wang Jie Liu Wei Zhang Yin-Shan Fang Zhi-Fei Zhang Hua-Ping Dai Wen Ning Chen Wang Department of Respiratory and Critical Care Medicine Beijing Chao-Yang Hospital Capital Medical University Beijing 100020 China Department of Respiratory Disease Beijing Key Laboratory of Respiratory and Pulmonary Circulation Disorders Capital Medical University Beijing 100020 China Department of Respiratory Disease Capital Medical University Beijing 100020 China Department of Life Sciences State Key Laboratory of Medicinal Chemical Biology College of Life Sciences Nankai University Tianjin 300071 China Department of Physiology and Pathophysiology Capital Medical University Beijing 100069 China

Background： Follistatin-like I （FSTL 1） is a novel profibrogenic factor that induces pulmonary fibrosis （PF） through the transforming growth factor-beta 1 （TGF-[B 1 ）/Smad signaling. Little is known about its effects on PF through the non-Smad signaling, like the mitogen-activated protein kinase （MAPK） pathway. Therefore, this study aimed to investigate the role ofFSTL 1 in PF through the MAPK signaling pathway and its mechanisms in lung fibrogenesis. Methods： PF was induced in Fstll~ and wild-type （WT） C57BL/6 mice with bleomycin. After 14 days, the mice were sacrificed, and lung tissues were stained with hematoxylin and eosin; the hydroxyproline content was measured to confirm PF. The mRNA and protein level of FSTLI and the change of MAPK phosphorylation were measured by quantitative polymerase chain reaction and Western blotting. The effect of Fst11 deficiency on fibroblasts differentiation was measured by Western blotting and cell immunofluorescence. MAPK signaling activation was measured by Western blotting in Fst11＋/ and WT fibroblasts treated with recombinant human FSTLI protein. We pretreated mouse lung fibroblast cells with inhibitors of the extracellular signal-regulated kinase （ERK）, p38, and Jun N-terminal kinase （JNK） signaling and analyzed their differentiation, proliferation, migration, and invasion by Western blotting, 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide analysis, and transwell assays. The Student＇s t-test was used to compare the differences between two groups. Results： Fstll deficiency attenuated phosphorylation of the ERK, p38, and JNK signaling in bleomycin-induced fibrotic lung tissue 14 days after injury （0.67 ± 0.05 vs. 1.22 ± 0.03, t = 14.92, P = 0.0001; 0.41 ± 0.01 vs. 1.15 ± 0.07; t = 11.19; P = 0.0004; and 0.41 ± 0.01 vs. 1.07± 0.07, t = 8.92, P = 0.0009; respectively）, compared with WT lungs at the same time and in primary lung fibroblasts （0.82 ± 0.01 vs. 1.01 ±0.04, t = 4.06, P = 0.0150; 1.04 ±0.03 vs. 1.24 ± 0.03, t= 4.44, P = 0.0100： and 0.76 ±0.05 vs. 0.99±

关键词： Follistatin-Like 1 mitogen-activated protein kinase Pulmonary Fibrosis Transforming Growth Factor Beta 1

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Effect of cigarette smoke extract on lipopolysaccharide-activated mitogen-activated protein kinase signal transduction pathway in cultured cells

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Chinese Medical Journal 2007年第12期120卷 1075-1081页

作者： LI Wen XU Yong-jian SHEN Hua-hao Department of Respiratory Medicine Second Affiliated Hospital College of Medicine and Institute of Respiratory Diseases Zhejiang University Hangzhou 310009 China Department of Respiratory Medicine Tongji Hospital of Tongji Medical College Huazhong University of Science and Technology Wuhan 430030 China

Background Lipopolysaccharide （LPS） forms outer membrane of the wall of Gram-negative cells. LPS can directly cause damage to epithelia of respiratory tract and is the major factor responsible for the chronic inflammation of respiratory passage. The mitogen-activated protein kinase （MAPK） signal transduction pathway of the airway epithelia is intimately associated with the action of LPS. The chronic inflammation of respiratory tract and smoking are interrelated and entwined in the development and progression of chronic lung diseases. This study was designed to examine the effects of cigarette smoke extract （CSE） and LPS on MAPK signal transduction pathway in order to further understand the roles CSE and LPS play in chronic lung inflammation. Methods Cultured primary human epithelial cells of airway were divided into four groups according to the stimulants used： blank control group, LPS-stimulation group, CSE-stimulation group and CSE plus LPS group. Western blotting was employed for the detection of phosphorylation level of extracellular-signal-regulated-kinase （ERK1/2）, p38 MAPK and c-Jun N-terminal kinase （JNK）. The expression of cytokines of MAPK transduction pathway （granulocyte-macrophage colony stimulating factor （GM-CSF） and mRNA of IL-8） in the primary epithelial cells of respiratory tract was also determined. Results Western blotting revealed that the phosphorylation levels of ERK1/2, p38 MAPK and JNK were low and 2 hours after the LPS stimulation, the phosphorylation of ERK1/2, p38 MAPK and JNK were all increased. There was a significant difference in the phosphorylation between the LPS-stimulation group and blank control group （P〈0.05）; no significant difference was found between CSE-stimulation group and blank control group （P〉0.05）; there was a significant difference between CSE ＋ LPS group and blank control group and between CSE ＋ LPS group and LPS group （P〈0.05）. The phosphorylation of CSE-LPS group was higher than that of blank control group but lower than that of LPS group. In blank control g

关键词： smoking lipopolysaccharide mitogen-activated protein kinase signal transduction pathway interleukin-8 epithelial cells granulocyte-macrophage colony stimulating factor

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Advanced oxidation protein products induce monocyte chemoattractant protein-1 expression via p38 mitogen-activated protein kinase activation in rat vascular smooth muscle cells

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Chinese Medical Journal 2006年第13期119卷 1088-1093页

作者： PENG Kan-fu WU Xiong-fei ZHAO Hong-wen SUN Yan Department of Nephrology Southwest Hospital Third Military Medical University Chongqing 400038 China

Background Advanced oxidation protein products （AOPPs） are new uremic toxins reported by Witko-Sarsat in 1996, which are associated with the pathogenesis of atherosclerosis. However, the mechanisms by which AOPPs enhance atherosclerosis have not been fully understood. Monocyte chemoattractant protein-1 （MCP-1） is a chemokine which stimulates migration of monocytes and plays a critical role in the development of atherosclerosis. In this study, we investigated the effect of AOPPs on MCP-1 expression in cultured vascular smooth muscle cells （VSMCs）.

关键词： atherosclerosis advanced oxidation protein products monocyte chemoattractant protein-1 mitogen-activated protein kinase myocytes, smooth muscle

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EFFECT OF HIGH TIDAL VOLUME VENTILATION AND LIPOPOLYSACCHARIDE ON mitogen-activated protein kinase IN RAT LUNG TISSUE

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Chinese Medical Journal 2006年第1期119卷 53-56页

作者： QIU Hai-bo LU Xiao-min ZHOU Shao-xia YANG Yi GUO Feng-mei Department of Critical Care Medicine Zhong-da Hospital and School of Clinical Medicine Southeast University Nanjing 210009 China

Mechanical ventilation, a crucial therapy to acute respiratory distress syndrome （ARDS）,could exacerbate lung injury, and even result in ventilator-induced lung injury （VILI） if misused in some condition1. Over-activating inflammatory cells and expanding inflammatory responses, which are induced by infection, are fundamental reasons for ARDS. Among them,

关键词： mechanical ventilation high tidal volume lipopolysaccharide mitogen-activated protein kinase inflammatory mediator

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mitogen-activated protein kinase-dependent apoptosis in norcan-tharidin-treated A375-S2 cells is proceeded by the activation of protein kinase C

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Chinese Medical Journal 2005年第3期118卷 198-203页

作者： ANWei-wei WANGMin-wei TashiroShin-ichi OnoderaSatoshi IkejimaTakashi China-JapanResearchInstituteofMedicalandPharmaceuticalSciences ShenyangPharmaceuticalUniversityShenyang110016China DepartmentofPharmacology ShenyangPharmaceuticalUniversityShenyang110016China DepartmentofClinicalandBiomedicalSciences ShowaPharmaceuticalUniversityTokyo19-8543Japan

We have reported that norcantharidin (NCTD) induces human melanoma A375-S2cell apoptosis and that the activation of caspase and the mitochondrial pathway are involved in theapoptotic process. This study aimed at investigating the roles of mitogen-activated protein kinase(MAPK) and protein kinase C (PKC) in A375-S2 cell apoptosis induced by NCTD. We assessed theeffects of NCTD on cell growth inhibition using the 3-(4,5-dimethylthiazol-2-yl)-2 ,5-dipheyltetrazolium bromide ( MTT) assay, DNA fragmentation ( DNA agarose gel electrophoresis ) ,and MAPK protein levels (Western blot analysis) in A375-S2 cells. Photomicroscopic data were alsocollected. The NCTD inhibitory effect on A375-S2 cells was partially reversed by MAPK and PKCinhibitors. The expression of phosphorylated JNK and p38 also increased after the treatment withNCTD, and inhibitors of c-Jun NH2 - terminal kinase (JNK) and p38 ( SP600125 and SB203580,respectively) had significant inhibitory effects on the upregulation of phosphorylated JNK and p38expression. Simultaneously, the PKC inhibitor staurosporine blocked the upregulation ofphosphorylated JNK and phosphorylated p_(38), but had little effect on extracellularsignal-regulated kinase (ERK) expression. These results suggest that the activation of JNK andp_(38) MAPK promotes the process of NCTD-induced A375-S2 cell apoptosis and that PKC plays animportant regulation role in the activation of MAPKs.

关键词： norcantharidin A375-S2 cells mitogen-activated protein kinase proteinkinase C staurosporine

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Effects of mitogen-activated protein kinase Signal Pathway on Heat Shock protein 27 Expression in Human Lens Epithelial Cells Exposed to Sodium Salicylate in vitro

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2009年第3期29卷 377-382页

作者：王智高瑞莹黄渝侃田博周龑莉 Deppartment of Ophthalmology Union Hospital of Tongji Medical College Huazhong University of Science and Technology Aier Eye Hospital

The roles of mitogen-activated protein kinase （MAPK） signal pathway in sodium salieylate-induced expression of heat shock protein 27 （HSP27） in human lens epithelial cells （HLECs-B3） in vitro were investigated. HLECs-B3 were incubated in the fresh media containing sodium salicylate at different concentrations for different durations, and allowed to be recovered in fresh medium without sodium salicylate for different durations with or without pretreatment with p38MAPK inhibitor （SB203580）, ERK1/2 inhibitor （PD98059） and JNK/SAPK inhibitor （SP600125）. The expression of P38MAPK, ERK1/2, JNK/SAPK, phosphorylated P38MAPK, phosphorylated ERK1/2, phosphorylated JNK/SAPK and HSP27 was detected by Western blot. The expression of HSP27 mRNA and protein was detected by RT-PCR and immunohistochemistry respectively. It was found there was only weak expression of HSP27 in normal HLECs. The expression of HSP27 was not detectable in HLECs-B3 that were exposed to sodium salicylate （55 retool/L） for 1-5 h. It was indicated that recovery from sodium salicylate （〉35 mmol/L） significantly increased the synthesis of HSP27. The expression of HSP27 was up-regulated in HLECs-B3 under sodium salicylate recovery for 3 h, reached the peak level for 6 h, and returned to the level of control cells by 24 h. Activation of P38MAPK from sodium salicylate stimulation occurred at 30th rain, and increased significantly at 1st h, then declined and renamed to baseline level at 3rd h under sodium salicylate recovery. Activation of ERK1/2 occurred at 1st h and reached the peak level at 6th h under sodium salicylate recovery. However, JNK/SAPK was inactivated by sodium salicylate. The expression of HSP27 could be down-regulated with the pretreatment of SB203580 and PD98059 jointly. It is concluded that sodium salicylate can induce the expression of HSP27 in HLECs-B3. The effects are mediated, at least in part, through the activation of P38MAPK and ERK1/2 signaling pathway.

关键词： sodium salicylate human lens epithelial cells mitogen-activated protein kinase heat shock protein

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Antithrombin-Ⅲ without concomitant heparin improves endotoxin-induced acute lung injury rats by inhibiting the activation of mitogen-activated protein kinase

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Chinese Medical Journal 2009年第20期122卷 2466-2471页

作者： SUN Hui-ming HONG Ling-zhi SHEN Xiao-kun LIN Xin-qing SONG Yong SHI Yi Department of Respiratory Diseases Clinical School of Nanjing University Nanjing General Hospital of Nanjing Military Command Nanjing Jiangsu 210002 China

Background Antithrombin-Ⅲ （AT-Ⅲ）, the major inhibitor of thrombin in plasma, also has anti-inflammation property and might have positive effect on sepsis. The present study aimed to investigate the effects of AT-Ⅲ on inflammatory reaction and pulmonary protection in endotoxin-induced acute lung injury （ALI） rat. Methods Sixty male Sprague-Dawley rats were randomly assigned equally to normal control group, ALl group, AT-Ⅲ treatment group, AT-Ⅲ＋heparin treatment group, and heparin treatment group. The pulmonary vascular permeability index （PVPI） was measured by single nuclide tracer technique. The activity of AT-Ⅲ in plasma was determined by the method of synthetic chromogenic substrata. Tumor necrosis factor-a （TNF-a） and interleukin-6 （IL-6） levels in serum were determined by enzyme-linked immunosorbent assay. The expressions of lung tissue mitogen-activated protein kinases （ERK1/2, P38 and JNK MAPK） were determined by Western blotting. Results Rats had significantly improved lung histopathology in the AT-Ⅲ treatment group and heparin treatment group compared with the ALl group, The PVPI of the ALl group was 0.38±0.04, significantly higher than that of the normal control group （0.20±0.02, P 〈0.01）, AT-Ⅲ treatment group （0.30±0.04, P 〈0.01） and heparin treatment group （0.28±0.04, P 〈0.01） respectively. There were no significant differences of PVPI in the ALl group and AT-Ⅲ＋heparin treatment group. The activity of AT-Ⅲ in plasma in the ALl group was （76±8）%, significantly lower than that of the normal control group （（96±11）%, P 〈0.05） and AT-Ⅲ treatment group （（105±17）%, P 〈0.05） respectively. The serum levels of TNF-α and I L-6 of the ALl group were （2.770±0.373） μg/L and （1.615±0.128） ng/ml respectively, significantly higher than those of the normal control group （0.506±0.093） μg/L and （0.233±0.047） ng/ml respectively, all P 〈0.01）, AT-Ⅲ treatment group （（1.774±0.218） pg/L and （1.140±0145） ng/ml respectively, all P 〈0.01） and heparin treatment group （（1.924±0.349） μg/L and （1.223±0.127） ng/ml respectively, all P

关键词： antithrombin-lll heparin mitogen-activated protein kinase endotoxin acute lung injury

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