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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Iranian Journal of Immunology
- نوع مقاله: Journal Article
- کلمات کلیدی: multiple myeloma,Bone marrow mesenchymal stromal cells,CD8+ T Cell Anergy,Fibroblast Activation Protein a
- چکیده:
- چکیده انگلیسی: Background: Multiple myeloma (MM) is a malignant plasma cell proliferative disorder with limited immunotherapy treatment because of T cell dysfunction. Objective: To investigate the immunomodulatory function of bone marrow mesenchymal stromal cells (MM-BMSCs) on CD8+ T cells. Methods: Proliferation and cytotoxicity were detected by cell counting kit-8 assay. Cell cycle was detected by flow cytometry, and p16 expression was detected by PCR. The expression of fibroblast activation protein α (FAPα) was evaluated by immunohistochemistry. Results: Co-culture of CD8+ T cells with MM-BMSCs decreased the cell survival rate and increased the killing rate (p=0.03, p=0.001, respectively), the percentage of cells in G0/G1 phase and p16 expression (p<0.001). FAPα was mainly in the mesenchymal matrix of the MM microenvironment and elevated in MM derived bone marrow compared to healthy donors (p<0.001). The FAPα inhibitor PT-100, increased survival and the killing rate (p<0.001, p=0.043, respectively), and decreased the percentage of cells in G0/G1 phase and p16 expression (p=0.024, p=0.004, respectively). Conclusion: Therefore, MM-BMSCs inhibit the proliferation and cytotoxicity of CD8+ T cells, significantly block the cell cycle and increase p16 expression in co-cultured CD8+ T cells in a cell-cell contact-dependent manner.
- انتشار مقاله: 07-05-1398
- نویسندگان: Yadan Wang,Xiaofei Wu,Yu Hu
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: oxidative stress,Inflammation,Brain injury,Ginkgo biloba extract,Subarachnoid Hemorrhage
- چکیده:
- چکیده انگلیسی: Objective(s): To investigate the effect of Ginkgo biloba extract EGb761 in early brain injury (EBI) after subarachnoid hemorrhage (SAH) and its mechanism.
Materials and Methods: The SAH rat model was constructed and pre-treated with EGb761.The neurological function, severity of SAH, water content of brain tissue, damage degree of the blood-brain barrier, related indexes of oxidative stress, and the level of inflammatory cytokines were compared among the groups. The expression of TXNIP/NLRP3 signaling pathway-related proteins in brain tissues was detected by Western blot.
Results: After SAH modeling, the neurological function score was significantly reduced, the degree of brain injury, levels of oxidative stress, inflammatory factors, expression of NLRP3 and TXNIP were all increased. Compared with the SAH rats, the neurological function score of rats pre-treated by EGb761 was higher, the degree of brain injury, levels of oxidative stress and inflammatory factors, expression of NLRP3 and TXNIP were all lower.
Conclusion: EGb761 could protect neurological injury after SAH and its mechanism may be that EGb761 could inhibit the activation of the TXNIP/NLRP3 signaling pathway and inflammatory reaction after oxidative stress.- انتشار مقاله: 07-06-1398
- نویسندگان: Chuan Du,Chao Xi,Chunxiao Wu,Jichang Sha,Jinan Zhang,Chao Li
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: oxidative stress,Inflammation,Brain injury,Ginkgo biloba extract,Subarachnoid Hemorrhage
- چکیده:
- چکیده انگلیسی: Objective(s): To investigate the effect of Ginkgo biloba extract EGb761 in early brain injury (EBI) after subarachnoid hemorrhage (SAH) and its mechanism.
Materials and Methods: The SAH rat model was constructed and pre-treated with EGb761.The neurological function, severity of SAH, water content of brain tissue, damage degree of the blood-brain barrier, related indexes of oxidative stress, and the level of inflammatory cytokines were compared among the groups. The expression of TXNIP/NLRP3 signaling pathway-related proteins in brain tissues was detected by Western blot.
Results: After SAH modeling, the neurological function score was significantly reduced, the degree of brain injury, levels of oxidative stress, inflammatory factors, expression of NLRP3 and TXNIP were all increased. Compared with the SAH rats, the neurological function score of rats pre-treated by EGb761 was higher, the degree of brain injury, levels of oxidative stress and inflammatory factors, expression of NLRP3 and TXNIP were all lower.
Conclusion: EGb761 could protect neurological injury after SAH and its mechanism may be that EGb761 could inhibit the activation of the TXNIP/NLRP3 signaling pathway and inflammatory reaction after oxidative stress.- انتشار مقاله: 07-06-1398
- نویسندگان: Chuan Du,Chao Xi,Chunxiao Wu,Jichang Sha,Jinan Zhang,Chao Li
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Mice,Immune thrombocytopenia,Norepinephrine VIP,β-EP,5-HT
- چکیده:
- چکیده انگلیسی: Objective(s): The main objective of this study was to investigate the variations of β-endorphin (β-EP), vasoactive intestinal peptide (VIP), serotonin (5-HT) and norepinephrine (NE) of immune thrombocytopenia (ITP) mice as well as the regulatory mechanism of prednison. Materials and Methods: Sixty BALB/c mice were randomly divided into control group, model group and prednison intervention group. ITP mice model was duplicated by injecting with glycoprotein-antiplatelet serum (GP-APS) except in control group. After ITP disease model was successful established, prednison was used in prednison intervention group. The β-EP, VIP, 5-HT and NE contents of ITP mice were detected by enzyme linked immunosorbent assay (ELISA). Results:Compared with the values in control group, the detection values of VIP and 5-HT in model group declined, while the detection values of β-EP and NE increased. Compared with prednison intervention group, the detection values of VIP and 5-HT in model group increased, while the detection values of β-EP and NE showed no significant change. Conclusion: In this study, the β-EP, VIP, 5-HT and NE contents in ITP mice injected with GP-APS were changed by prednison. It shows that prednison as the first-line therapy for ITP with effective hemostasis function is likely to increasing the contents of VIP and 5-HT. These results suggest the therapeutic value of prednison for the treatment of ITP.
- انتشار مقاله: 04-07-1395
- نویسندگان: Ling Zhang,Ke Chen,Tiantian Li,Hao He,Li Hou,Xiaoyong Wu,Yanping Sun,Lei Zheng,Zhixiong Chen,Bei Qin,Xinyi Chen,Shaodan Tian
- مشاهده
- جایگاه : پژوهشی
- مجله: Iranian Journal of Basic Medical Sciences
- نوع مقاله: Journal Article
- کلمات کلیدی: Degeneration,Apoptosis,senescence,Acidic,Acid-sensing ion channel 1a,Intervertebral disc,Nucleus pulposus cells
- چکیده:
- چکیده انگلیسی: Objective(s): Activation of acid-sensing ion channel 1a (ASIC1a) is responsible for tissue injury caused by acidosis in nervous systems. But its physiological and pathological roles in nucleus pulposus cells (NPCs) are unclear. The aim of this study is to investigate whether ASIC1a regulates the survival of NPCs in the acidic environment of degenerated discs. Materials and Methods: NPCs were isolated and cultured followed by immunofluorescent staining and Western-blot analysis for ASIC1a. Intracellular calcium ([Ca2+]i) was determined by Ca2+-imaging using Fura-2-AM. Cell necrosis, apoptosis, and senescence following acid exposure were determined using lactate dehydrogenase (LDH) release assay, annexin V-fluorescein isothiocyanate/propidium iodide dual-staining and cell cycle analysis, respectively, followed by Western-blot analysis for apoptosis-related proteins (Bax, Bcl-2, and caspase-3) and senescence-related proteins (p53, p21, and p16). Effects of treatment with psalmotoxin-1 (PcTX1, blocker of ASIC1a) on [Ca2+]i and cell survival were investigated. Results:ASIC1a was detected in healthy NPCs, and its expression was significantly higher in degenerated cells. When NPCs were treated with PcTX1, acid-induced increases in [Ca2+]i were significantly inhibited. PcTX1 treatment also resulted in decreased LDH release, cell apoptosis and cell cycle arrest in acid condition. Acid exposure decreased the expression of Bcl-2 and increased the expression of Bax, cleaved caspase-3 and senescence-related proteins (p53, p21, and p16), which was inhibited by PcTX1. Conclusion: The present findings suggest that further understanding of ASIC1a functionality may provide not only a novel insight into intervertebral disc biology but also a novel therapeutic target for intervertebral disc degeneration.
- انتشار مقاله: 10-06-1395
- نویسندگان: Feng Cai,Feng Wang,Xin Hong,Xin-Hui Xie,Rui Shi,Zhi-Yang Xie,Xiao-Tao Wu
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Apoptosis,Lung cancer,Bcl-2,Bax,croton tiglium
- چکیده:
- چکیده انگلیسی:
Objective: To investigate the impact of a Croton tiglium extract on cellular proliferation and apoptosis in a non-small cell lung cancer cell line (A549) in vitro. Methods: A Croton tiglium seed methanol extract was prepare and assessed for effects on A549 cells regarding cellular proliferation, apoptotic rates, and expression of apoptosis related genes and proteins using real-time PCR and immunofluorescence. Results: The tested Croton tiglium extract inhibited A549 cell proliferation in a dose- and time-dependent manner, with significant elevation of apoptotic indexes at various concentrations after 24 h. In addition, rates in both early and late stages were higher in treated than untreated groups, the 100 μg/ml dose causing the highest levels of apoptosis. RT-PCR showed that A549 cells treated with 100 μg/ml Croton tiglium extract for 24 h has markedly higher Bax mRNA expression levels and obviously lower Bcl-2 expression levels than controls, equivalent results being observed for proteins by immunofluorescence. However, the mRNA expression levels of Fas and caspase-8 were not significantly altered. Conclusion: A Croton tiglium extract can inhibit proliferation of A549 cells and promote apoptosis though Bax/Bcl-2 pathways.- انتشار مقاله: 09-06-1395
- نویسندگان: Changyou Li,Xiao Wu,Rongli Sun,Peng Zhao,Fengjuan Liu,Chunling Zhang
- مشاهده