共查询到20条相似文献,搜索用时 15 毫秒
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Shaohui Lin Shaojun Ma Ping Lu Wenwei Cai Yi Chen Jing Sheng 《International journal of clinical and experimental pathology》2014,7(5):2199-2208
CTRP3, discovered as novel adipokines, is a member of the C1q tumor necrosis factor (TNF) related protein (CTRP) super-family. CTRP3 is found to function as adipokines that display diverse biological activities in metabolic and cardiovascular diseases. Recent study demonstrated that CTRP3 was protective against pathological cardiac remodeling in mice. Nevertheless, the effect of CTRP3 on vascular remodeling remains undefined. Our present study aimed to explore the effects of adipokine CTRP3 on the activation of adventitial fibroblasts (AFs) induced by TGF-β1. Immunofluorescent staining, real-time PCR and Western blot were conducted to evaluate the expression of α-smooth muscle-actin (α-SMA) and collagen I. The expression of CTGF was evaluated by enzymelinked immunosorbent assay (ELISA), while the proliferation and migration of adventitial fibroblasts were detected by using cell counting kit-8 (CCK-8) assay and Transwell technique, respectively. Functional analysis showed that CTRP3 inhibited TGF-β1 inducing AFs phenotypic conversion, collagen synthesis, proliferation and migration. The secretion of CTGF was also inhibited by CTRP3. Our findings suggest that CTRP3 may be beneficial to the prevention of cardiovascular diseases and provide a promising therapeutic strategy to attenuate vascular remodeling. 相似文献
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Yun Bai Huixin Bi Lixin Li Jingwei Li Xiuju Yu Huawei Ren Yilei Li Yunyan Ji Hongquan Li Haidong Wang 《Acta histochemica》2019,121(3):323-329
Myostatin (MSTN) is a key negative regulator of muscle growth and development. Skeletal, cardiac, and smooth muscles were isolated from MSTN knockout (MSTN?∕?) and control mice to investigate the effect of knocking out MSTN on peroxisome proliferator-activated receptor 1 coactivator (PGC-1α)-III and fibronectin domain 5 (FNDC5) expression. Various molecular biology techniques were used to analyze the changes in PGC-1α-FNDC5 in different muscle types from MSTN?∕? mice. The expression levels of PGC-1α and FNDC5 in the skeletal, cardiac, and smooth muscles of MSTN?∕? mice differed from those in the skeletal, cardiac, and smooth muscles of normal mice. This study revealed that knocking out MSTN resulted in inconsistent PGC-1α and FNDC5 expression in specific muscles. It proved for the first time that MSTN deletion attenuated the expression of PGC-1α and FNDC5 in three different murine muscle types. MSTN deletion may have additional effects on the status ofFNDC5 expression. Further research, however, is needed to confirm this conclusion. 相似文献
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Umit Yilmaz Suat Tekin Mehmet Demir Yilmaz Cigremis Suleyman Sandal 《The journal of physiological sciences : JPS》2018,68(6):781-788
The aim of this study was to evaluate the impact of intracerebroventricular chronic fibroblast growth factor 21 (FGF21) infusion on hypothalamic–pituitary–thyroid (HPT) axis, energy metabolism, food intake and body weight. Thirty male Wistar albino rats were used and divided into three groups including control, sham (vehicle) and FGF21 infused groups (n = 10). Intracerebroventricularly, FGF21 and vehicle groups were infused for 7 days with FGF21 (0.72 µg/day) and artificial cerebrospinal fluid, respectively. During the experimental period, changes in food intake and body weight were recorded daily. Serum thyroid stimulating hormone (TSH), Triiodothyronine (T3) and thyroxine (T4) levels were measured using ELISA. TRH and uncoupling protein 1 (UCP1) gene expressions were analyzed by using RT-PCR in hypothalamus and adipose tissues, respectively. Chronic infusion of FGF21 significantly increased serum TSH (p < 0.05), T3 (p < 0.05) and T4 (p < 0.001) levels. Additionally, hypothalamic TRH (p < 0.05) and UCP1 gene expressions (p < 0.05) in white adipose tissue were found to be higher than in the vehicle and control groups. While FGF21 infusion did not cause a significant change in food consumption, it caused a reduction in the body weight of rats (p < 0.05). Our findings indicate that FGF21 may have an effect on energy metabolism via the HPT axis. 相似文献
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Effects of Fas,NF-κB and caspases on rat microvascular endothelial cell apoptosis induced by TNFα 下载免费PDF全文
Effects of Fas,NF-κB and caspases on rat microvascular endothelial cell apoptosis induced by TNFα 相似文献
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γ-terpineol inhibits cell growth and induces apoptosis in human liver cancer BEL-7402 cells in vitro
Zi-Li wu Zhong-Qiong Yin Yong-Hua Du Rui-Zhang Feng Kui-Chuan Ye Qin Wei Yong Hu Lin He Lin Liao Yu Wang 《International journal of clinical and experimental pathology》2014,7(10):6524-6533
To investigate the effect of γ-terpineol on cell proliferation and apoptosis of human hepatoma BEL-7402 cells to elucidate its molecular mechanism. Here, BEL-7402 cells were treated with various concentrations (40, 80, 160, 320 and 640 μg/ml) of γ-terpineol for 48 h, cell proliferation was determined by 3-(4,5-dimethyl-thiazolyl-2)-2,5-diphenyl tetrazolium bromides (MTT) assay. Cell colony inhibition was determined by soft agar assay. Apoptosis and possible molecular mechanisms were evaluated by morphological observation, flow cytometry analysis, and DNA fragmentation assay. The γ-terpineol significantly suppressed BEL-7402 cell proliferation in a dose-dependent manner. Characteristic morphological and biochemical changes associated with apoptosis such as cells shrinkage, deformation and vacuolization of mitochondria, nuclear chromatin condensation and fragmentation, formation of apoptotic bodies were observed after BEL-7402 cells treated with γ-terpineol for 24 h and 48 h. Cell cycle were displayed by flow cytometry analysis, the γ-terpineol treatment resulted in accumulation of cells at G1 or S phase and a blockade of cell proliferation compared to control group. Treating BEL-7402 cells with 320 μg/ml of γ-terpineol for 36 h and 48 h, a typical apoptotic “DNA ladder” was observed using DNA fragmentation assay. The present study demonstrated that possible anti-cancer mechanism of γ-terpineol on human hematomas cells is through inducing cell apoptosis to suppress tumor cell growth. 相似文献
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Interleukin 1 alpha (IL1) and tumor necrosis factor alpha (TNF) have been successfully incorporated into specific phosphatidylcholine (PC) and phosphatidylserine (PS) multilamellar vesicle (MLV) liposomes by modifying the concentration of calcium ion and pH of the encapsulation buffer. Under these conditions, some of the cytokines may attach to the exterior surface of the MLV and therefore be readily accessible to target cells for receptor binding and signal transduction. These cytokine-associated liposomes are stable for up to 2 weeks in serum-free buffer, and leakage of cytokines into medium containing 10% fetal bovine serum was about 50% at the end of a 3-day incubation period at 37°C. The biological activities mediated by liposomal IL1 and TNF were specific: the stimulation of thymidine uptake in T-helper D10 lymphocytes and the cytolysis of TNF-sensitive L929 target cells could be blocked by specific neutralizing antibodies in a dose-dependent fashion. When administered intravenously into C57BL/6 mice bearing the syngeneic B16F10 murine melanoma cells, dual entrapment of liposomal IL1 and TNF significantly reduced the number of metastatic tumor nodules in the lungs and prolonged the life span of the animals. Thus, liposomal IL1 and TNF displayed significant in vivo antitumor activity against the IL1- and TNF-resistant B16F10 metastatic murine melanoma. 相似文献
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Belogolovskaya EG Oreshchenko AV Durnev AD Seredenin SB Litvinova EV Zubtsov YN 《Bulletin of experimental biology and medicine》2000,130(11):1102-1105
Antimutagenic effects of combination of aspartame (0.4 and 4 mg/kg) and -carotene (0.15-15 mg/kg) were studied by estimation of chromosome aberrations in bone marrow cells of C57Bl/6 mice. Single and 5-day treatment with this combination decreased the clastogenic effects of dioxidine and cyclophosphamide and produced a more potent and universal antimutagenic effect than its constituents. 相似文献
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E. G. Belogolovskaya A. V. Oreshchenko A. D. Durnev S. B. Seredenin E. V. Litvinova Y. N. Zubtsov 《Bulletin of experimental biology and medicine》2000,130(5):1102-1105
Antimutagenic effects of combination of aspartame (0.4 and 4 mg/kg) and β-carotene (0.15–15 mg/kg) were studied by estimation
of chromosome aberrations in bone marrow cells of C57Bl/6 mice. Single and 5-day treatment with this combination decreased
the clastogenic effects of dioxidine and cyclophosphamide and produced a more potent and universal antimutagenic effect than
its constituents.
Translated fromByulleten’ Eksperimental’noi Biologii i Meditsiny, Vol. 130, No. 11, pp. 570–573, November, 2000 相似文献
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Giulio Cavalli Serena Colafrancesco Giacomo Emmi Massimo Imazio Giuseppe Lopalco Maria Cristina Maggio Jurgen Sota Charles A. Dinarello 《Autoimmunity reviews》2021,20(3):102763
The interleukin (IL)-1 family member IL-1α is a ubiquitous and pivotal pro-inflammatory cytokine. The IL-1α precursor is constitutively present in nearly all cell types in health, but is released upon necrotic cell death as a bioactive mediator. IL-1α is also expressed by infiltrating myeloid cells within injured tissues. The cytokine binds the IL-1 receptor 1 (IL-1R1), as does IL-1β, and induces the same pro-inflammatory effects. Being a bioactive precursor released upon tissue damage and necrotic cell death, IL-1α is central to the pathogenesis of numerous conditions characterized by organ or tissue inflammation. These include conditions affecting the lung and respiratory tract, dermatoses and inflammatory skin disorders, systemic sclerosis, myocarditis, pericarditis, myocardial infarction, coronary artery disease, inflammatory thrombosis, as well as complex multifactorial conditions such as COVID-19, vasculitis and Kawasaki disease, Behcet’s syndrome, Sjogren Syndrome, and cancer.This review illustrates the clinical relevance of IL-1α to the pathogenesis of inflammatory diseases, as well as the rationale for the targeted inhibition of this cytokine for treatment of these conditions. Three biologics are available to reduce the activities of IL-1α; the monoclonal antibody bermekimab, the IL-1 soluble receptor rilonacept, and the IL-1 receptor antagonist anakinra. These advances in mechanistic understanding and therapeutic management make it incumbent on physicians to be aware of IL-1α and of the opportunity for therapeutic inhibition of this cytokine in a broad spectrum of diseases. 相似文献
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Xu X Tu L Jiang W Feng W Zhao CX Wang DW 《International journal of molecular medicine》2012,29(5):891-898
The kallikrein-kinin system (KKS) is a complex multi-enzyme system which is composed of circulating and tissue kallikrein and kinin. It is well established that tissue kallikrein and kinin play crucial and diverse roles in cardiovascular and renal homeostasis. Recent data indicate that kallikrein gene delivery reduces insulin resistance in STZ-treated rats suggesting a protective role for kinin in the development of diabetes. This study investigated the effects of exogenous bradykinin (BK) on the apoptosis of NIT-1 cells, a pancreatic β-cell line in?vitro. Exogenous BK significantly protected NIT-1 cells from TNF-α-induced apoptosis. These effects were associated with upregulation of Bcl-2 and Bcl-xL protein expression levels as well as with downregulation of Bax expression levels via the activation of the mitogen-activated protein kinase and PI3K/Akt signaling pathways. In conclusion, these data highlight the beneficial roles of BK on pancreatic β-cell function. 相似文献
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H.H. Guo C.C. Yu S.X. Sun X.J. Ma X.C. Yang K.N. Sun Q.H. Jin 《Brazilian journal of medical and biological research》2013,46(10):831-838
Wear particles are phagocytosed by macrophages and other inflammatory cells,
resulting in cellular activation and release of proinflammatory factors, which
cause periprosthetic osteolysis and subsequent aseptic loosening, the most
common causes of total joint arthroplasty failure. During this pathological
process, tumor necrosis factor-alpha (TNF-α) plays an important role in
wear-particle-induced osteolysis. In this study, recombination adenovirus (Ad)
vectors carrying both target genes [TNF-α small interfering RNA (TNF-α-siRNA)
and bone morphogenetic protein 2 (BMP-2)] were synthesized and transfected into
RAW264.7 macrophages and pro-osteoblastic MC3T3-E1 cells, respectively. The
target gene BMP-2, expressed on pro-osteoblastic MC3T3-E1 cells and silenced by
the TNF-α gene on cells, was treated with titanium (Ti) particles that were
assessed by real-time PCR and Western blot. We showed that recombinant
adenovirus (Ad-siTNFα-BMP-2) can induce osteoblast differentiation when treated
with conditioned medium (CM) containing RAW264.7 macrophages challenged with a
combination of Ti particles and Ad-siTNFα-BMP-2 (Ti-ad CM) assessed by alkaline
phosphatase activity. The receptor activator of nuclear factor-κB ligand was
downregulated in pro-osteoblastic MC3T3-E1 cells treated with Ti-ad CM in
comparison with conditioned medium of RAW264.7 macrophages challenged with Ti
particles (Ti CM). We suggest that Ad-siTNFα-BMP-2 induced osteoblast
differentiation and inhibited osteoclastogenesis on a cell model of a Ti
particle-induced inflammatory response, which may provide a novel approach for
the treatment of periprosthetic osteolysis. 相似文献
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《Journal of immunotoxicology》2013,10(2):201-209
The current study investigated the effects of 14-day pioglitazone (PIO) and/or simvastatin (SIM) treatments on serum adiponectin (Adp) and TNFα levels (markers of adipocyte dysfunction), as well as on metabolic perturbations that arise from prolonged (8 week) consumption of a high fructose (HFD; 60%) diet in a rat model of pre-diabetic insulin resistance. The HFD induced a deranged lipid profile that was associated with adipose tissue hypertrophy, increased ratios of visceral and epididymal fats to body weight, and fatty liver. These perturbations were associated with hypo-adiponectinemia (50.8%) and increased serum TNFα (6.5-fold) levels. Treatment with PIO ameliorated the altered blood and hepatic glucose metabolism via an Adp-dependent mechanism; PIO also mitigated the changes in blood TNFα and led to a hyperelevation of Adp levels. SIM amended hepatic and overall lipid metabolism, regulated TNFα, but failed to alter the glucose intolerance or significantly impact on the HFD-altered Adp levels. Coadministration of SIM + PIO was superior in improving overall metabolic parameters compared to each monotherapy. Cotreatment was optimal in reestablishing insulin resistance, most efficacious in improving serum lipid profiles, normalizing percentage ratios of epididymal and visceral fats to body weight, and augmenting Adp/reducing TNFα levels relative to that in the HFD group or with HFD + each drug alone. The results here show that use of either monotherapy or a combined SIM + PIO approach might, from a clinical perspective, provide an ability to delay progression to Type 2 diabetes and its associated inflammatory/cardiovascular effects. 相似文献
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Janich MA Menzel MI Wiesinger F Weidl E Khegai O Ardenkjaer-Larsen JH Glaser SJ Haase A Schulte RF Schwaiger M 《NMR in biomedicine》2012,25(1):142-151
Real-time in vivo measurements of metabolites are performed by signal enhancement of [1-(13)C]pyruvate using dynamic nuclear polarization, rapid dissolution and intravenous injection, acquisition of free induction decay signals and subsequent quantification of spectra. The commonly injected dose of hyperpolarized pyruvate is larger than typical tracer doses, with measurement before complete dilution of the injected bolus. Pyruvate is in exchange with its downstream metabolites lactate, alanine and bicarbonate. A transient exposure to high pyruvate blood concentrations may cause the saturation of cellular uptake and metabolic conversion. The goal of this study was to examine the effects of a [1-(13)C]pyruvate bolus on metabolic conversion in vivo. Spectra were quantified by three different methods: frequency-domain fitting with LCModel, time-domain fitting with AMARES and simple linear least-squares fitting in the time domain. Since the simple linear least-squares approach showed bleeding artifacts and LCModel produced noisier time signals. AMARES performed best in the quantification of in vivo hyperpolarized pyruvate spectra. We examined pyruvate doses of 0.1-0.4 mmol/kg (body mass) in male Wistar rats by acquiring slice-selective free induction decay signals in slices dominated by heart, liver and kidney tissue. Dose effects were noted in all cases, except for alanine in the cardiac slice below the dose of 0.2 mmol/kg. Our results indicate unlimited cellular uptake of pyruvate up to this dose and limited enzymatic activity of lactate dehydrogenase. In the cardiac slice above 0.2 mmol/kg and in liver and kidney slices, reflect limited cellular uptake or enzymatic activity, or a combination of both effects. The results indicate that the dose of pyruvate must be recognized as an important determinant for metabolic tissue kinetics, and saturation effects must be taken into account for the quantitative interpretation of the observed results. 相似文献
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Schaalan MF 《Journal of immunotoxicology》2012,9(2):201-209
The current study investigated the effects of 14-day pioglitazone (PIO) and/or simvastatin (SIM) treatments on serum adiponectin (Adp) and TNFα levels (markers of adipocyte dysfunction), as well as on metabolic perturbations that arise from prolonged (8 week) consumption of a high fructose (HFD; 60%) diet in a rat model of pre-diabetic insulin resistance. The HFD induced a deranged lipid profile that was associated with adipose tissue hypertrophy, increased ratios of visceral and epididymal fats to body weight, and fatty liver. These perturbations were associated with hypo-adiponectinemia (50.8%) and increased serum TNFα (6.5-fold) levels. Treatment with PIO ameliorated the altered blood and hepatic glucose metabolism via an Adp-dependent mechanism; PIO also mitigated the changes in blood TNFα and led to a hyperelevation of Adp levels. SIM amended hepatic and overall lipid metabolism, regulated TNFα, but failed to alter the glucose intolerance or significantly impact on the HFD-altered Adp levels. Coadministration of SIM + PIO was superior in improving overall metabolic parameters compared to each monotherapy. Cotreatment was optimal in reestablishing insulin resistance, most efficacious in improving serum lipid profiles, normalizing percentage ratios of epididymal and visceral fats to body weight, and augmenting Adp/reducing TNFα levels relative to that in the HFD group or with HFD + each drug alone. The results here show that use of either monotherapy or a combined SIM + PIO approach might, from a clinical perspective, provide an ability to delay progression to Type 2 diabetes and its associated inflammatory/cardiovascular effects. 相似文献
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Hui Peng Wenyu Zhong Hong Zhao Li Chen Xiao Zhou Feng Li Weiwei Zhu Guimei Li 《International journal of clinical and experimental pathology》2015,8(5):4639-4650
Endothelial cells (ECs) apoptosis induced by hyperglycemia is intimately involved in the pathophysiology of diabetes and its complication. Although PGC-1α is known for its role in glucose metabolism, its role in ECs injury caused by high glucose milieu is still unclear. Therefore, this study aims to investigate whether PGC-1α participates in ECs apoptosis under high glucose condition. Human umbilical vein endothelial cells (HUVECs) were down-regulated PGC-1α expression by adenovirus-mediated PGC-1α specific siRNA (Ad-shPGC-1α) and exposed to high glucose. Cell viability, apoptosis, mitochondrial membrane permeability, apoptotic marker, reactive oxygen species (ROS), and expression of PGC-1α and VDAC isoforms were studied. Our results showed that high glucose-induced cell apoptosis was associated with an obvious decrease in PGC-1α expression. Lack of PGC-1α exacerbated high glucose-induced cell apoptosis, inner mitochondrial membrane permeabilization, mitochondrial cytochrome c release into cytoplasm and caspases activation; while further decreased cell viability and mitochondrial membrane potential. Analysis of apoptotic markers (Bcl-2, Bax), intracellular ROS and endoplasmic reticulum stress revealed that these mechanisms were not accounted for the effects of Ad-shPGC-1α on apoptosis. However, we found silencing PGC-1α further increased high glucose-induced VDAC1 expression. The pharmacological inhibition of VDAC1 with 4,4’-diisothiocyanostilbene-2,2’-disulfonic acid (DIDS) inhibited the increased apoptosis in high glucose-treated PGC-1α knockdown cells. These findings strongly suggest that PGC-1α defect is one of the major mechanisms for ECs apoptosis under high glucose condition, and provide a novel strategy to prevent endothelial dysfunction in diabetes. 相似文献