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[PMID]: 29499191
[Au] Autor:Salama SA; Arab HH; Omar HA; Gad HS; Abd-Allah GM; Maghrabi IA; Al Robaian MM
[Ad] Address:Division of Biochemistry, Department of Pharmacology and GTMR Unit, College of Clinical Pharmacy, Taif University, Taif, 21974, Saudi Arabia; Department of Biochemistry, Faculty of Pharmacy, Al-Azhar University, Cairo, 11751, Egypt. Electronic address: salama.3@buckeyemail.osu.edu.
[Ti] Title:L-carnitine mitigates UVA-induced skin tissue injury in rats through downregulation of oxidative stress, p38/c-Fos signaling, and the proinflammatory cytokines.
[So] Source:Chem Biol Interact;285:40-47, 2018 Feb 27.
[Is] ISSN:1872-7786
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:UVA comprises more than 90% of the solar UV radiation reaching the Earth. Artificial lightening lamps have also been reported to emit significant amounts of UVA. Exposure to UVA has been associated with dermatological disorders including skin cancer. At the molecular level, UVA damages different cellular biomolecules and triggers inflammatory responses. The current study was devoted to investigate the potential protective effect of L-carnitine against UVA-induced skin tissue injury using rats as a mammalian model. Rats were distributed into normal control group (NC), L-carnitine control group (LC), UVA-Exposed group (UVA), and UVA-Exposed and L-carnitine-treated group (UVA-LC). L-carnitine significantly attenuated UVA-induced elevation of the DNA damage markers 8-oxo-2'-deoxyguanosine (8-oxo-dG) and cyclobutane pyrimidine dimers (CPDs) as well as decreased DNA fragmentation and the activity of the apoptotic marker caspase-3. In addition, L-carnitine substantially reduced the levels of lipid peroxidation marker (TBARS) and protein oxidation marker (PCC) and significantly elevated the levels of the total antioxidant capacity (TAC) and the antioxidant reduced glutathione (GSH) in the skin tissues. Interestingly, L-carnitine upregulated the level of the DNA repair protein proliferating cell nuclear antigen (PCNA). Besides it mitigated the UVA-induced activation of the oxidative stress-sensitive signaling protein p38 and its downstream target c-Fos. Moreover, L-carnitine significantly downregulated the levels of the early response proinflammatory cytokines TNF-α, IL-6, and IL-1ß. Collectively, our results highlight, for the first time, the potential attenuating effects of L-carnitine on UVA-induced skin tissue injury in rats that is potentially mediated through suppression of UVA-induced oxidative stress and inflammatory responses.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1803
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher

  2 / 18065 MEDLINE  
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[PMID]: 29325918
[Au] Autor:Nan X; Su S; Ma K; Ma X; Wang X; Zhaxi D; Ge R; Li Z; Lu D
[Ad] Address:Research Center for High Altitude Medicine, Qinghai University, Xining 810001, China; Key Laboratory of Application and Foundation for High Altitude Medicine Research in Qinghai Province, Xining 810001, China.
[Ti] Title:Bioactive fraction of Rhodiola algida against chronic hypoxia-induced pulmonary arterial hypertension and its anti-proliferation mechanism in rats.
[So] Source:J Ethnopharmacol;216:175-183, 2018 Apr 24.
[Is] ISSN:1872-7573
[Cp] Country of publication:Ireland
[La] Language:eng
[Ab] Abstract:ETHNOPHARMACOLOGICAL RELEVANCE: Rhodiola algida var. tangutica (Maxim.) S.H. Fu is a perennial plant of the Crassulaceae family that grows in the mountainous regions of Asia. The rhizome and roots of this plant have been long used as Tibetan folk medicine for preventing high latitude sickness. AIM OF THE STUDY: The aim of this study was to determine the effect of bioactive fraction from R. algida (ACRT) on chronic hypoxia-induced pulmonary arterial hypertension (HPAH) and to understand the possible mechanism of its pharmacodynamic actions. MATERIALS AND METHODS: Male Sprague-Dawley rats were separated into five groups: control group, hypoxia group, and hypoxia+ACRT groups (62.5, 125, and 250mg/kg/day of ACRT). The chronic hypoxic environment was created in a hypobaric chamber by adjusting the inner pressure and oxygen content for 4 weeks. After 4 weeks, major physiological parameters of pulmonary arterial hypertension such as mPAP, right ventricle index (RV/LV+S, RVHI), hematocrit (Hct) levels and the medial vessel thickness (wt%) were measured. Protein and mRNA expression levels of proliferating cell nuclear antigen (PCNA), cyclin D1, p27Kip1 and cyclin-dependent kinase 4 (CDK4)) were detected by western blotting and real time PCR respectively. Chemical profile of ACRT was revealed by ultra performance liquid chromatography coupled with quadrupole time of flight mass spectrometry (UHPLC-Q-TOF-MS/MS). RESULTS: The results showed that a successful HPAH rat model was established in a hypobaric chamber for 4 weeks, as indicated by the significant increase in mPAP, RV/LV+S, RV/BW and wt%. Compared with the normal group, administration of ACRT reduced mPAP, right ventricular hypertrophy, pulmonary small artery wall thickness, and damage in ultrastructure induced by hypoxia in rats. PCNA, cyclin D1, and CDK4 expression was reduced (p<0.05), and p27Kip1 expression increased (p<0.05) in hypoxia+ACRT groups compared to hypoxia. 38 constituents in bioactive fraction were identified by UHPLC-Q-TOF-MS/MS. CONCLUSION: Our results suggest that ACRT could alleviate chronic hypoxia-induced pulmonary arterial hypertension. And its anti-proliferation mechanism in rats based on decreasing PCNA, cyclin D1, CDK4 expression level and inhibiting p27Kip1 degradation.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1801
[Cu] Class update date: 180310
[Lr] Last revision date:180310
[St] Status:In-Process

  3 / 18065 MEDLINE  
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[PMID]: 29484407
[Au] Autor:Yu S; Chen Y; Chen S; Ye N; Li Y; Sun Y
[Ad] Address:Department of Cardiology, The First Hospital of China Medical University, Shenyang, Liaoning 110001, P.R. China.
[Ti] Title:Regulation of angiotensin II-induced B-cell lymphoma-2-associated athanogene 3 expression in vascular smooth muscle cells.
[So] Source:Mol Med Rep;17(4):6156-6162, 2018 Apr.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Previous studies have demonstrated that angiotensin II (Ang II) is involved in the process of atherosclerosis and vascular restenosis through its proinflammatory effect. Bcl­2­associated athanogene 3 (BAG3) had been suggested to be associated with proliferation, migration and invasion in many types of tumor. However, the role of BAG3 among the proliferative process of vascular smooth muscle cells (VSMCs) induced by Ang II, to the best of our knowledge, remains to be investigated. The present study demonstrated that in growth­arrested VSMCs, Ang II­induced VSMC proliferation, accompanied by increased BAG3 mRNA and protein expression levels in a dose­ and time­dependent manner. BAG3 expression levels were measured in VSMCs treated in the presence or absence of Ang II. The proliferation of VSMCs was assessed using manual cell counting and Cell Counting kit­8 assays. mRNA and protein expression levels of BAG3, Toll­like receptor 4 (TLR4), proliferating cell nuclear antigen, nuclear factor (NF)­κB p65, smooth muscle protein 22α and phosphorylated NF­κB p65 were assessed by reverse transcription­quantitative polymerase chain reaction and western blotting, respectively. In non­transfected or scramble short hairpin RNA (shRNA)­transfected VSMCs cells, Ang II significantly induced VSMC proliferation. However, this Ang II­induce proliferation was attenuated when BAG3 was silenced, suggesting that inhibition of BAG3 may somehow reduce proliferation in Ang II­induced VSMCs. Furthermore, the TLR4/NF­κB p65 signaling pathway was involved in BAG3 gene upregulation. In conclusion, to the best of our knowledge, the present study demonstrated for the first time that inhibition of BAG3 attenuates cell proliferation. Furthermore, Ang II induced VSMCs proliferation through regulation of BAG3 expression via the TLR4/NF­κB p65 signaling pathway.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.3892/mmr.2018.8630

  4 / 18065 MEDLINE  
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[PMID]: 29451151
[Au] Autor:Luo L; Yu ZP; Qin H; Zhu ZX; Liao MH; Liao HT; Yuan KF; Zeng Y
[Ad] Address:Department of Liver Surgery, Liver Transplantation Division, West China Hospital, Sichuan University, Chengdu, Sichuan 610041, China.
[Ti] Title:Exosomal MicroRNA-10a Is Associated with Liver Regeneration in Rats through Downregulation of EphA4.
[So] Source:Chin Med J (Engl);131(4):454-460, 2018 Feb 20.
[Is] ISSN:0366-6999
[Cp] Country of publication:China
[La] Language:eng
[Ab] Abstract:Background: MicroRNAs (miRNAs) have been reported to play vital roles in liver regeneration. Previous studies mainly focused on the functions of intracellular miRNAs, while the functions of circulating exosomal miRNAs in liver regeneration remain largely unknown. The aim of this study was to identify the key exosomal miRNA that played vital roles in liver regeneration. Methods: The Sprague-Dawley male rats were assigned to 70% partially hepatectomized group (n = 6) and sham surgery group (n = 6). The peripheral blood of both groups was collected 24 h after surgery. The exosomal miRNAs were extracted, and microarray was used to find out the key miRNA implicated in liver regeneration. Adenovirus was used to overexpress the key miRNA in rats, and proliferating cell nuclear antigen (PCNA) staining was applied to study the effect of key miRNA overexpression on liver regeneration. Western blotting was used to validate the predicted target of the key miRNA. Results: Exosomal miR-10a was upregulated more than nine times in hepatectomized rats. The level of miR-10a was increased in the early phase of liver regeneration, reached the top at 72 h postsurgery, and decreased to perioperative level 168 h after surgery. Moreover, enforced expression of miR-10a by adenovirus facilitated the process of liver regeneration as evidenced by immunohistochemical staining of PCNA. Erythropoietin-producing hepatocellular receptor A4 (EphA4) has been predicted to be a target of miR-10a. The protein level of EphA4 was decreased in the early phase of liver regeneration, reached the bottom at 72 h postsurgery, and rose to perioperative level 168 h after surgery, which was negatively correlated with miR-10a, confirming that EphA4 served as a downstream target of miR-10a. Moreover, inhibition of EphA4 by rhynchophylline could promote the proliferation of hepatocytes by regulating the cell cycle. Conclusion: Exosomal miR-10a might accelerate liver regeneration through downregulation of EphA4.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.4103/0366-6999.225057

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[PMID]: 29440488
[Au] Autor:Janke R; King GA; Kupiec M; Rine J
[Ad] Address:Department of Molecular and Cell Biology, University of California, Berkeley, CA 94720.
[Ti] Title:Pivotal roles of PCNA loading and unloading in heterochromatin function.
[So] Source:Proc Natl Acad Sci U S A;115(9):E2030-E2039, 2018 Feb 27.
[Is] ISSN:1091-6490
[Cp] Country of publication:United States
[La] Language:eng
[Ab] Abstract:In , heterochromatin structures required for transcriptional silencing of the and loci are duplicated in coordination with passing DNA replication forks. Despite major reorganization of chromatin structure, the heterochromatic, transcriptionally silent states of and are successfully maintained throughout S-phase. Mutations of specific components of the replisome diminish the capacity to maintain silencing of and through replication. Similarly, mutations in histone chaperones involved in replication-coupled nucleosome assembly reduce gene silencing. Bridging these observations, we determined that the proliferating cell nuclear antigen (PCNA) unloading activity of Elg1 was important for coordinating DNA replication forks with the process of replication-coupled nucleosome assembly to maintain silencing of and through S-phase. Collectively, these data identified a mechanism by which chromatin reassembly is coordinated with DNA replication to maintain silencing through S-phase.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Data-Review
[do] DOI:10.1073/pnas.1721573115

  6 / 18065 MEDLINE  
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[PMID]: 29431281
[Au] Autor:Wang P; Han J; Wei M; Xu Y; Zhang G; Zhang H; Shi L; Liu X; Hamblin MR; Wang X
[Ad] Address:Institute of Photomedicine, Shanghai Skin Disease Hospital, Tongji University School of Medicine, Shanghai, China.
[Ti] Title:Remodeling of dermal collagen in photoaged skin using low-dose 5-aminolevulinic acid photodynamic therapy occurs via the TGF-ß pathway.
[So] Source:J Biophotonics;, 2018 Feb 12.
[Is] ISSN:1864-0648
[Cp] Country of publication:Germany
[La] Language:eng
[Ab] Abstract:5-Aminolevulinic acid photodynamic therapy (ALA-PDT) is known to be effective in the treatment of photoaged skin. However, the molecular mechanisms still remain elusive. Protoporphyrin IX (PpIX) fluorescence is primarily located in the epidermis while ALA-PDT affects the dermal collagen, presumably by an indirect mechanism. This study aimed to investigate the molecular communication in low-dose ALA-PDT occurring between epidermal keratinocytes and dermal fibroblasts. Western blotting and enzyme-linked immunosorbent assays were performed to evaluate collagen expression and transforming growth factor-ß (TGF-ß) signaling in human keratinocytes and dermal fibroblasts. The impact on fibroblast proliferation was assessed by morphology and proliferating cell nuclear antigen immunofluorescence. Skin biopsies from mice were used to analyze the histological changes in dermal collagen and PpIX distribution. When fibroblasts were co-cultured with keratinocytes treated with low-dose ALA-PDT, collagen synthesis and fibroblast proliferation were enhanced. Low-dose ALA-PDT stimulated TGF-ß1 expression in keratinocytes. Fibroblasts co-cultured with low-dose ALA-PDT treated keratinocytes also showed activation of the TGF-ß pathway. In vivo, PpIX fluorescence was densely distributed in photoaged mouse epidermis while collagen in the mouse dermis underwent remodeling. This study suggests that low-dose ALA-PDT can stimulate keratinocytes to release TGF-ß1, activating the TGF-ß pathway in dermal fibroblasts to remodel collagen in the dermis.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:Publisher
[do] DOI:10.1002/jbio.201700357

  7 / 18065 MEDLINE  
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[PMID]: 29393459
[Au] Autor:Zhao W; Zhang X; Zhou Z; Sun B; Gu W; Liu J; Zhang H
[Ad] Address:Key Laboratory of Hormones and Development (Ministry of Health), Tianjin Key Laboratory of Metabolic Diseases, Tianjin Metabolic Diseases Hospital and Tianjin Institute of Endocrinology, Tianjin Medical University, Tianjin 300070, P.R. China.
[Ti] Title:Liraglutide inhibits the proliferation and promotes the apoptosis of MCF-7 human breast cancer cells through downregulation of microRNA-27a expression.
[So] Source:Mol Med Rep;17(4):5202-5212, 2018 Apr.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:The use of glucagon-like peptide-1 analogues, such as liraglutide, as hypoglycemic drugs has been widely employed in clinical practice. Liraglutide is reported to exert potential anti­breast cancer effects, however the specific mechanisms of this action remain unknown. In the present study, MCF­7 human breast cancer cells were cultured in vitro and treated with various concentrations of liraglutide. Cell Counting Kit­8, colony formation and flow cytometry assays were performed to determine the proliferation and apoptosis of cells following treatment. Furthermore, reverse transcription­quantitative polymerase chain reaction was employed to measure the expression level of microRNA (miRNA/miR)-27a. In addition, miR­27a mimics, inhibitors and negative controls were transfected into MCF­7 cells and the proliferation and apoptosis of cells following transfection was subsequently determined. Western blotting was performed to detect alterations in the protein expression of AMP­activated protein kinase catalytic subunit α2 (AMPKα2), proliferating cell nuclear antigen and cleaved­caspase­3 following treatments. The results demonstrated that, following treatment with liraglutide, the proliferation of MCF­7 cells was reduced and the apoptosis was increased, compared with the control group; this effect was increased with increasing concentrations of liraglutide. In addition, liraglutide treatment downregulated miR­27a expression in MCF­7 cells. While the overexpression of miR­27a promoted cell proliferation and inhibited apoptosis, knockdown of endogenous miR­27a inhibited cell proliferation and promoted apoptosis in MCF­7 cells. Furthermore, the expression of AMPKα2 protein in the group transfected with miR­27a mimics was decreased, while it was increased in MCF­7 cells transfected with miR­27a inhibitors. In conclusion, liraglutide may have a role in the inhibition of proliferation and promotion of apoptosis in MCF­7 cells. Concerning the mechanism of these effects, liraglutide may inhibit miR­27a expression, which subsequently increases the expression of AMPKα2 protein. The present study provides an experimental basis for the clinical treatment strategies of T2DM patients with breast cancer.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.3892/mmr.2018.8475

  8 / 18065 MEDLINE  
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[PMID]: 29393453
[Au] Autor:Liu J; Liu Z; Hu X; Zhang Y; Zhang S
[Ad] Address:Department of Neurosurgery, The First Affiliated Hospital of Soochow University, Suzhou, Jiangsu 215006, P.R. China.
[Ti] Title:Synthetic E-selectin prevents postoperative vascular restenosis by inhibiting nuclear factor κB in rats.
[So] Source:Mol Med Rep;17(4):5065-5073, 2018 Apr.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:During the development of postoperative vascular restenosis, the aberrant proliferation of vascular smooth muscle cells (VSMCs) is a critical event resulting in intimal hyperplasia. Inflammatory responses involving the activation of nuclear factor (NF)­κB are among the major molecular processes underlying restenosis. The present study aimed to investigate the roles of NF­κB in VSMC proliferation and restenosis following vascular anastomosis, as well as to evaluate the potential of synthetic E­selectin to downregulate NF­κB and thus inhibit vascular hyperplasia. A total of 72 adult male Sprague­Dawley rats were randomly assigned to three groups: Control, operation and treatment groups. Rats in the operation and treatment groups received longitudinal incisions in the right carotid arteries, which were closed using interrupted sutures. Following vascular anastomosis, synthetic E­selectin (10 mg/kg), or an equal volume of saline, was immediately injected into the right femoral vein of rats in the treatment and operation groups, respectively. Following surgery, the mRNA and protein expression levels of NF­κB at the site of anastomosis, the levels of tumor necrosis factor­α and interleukin­6 in the serum, NF­κB binding activity, and the presence of proliferating cell nuclear antigen (PCNA)­positive cells were evaluated by western blotting, reverse transcription­quantitative polymerase chain reaction, ELISA, electrophoretic mobility shift assay and immunofluorescence staining. The present results demonstrated that following treatment with synthetic E­selectin, the levels of NF­κB and the inflammatory response, as well as the presence of PCNA­positive cells, were significantly reduced (P<0.01). In conclusion, the results of the present study suggested that synthetic E­selectin may exert anti­inflammatory and anti­restenotic effects following vascular anastomosis in vivo.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.3892/mmr.2018.8536

  9 / 18065 MEDLINE  
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[PMID]: 29393448
[Au] Autor:Huang J; Zhang D; Lin L; Jiang R; Dai J; Tang L; Yang Y; Ge P; Wang B; Zhang L
[Ad] Address:Department of Pathophysiology, Chongqing Medical University, Chongqing 400016, P.R. China.
[Ti] Title:Potential roles of AMP-activated protein kinase in liver regeneration in mice with acute liver injury.
[So] Source:Mol Med Rep;17(4):5390-5395, 2018 Apr.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:Liver regeneration post severe liver injury is crucial for the recovery of hepatic structure and function. The energy sensor AMP­activated protein kinase (AMPK) has a crucial role in the regulation of nutrition metabolism in addition to other energy­intensive physiological and pathophysiological processes. Cellular proliferation requires intensive energy and nutrition support, therefore the present study investigated whether AMPK is involved in liver regeneration post carbon tetrachloride (CCl4)­induced acute hepatic injury. The experimental data indicated that phosphorylation level of AMPK increased 48 h post­CCl4 exposure, which was accompanied with upregulation of proliferating cell nuclear antigen (PCNA) and recovery of alanine aminotransferase (ALT) level. Pretreatment with the AMPK inhibitor compound C had no obvious effects on ALT elevation in plasma and histological abnormalities in liver 24 h post CCl4 exposure. However, treatment with compound C 24 h post CCl4 exposure significantly suppressed CCl4­induced AMPK phosphorylation, PCNA expression and ALT recovery. These data suggest that endogenous AMPK was primarily activated at the regeneration stage in mice with CCl4­induced acute liver injury and may function as a positive regulator in liver regeneration.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.3892/mmr.2018.8522

  10 / 18065 MEDLINE  
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[PMID]: 29393352
[Au] Autor:Zhang J; Zhang J; Li T; Zhang N; Tang S; Tao Z; Zhou X; Sun X; Chen H
[Ad] Address:School of Medicine, Jiangsu University, Zhenjiang, Jiangsu 212001, P.R. China.
[Ti] Title:Effect of idebenone on bone marrow mesenchymal stem cells in vitro.
[So] Source:Mol Med Rep;17(4):5376-5383, 2018 Apr.
[Is] ISSN:1791-3004
[Cp] Country of publication:Greece
[La] Language:eng
[Ab] Abstract:In recent years, stem cell research has continued to benefit from its crossover with chemistry, particularly the investigation of small molecular drugs modulating specific targets to regulate stem cell fate. Idebenone (IDB) is a yellow crystalline powder that is used in the treatment of chronic cerebrovascular diseases. The objective of the present study was to examine whether IDB had an influence on bone marrow­derived mesenchymal stem cells (BMSCs) extracted from the bone marrow of Sprague­Dawley rats. The effects of IDB on cell proliferation, cell cloning and migration were investigated. Cell cycle, apoptosis, DAPI nuclear staining and senescence­associated ß­galactosidase (SA­ß­gal) staining were also examined. The results revealed that IDB at suitable concentrations enhanced cell cloning capacity, promoted the proliferation of BMSCs, delayed cellular senescence, and inhibited cell apoptosis and migration. Western blot analysis indicated that IDB increased the expression of B­cell lymphoma 2 (Bcl­2), signal transducer and activator of transcription­3, Nanog, octamer­binding transcription factor 4, E­cadherin, proliferating cell nuclear antigen, cyclinD1 and cyclinD3, and decreased the expression of Bcl­2­associated X protein, cleaved caspase­3, N­cadherin, vimentin and α­smooth muscle actin. In conclusion, these experiments confirmed that IDB in low doses had no toxic effect and may exert protective effects on BMSCs.
[Pt] Publication type:JOURNAL ARTICLE
[Em] Entry month:1802
[Cu] Class update date: 180309
[Lr] Last revision date:180309
[St] Status:In-Process
[do] DOI:10.3892/mmr.2018.8506


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