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Xiaokeping-containing serum suppresses high-glucose-induced proliferation of mesangial cells involved in the regulation of cell cycle progression and the p38 mitogen-activated protein kinase pathway

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Journal of Traditional Chinese Medicine 2021年第1期41卷 44-50页

作者： XIN Chuanwei XIA Zhongni YANG Bo LU Lisong Department of Pharmacy Zhejiang Academy of Traditional Chinese MedicineTongde Hospital of Zhejiang ProvinceHangzhou 310012China

OBJECTIVE: To investigate the efficacy of Xiaokeping(XKP)-containing serum on the proliferation of high-glucose-induced mesangial cells(MCs)and the potential underlying ***: XKP-containing serum was prepared by the intragastric administration of XKP in ***-1 cells were cultured with normal glucose(NC group), high glucose(HG group), and high glucose with different XKP concentrations. Cell proliferation was assessed by the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay,and the cell cycle distribution was detected by flow cytometry. The expression of p38 mitogen-activated protein kinase(p38 MAPK) pathway components in MCs was detected by Western blotting and quantitative real-time polymerase chain ***: The MC proliferation level in the high-glucose group was significantly higher than that in the normal control group, and XKP suppressed the HG-induced proliferation of MCs dose dependently. Moreover, flow cytometry revealed that XKP blocked cell cycle progression by inducing cell cycle arrest in G1 phase and inhibiting S phase entry. XKP down-regulated the protein and m RNA expression of p38 MAPK in MCs(P < 0.05 vs HG).CONCLUSION: The present study demonstrated that XKP-containing serum inhibits high-glucoseinduced proliferation of MCs by causing cell cycle arrest at G1 phase and inhibiting S phase entry. The underlying mechanism involves the down-regulation of the p38 MAPK signaling pathway, providing a theoretical basis for the use of XKP to treat diabetic kidney disease.

关键词： mesangial cells cell proliferation cell cycle p38 mitogen-activated protein kinase Xiaokeping mixture

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Effects of Herbal Compound 861 on Collagen Synthesis and Degradation in Rat mesangial cells Exposed to High Glucose

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Chinese Journal of Integrative Medicine 2014年第3期20卷 209-215页

作者：马清张丽姚兰陈海平王宝恩 Department of Gerontology Beijing Friendship HospitalCapital Medical University

Objective： To investigate the effects of Herbal Compound 861 （Cpd 861） on collagen synthesis and degradation in rat mesangial cells exposed to high glucose. Methods： The third to fifth passage of rat mesangial cells were exposed to high glucose and Cpd 861 at a concentration of 0.25-4.00 g/L for 24, 48 and 72 h, respectively. Benazepril （107-10s mmol/L） was selected as positive control. The methyl thiazolyl tetrazolium colorimetric assay was used to evaluate the effect of Cpd 861 on cell proliferation. After incubation with Cpd 861 at a concentration of 2.00 g/L for 48 h, the protein secretions of collagen type IV, matrix metallopeptidase 9 （MMP-9）, tissue inhibitor of metalloproteinase-1 （TIMP-1）, transforming growth factor beta 1 （TGF-131）, and hepatocyte growth factor （HGF） were detected by enzyme-linked immunosorbent assay method. And rat mesangial cells were harvested to determine MMP-9, TIMP-1, TGF-131 and HGF mRNA expression by revers^transcription polymerase chain reaction. Results： Cpd 861 inhibited cell proliferation induced by high glucose in a dose- and time-dependent manner. Compared with high glucose, collagen type IV production was decreased significantly by Cpd 861 （P〈0.01）. Cpd 861 increased the protein secretions and mRNA expressions of MMP-9 and HGF, whereas the protein secretions and mRNA expressions of TIMP-1 and TGF-131 were reduced markedly （P〈0.05）. The ratio of MMP-9 to TIMP-1 was enhanced by Cpd 861 significantly. There was no significant difference in all above-mentioned effects between Cpd 861 （2.00 g/L） and benazepril （10-5 mmol/L）. Conclusion： The anti-glomerulosclerosis mechanisms of Cpd 861 were partly attributed to its effects of inhibiting mesangial cell proliferation, decreasing collagen synthesis and enhancing collagen degradation.

关键词： Herbal Compound 861 mesangial cells collagen type IV matrix metalloproteinase cytokine

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IDENTIFICATION OF GLUCOSE TRANSPORTER- 1 AND ITS FUNCTIONAL ASSAY IN MOUSE GLOMERULAR mesangial cells CULTURED IN VITRO

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Chinese Medical Sciences Journal 2001年第1期16卷 35-39页

作者：章精刘志红刘栋黎磊石 Research Institute of Nephrology Jingling Hospital Nanjing University School of Medicine Nanjing 210002 esearch Institute of Nephrology Jingling Hospital Nanjing University School of Medicine Nanjing 210002

To evaluate the role of glucose transporter- l (GLUT1) in the glucose uptake of glomerular mesangial cells. Methods. Cultured C57/SJL mouse mesangial cells were used in the study. The expression of GLUT1 mRNA was detected by RT- PCR. The expression of GLUT1 protein was detected by immunofluorescence and flow cytometry. The uptake of glucose and its kinetics were determined by 2- deoxy- [3H]- D- glucose uptake. Results. Both GLUT1 mRNA and protein were found in mouse glomerular mesangial cells. 2- deoxy- D- glucose uptake and kinetics assay showed that this glucose transporter had high affinity for glucose and the glucose uptake specificity was further confirmed by phloretin. Conclusion. Functional GLUT1 did present in mouse mesangial cells cultured in vitro and it might be the predominant transporter mediated the uptake of glucose into mesangial cells.

关键词： glucose transporter- 1 mesangial cells phloretin diabetic nephropathy

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Interleukin-13 inhibits cytokines synthesis by blocking nuclear factor-κB and c-Jun N-terminal kinase in human mesangial cells

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The Journal of Biomedical Research 2010年第4期24卷 308-316页

作者： Chunhua Zhu Aihua Zhang Songming Huang GuixiaDing Xiaoqin Pan Ronghua Chen Nanjing Children 's Hospital Affiliated to Nanjing Medical University Nanjing 210008 Jiangsu Province China Institute of Pediatrics Nanjing Medical University Nanjing 210029 Jiangsu Province China

Objective： Monocytes/macrophages, proinflammatory cytokines and chemokines are important in the pathogenesis of glomerulonephritis. Interleukin （IL） -13 has been shown to exert potent anti-inflammatory properties. This study was designed to investigate the effect of IL-13 on the expression of proinflammatory cytokines, chemokines and profibrogenic cytokines and the involved molecular mechanism in cultured human mesangial cells （HMCs）. Methods： The expressions of proinflammatory cytokines, chemokines and profibrogenic cytokines were determined by ribonuclease protection assay （RPA）. Activity of nuclear factor-kappa B （NF-κB） and activa- tor protein-1 （AP-1） was examined by electrophoretic mobility shift assay （EMSA）. NF-κB subunit p65 nuclear transportation and c-Jun N-terminal kinase （JNK） activity were assayed by immunoblot. Results： Recombinant IL-13 inhibited tumor necrosis factor-α （TNF-u）, IL-1α, IL-1β, monocyte chemoattractant protein-1 （MCP-1）, IL-8, and transforming growth factor-β1 （TGF-β1） mRNA expressions in a dose-dependent manner. Lipopoly- sacchorides （LPS） dramatically increased NF-κB DNA binding activity of HMCs, which was inhibited by IL-13 in a dose-dependent manner. LPS-activated NF-κB contained p50 and p65 dimers, but not c-Rel subunit. IL-13 blocked LPS-induced NF-κB subunit p65. LPS stimulated JNK/AP-1 activation, which was inhibited by IL-13 in a dose-dependent manner. Conclusion： IL-13 inhibits proinflammatory cytokines, chemokines, and profibrogenic cytokines synthesis by blocking NF-κB and JNK/AP-1 activation. These observations point to the importance of IL-13 in the modulation of inflammatory processes in the renal glomerulus.

关键词： mesangial cells interleukin-13 inflammation

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AP-1 mediated signal transduction in thrombin induced regulation of PAL-1 expression in human mesangial cells

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Chinese Medical Journal 2000年第6期 34-39页

作者：陈香美何庆南刘文虎徐启河叶一舟傅博于力方

Objective To evaluate activator protein 1(AP 1) mediated mechanisms in thrombin induced qlasmino^gen activator inhibitor 1 (PAI 1) expression in cultured human glomerular mesangial cells (MCs) Methods Electrophoretic mobility shift assay (EMSA) was employed to assess AP 1 DNA binding activity, and Western blot hybridization was used for quantification of c fos and c jun, two subunits of AP 1 dimers PAI 1 activity and mRNA expression were analysed by the fibrin plate assay and Northern hybridization, respectively Results Thrombin concentration enhanced PAI 1 activity in the supernatant and stimulated PAI 1 mRNA expression in cultured MCs PAI 1 activity was blocked by hirudin, a specific inhibitor of thrombin Further study demonstrated that thrombin promoted AP 1 DNA binding activity but exerted little effect on c fos or c jun Curcumin (AP 1 inhibitor), staurosporine (PKC inhibitor), and genistein (PTK inhibitor) all reduced AP 1 mediated PAI 1 mRNA expression induced by thrombin in cultured MCs Conclusion The present study indicates that in cultured human MCs, thrombin stimulates PAI 1 expression through an AP 1 signal pathway, which may be mediated by PKC and PTK

关键词： thrombin · activator protein-1 · plasminogen activator inhibitor-1 · mesangial cells

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Effects of Cyclosporin A on Proliferation of Cultured Rat mesangial cells

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Journal of Huazhong University of Science and Technology(Medical Sciences) 1997年第2期17卷 115-117页

作者：孙建平王韵琴 Department of Pediatrics Tongji Hospital Tongji Medical University Wuhan

The proliferation of mesangial cells on cyclosporin (CsA) test mediumwas studied by MTT assay and TNF-Q in cultured supernatant was examined byusing ELISA. The results showed that cyclosporin A significantly inhibited theproliferation of mesangial cells at the concentration between 0. 25 - 15 μg/ml(IC50 1μg/ml). This action appeared to be dose-dependent. Release of TNF-αfrom mesangial cells stimulated by LPS was also dose-dependently suppressed. Itis suggested that cyclosporin A play an important role in antiproliferation mecha-nism of mesangial cells in vitro.

关键词： cyclosporin A mesangial cells tumor necrosis factor-α

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Acortatarin A inhibits high glucose-induced extracellular matrix production in mesangial cells

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Chinese Medical Journal 2013年第7期126卷 1230-1235页

作者： ZHAO Zhi-fang ZHOU Li-li CHEN Xia CHENG Yong-xian HOU Fan-fan NIE Jing Division of Neph-rology Nanfang Hospital Southern Medical University Research Institute ofNephrology Guangdong Province Key Laboratory for Organ Failure Research Ministry of Education Guangzhou Guangdong 510515 China State Key Laboratory of Phytochemistry and Plant Resources in West China Kunming Institute of Botany Chinese Academy of Sciences Kunming Yunnan 650204 China

Background Diabetic nephropathy （DN） is the leading cause of end-stage renal disease. Various treatment regimens and combinations of therapies provide only partial renoprotection. Therefore new approaches are needed to retard the progression of DN. The aim of the present study was to evaluate the role of a novel spiroalkaloid from Acorus tatarinowii named acortatarin A （AcorA） in inhibiting high glucose-induced extracellular matrix accumulation in mesangial cells （MCs）. Methods The cytotoxity of AcorA on MCs was examined by 3-（4,5-dimethylthiazol-2-yl）-2.5-diphenyltetrazolium bromide （MTT） assay. The expression of fibronectin and collagen IV was examined by real time PCR and western blotting. The expression of p22phox and p47phox was detected by western blot. The interaction between p22phox and p47phox was examined by co-immunoprecipitation. The phosphorylation of p47phox was examined by immunoprecipitation. The phosphorylation of protein kinase C （PKC） α, PKCβ, phospholiase C gamma （PLCγ1）, and the p85 subunit of PI3K was determined by Western blotting. Results AcorA significantly inhibited high glucose-induced activation of NADPH oxidase, a ROS-generating enzyme, by increasing phosphorylation of p47phox and enhancing interaction between p22phox and p47phox. Preincubation of AcorA with MCs inhibited high glucose-induced collagen IV and fibronectin production in a dose-dependent manner. Moreover, AcorA attenuated high glucose enhanced phosphorylation of PKCα, PKCβ, PLCγ1, and the p85 subunit of PI3K. Conclusion AcorA inhibits high glucose-induced extracellular matrix production via blockinq NADPH oxidase activation.

关键词： acortatarin A high glucose mesangial cells extracellular matrix

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Pioglitazone inhibits the expression of nicotinamide adenine dinucleotide phosphate oxidase and p38 mitogen-activated protein kinase in rat mesangial cells

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Chinese Medical Journal 2013年第21期126卷 4054-4059页

作者： Wang Shan Ye Shan-dong Sun Wen-jia Hu Yuan-yuan Anhui Med Univ Anhui Prov Hosp Dept Endocrinol Hefei 230001 Anhui Peoples R China

Background Oxidative Stress and p38 mitogen-activated protein kinase （p38MAPK） play a vital role in renal fibrosis. Pioglitazone can protect kidney but the underlying mechanisms are less clear. The purpose of this study was to investigate the effect of pioglitazone on oxidative stress and whether the severity of oxidative stress was associated with the phosphorylation level of p38MAPK.

关键词： nicotinamide adenine dinucleotide phosphate oxidase p38 mitogen-activated protein kinase oxidative stress,"pioglitazone mesangial cells

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Proliferation of renal mesangial cells induced by very low density lipoprotein is mediated by p42/44 mitogen activated protein kinase

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Chinese Medical Journal 2010年第19期123卷 2710-2713页

作者： YU Guo-qing YUAN Wei-jie CUI Ruo-lan FU Peng Division of Nephrology Dongfang Hospital Fuzhou Fujian 350025 China Division of Nephrology Shanghai Jiao Tong University Affiliated First People's Hospital Shanghai 200080 China Division of Nephrology Changhai Hospital Second Military Medical University Shanghai 200433 China

Background The plasma concentration of very low density lipoprotein （VLDL） is negatively correlated to renal function in glomerular diseases. Effects of VLDL on renal function have been partially attributed to the proliferation of mesangial cells. This study examined the potential role of the p42/44 mitogen activated protein kinase （MAPK） in mesangial cell proliferation induced by VLDL. Methods mesangial cells were treated with VLDL at different concentrations or for different time. The cell cycle of the mesangial cells was analyzed by Xl-r assay and flow-cytometry; MAPK activity was also assayed. In some experiments, cells were treated with VLDL together with or without 0.1 pmol/L PD 98059. Results Ten to 500 μg/ml VLDL stimulated the proliferation of mesangial cells cultured in vitro in a concentration-dependent manner. The effect was associated with an increase in p42/44 MAPK activity. Increased proliferation of mesangial cells by VLDL was significantly attenuated by PD98059, a specific p42/44 MAPK inhibitor. Conclusion These results indicate that the p42/44 MAPK pathway is an important regulator of mesangial cell proliferation and of renal functions.

关键词： mesangial cells p42/44 mitogen activated protein kinase," proliferation," very low density lipoprotein

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Effects of advanced glycosylation end products and rosiglitazone on the expression and secretion of galectin-3 in human renal mesangial cells

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Chinese Medical Journal 2009年第9期122卷 1067-1071页

作者： SUN Zi-lin MA Chan-juan JIN Hui YUAN Yang LIU Nai-feng Department of Endocrinology Zhongda Hospital Southeast University Nanjing Jiangsu 210009China Department of Cardiology Zhongda Hospital SoutheastUniversity Nanjing Jiangsu 210009 China

Background Galectin-3 is the most recently identified advanced glycosylation end products （AGEs） binding protein. This study aimed to investigate the effects of AGEs and rosiglitazone on the expression and secretion of galectin-3 in cultured human renal mesangial cells （HRMCs）. Methods HRMCs were incubated with different concentrations of AGE-bovine serum albumin （BSA）（0, 50, 100, 200, and 400 mg/L） for different time （0, 24, 36, 48, and 72 hours）, and exposed to AGE-BSA in the presence of different concentrations of rosiglitazone （1, 10, and 100 μmol/L）. The mRNA and protein expression of galectin-3 in HRMCs were analyzed by reverse transcription polymerase chain reaction （RT-PCR） and Western blotting. The culture medium of HRMCs was collected and concentrated, and the content of galectin-3 in the medium was detected by Western blotting. Results Both RT-PCR and Western blotting revealed that AGE-BSA up-regulated the expression of galectin-3 in HRMCs in a concentration- （P 〈0.05） and time-dependent （P 〈0.05） manner compared with the control. Compared with the control, AGE-BSA elevated the content of galectin-3 in the culture medium of HRMCs time- and concentrationdependently （P 〈0.05, respectively）. Both protein and mRNA expression of galectin-3, and its content in the medium of HRMCs exposed to different concentrations of rosiglitazone in the presence of AGE-BSA were increased compared with those of cells exposed to AGE-BSA alone （P 〈0.05）. Rosiglitazone increased the expression and secretion of galectin-3 in a dose-dependent manner （P 〈0.05）. Conclusions AGEs up-regulates the expression and secretion of galectin-3 in HRMCs. Rosiglitazone further enhances the upregulation of galectin-3 in HRMCs induced by AGEs, which suggests that rosiglitazone may play a role of reno-protection via up-regulation of galectin-3.

关键词： glycosylation end products, advanced galectin 3 diabetic nephropathies rosiglitazone mesangial cells

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