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interleukin-1α, 6 regulate the secretion of vascular endothelial growth factor A, C in pancreatic cancer

Hepatobiliary & Pancreatic Diseases International 2005年第3期4卷 460-463页

作者： Department of Hepatobiliary Surgery (Tang RF, Zhang FR, Peng L, Wang SX, Xiao Y and Zhang M) and Department of Dermatology (Wang SX), 4th Hospital, Hebei Medical University, Shijiazhuang 050011, China Department of Hepatobiliary Surgery 4th Hospital Hebei Medical University Shijiazhuang 050011 China. tangreifeng@***

Vascular endothelial growth factor (VEGF, namely VEGF-A) is an angiogenic polypeptide and VEGF-C is a lymphangiogenic polypeptide that has been implicated in cancer growth, invasion and metastasis. Several cytokines and growth factors play an important part in cancer progression. These cytokines and growth factors are the principal mediators of cancer cells-stromal cell interaction , which is critical for invasion of cancer cells to the surrounding tissues and metastatic dissemination to distant organs. In this study, we studied VEGF-A, C expression in cultured human pancreatic cancer cell lines and whether the presence of VEGF-A, C in the cell lines is regulated by cytokines interleukin-lct (EL-1α), and interleukin-6 (IL-6). METHODS: We used Northern blot and Western blot methods to analyze expression of the gene and protein of VEGF-A, C in all 6 tested cell lines (ASPC-1, CAPAN-1, MIA-PaCa-2, PANC-1, COLO-357 and T3M4) respectively. To analyze what is the regulator for this VEGF-A, C expression in pancreatic cancer,we used the reverse transcription -polymerase chain reaction (RT-PCR) method to analyze VEGF-A, C expression in cultured human pancreatic cancer cell lines (CAPAN-1 and COLO-357) under the stimulation with IL-1α (10μg/L) or IL-6 (100 μg/L). RESULTS:Northern blot analysis revealed the presence of the 4.1-kb VEGF-A mRNA transcript and 2.4-kb VEGF-C mRNA transcript in all 6 tested cell lines. Immunoblotting with highly specific anti-VEGF-A, anti-VEGF-C antibody revealed the presence of a molecular weight of 43-kDa VEGF-A protein and 55-kDa VEGF-C protein in all the cell lines. RT-PCR analysis revealed the levels of the VEGF-A and VEGF-C gene were 1-2 fold and a 1-fold increase in the COLO-357 cell line by stimulation with IL-la, however, no effect was found in the CAPAN-1 cell line. The levels of the VEGF-A and VEGF-C gene were 2-5 fold and a 1-fold increase in the CAPAN-1 cell line by stimulation with IL-6, but, no effect was found in the COLO-357 cell li

关键词： pancreatic cancer vascular endothelial growth factor VEGF-C cytokine interleukin-1α interleukin-6

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Expression of Pigment Epithelium-derived Factor in Bladder Tumour Is Correlated with interleukin-8 yet Not with interleukin-1α

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Journal of Huazhong University of Science and Technology(Medical Sciences) 2011年第1期31卷 21-25页

作者：冯陈陈关明丁强张元芳姜昊文温晖王保勋吴忠 Department of Urology Huashan Hospital Fudan University Centre of Laboratory Medicine Huashan Hospital Fudan University Institute of Urology Huashan Hospital Fudan University Department of Surgery Huashan Hospital Fudan University

Pigment epithelium-derived factor （PEDF） is an antiangiogenic factor which is effective in tumour inhibition in a variety of tumours and has not yet been studied in bladder tumour before. In this study the expression of PEDF, interleukin-1α （IL-1α） and -8 （IL-8） in bladder tumours was investigated. Immunohistochemistry was performed on 64 bladder tumour and 23 normal uroepithelium samples. Expression change of the factors was compared with clinicopathological parameters. Correlations between PEDF, IL-1α and IL-8 were analyzed. None of the factors was in relation to gender, tumour occurrence, and size or onset pattern. PEDF （P=0.014） and IL-1α （P=0.049） expression was down-regulated with grade progression. PEDF expression was lower in normal uroepithelium than in papillary urothelial neoplasm of low malignant potential （PUNLMP）（P=0.000） and carcinoma （P=0.009） whilst IL-1α （P=0.000 and P=0.000 respectively） and IL-8 （P=0.000 and P=0.023 respectively） expression was higher in the same grouping. PEDF expression had a negative correlation with IL-8 in PUNLMP （P=0.049, r=-0.578） as well as in tumour grouping （P=0.033, r=-0.276）. Deranged expressional change of PEDF, IL-1α and IL-8 could be in relation to loss of differentiation from normal uroepithelium to papillary lesion and eventually to carcinoma.

关键词： angiogenesis bladder tumour interleukin-1α interleukin-8 pigment epithelium-derived factor

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Study of the Mechanism of Essential Garlic Oil Inhibiting interleukin1 Induced Monocyte Adhesion to Endothelial Cells

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Chinese Journal of Integrative Medicine 2001年第4期7卷 293-296页

作者：葛璐璐张薇戴云臧燕黄纯洁 The First Military Medical University Guangzhou510515

To observe the effects of essential garlic oil (EGO) on vascular cell adhesive molecule-1 (VCAM-1) expression of endothelial cells and monocyte-endothelial cell adhesion rate induced by interleukin-1α (IL-1α). Methods: Human umbilical vein endothelial cells (HUVEC) were isolated by trypsin digestion method and co-cultured with IL-1α or EGO+IL-1α in the absence or presence of U937 monocyte. Monocyte-endothelial cell adhesion rate was examined with reverted microscope. VCAM-1 expression of endothelial cells was measured by ACAS 570 confocal microscope, and the data were presented as mean fluorescent intensity. Results: EGO significantly inhibited IL-1α-induced endothelial expression of VCAM-1, and thus markedly decreased monocyte-endothelial cell adhesion rate. Conclusion: EGO has the effect on antagonizing adhesion of monocyte and vascular endothelial cell, which might be due to its inhibition on adhesive molecular expression on the surface of endothelial cells.

关键词： essential garlic oil endothelial cells monocytes vascular cell adhesive molecule-1 interleukin-1α

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UVB-irradiated human keratinocytes and interleukin-1■ indirectly increase MAP kinase/AP-1 activation and MMP-1 production in UVA-irradiated dermal fibroblasts

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Chinese Medical Journal 2006年第10期 827-831页

作者： WANG Xiao-yong BI Zhi-gang Department of Dermatology First Affiliated Hospital of NanjingMedical University Nanjing 210029 China

Background Solar ultraviolet （UV） irradiation induces the production of matrix metalloproteinases （MMPs） by activating cellular signalling transduction pathways. MMPs are responsible for the degradation and/or inhibition of synthesis of collagenous extracellular matrix in connective tissues. We mimicked the action of environmental ultraviolet on skin and investigated the effects of UVB-irradiated human keratinocytes HaCaT and IL-1α on mitogen activated protein （MAP） kinase activation, c-Jun and c-Fos （AP- 1 is composed of Jun and Fos proteins） mRNA expression and MMP-1 production in UVA-irradiated dermal fibroblasts.

关键词： ultraviolet keratinocytes fibroblasts interleukin-1α matrix metalloproteinase-1

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Inhibition of inflammatory mediator release from microglia can treat ischemic/hypoxic brain injury

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Neural Regeneration Research 2013年第13期8卷 1157-1168页

作者： Huaibo Wang Weitao Guo Hongliang Liu Rong Zeng Mingnan Lu Ziqiu Chen Qixian Xiao Department of Orthopedics Affiliated Hospital of Guangdong Medical College Chongqing Cancer Institute

interleukin-1α and interleukin-1β aggravate neuronal injury by mediating the inf1αmmatory reaction following ischemic/hypoxic brain injury. It remains unclear whether interleukin-1α and interleukin-1β are released by microglia or astrocytes. This study prepared hippocampal slices that were subsequently subjected to oxygen and glucose deprivation. Hematoxylin-eosin staining verified that neurons exhibited hypoxic changes. Results of enzyme-linked immunosorbent assay found that interleukin-1α and interleukin-1β participated in this hypoxic process. Moreover, when hypoxic injury occurred in the hippocampus, the release of interleukin-1α and interleukin-1β was mediated by the P2X4 receptor and P2X7 receptor. Immunofluorescence staining revealed that during ischemia/hypoxia, the P2X4 receptor, P2X7 receptor, interleukin-1α and interleukin-1β expression was detectable in rat hippocampal microglia, but only P2X4 receptor and P2X7 receptor expression was detected in astrocytes. Results suggested that the P2X4 receptor and P2X7 receptor, respectively, mediated interleukin-1α and interleukin-1β released by microglia, resulting in hippocampal ischemic/hypoxic injury. Astrocytes were activated, but did not synthesize or release interleukin-1α and interleukin-1β.

关键词： neural regeneration brain injury inflammatory P2X4 receptor P2X7 receptor interleukin-1α interleukin-1β microglia astrocytes oxygen-glucose deprivation hippocampal slices grants-supported paper neuroregeneration

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Role of inflammatory response in liver diseases: Therapeutic strategies

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World Journal of Hepatology 2018年第1期10卷 1-7页

作者： José A Del Campo Paloma Gallego Lourdes Grande Department of Digestive Diseases Valme University Hospital and CIBERehd

Inflammation and tumorigenesis are tightly linked pathways impacting cancer development. Inflammasomes are key signalling platforms that detect pathogenic microorganisms, including hepatitis C virus(HCV) infection, and sterile stressors(oxidative stress, insulin resistance, lipotoxicity) able to activate pro-inflammatory cytokines interleukin-1β and IL-18. Most of the inflammasome complexes that have been described to date contain a NOD-like receptor sensor molecule. Redox state and autophagy can regulate inflammasome complex and, depending on the conditions, can be either pro-or antiapoptotic. Acute and chronic liver diseases are cytokinedriven diseases as several proinflammatory cytokines(IL-1α, IL-1β, tumor necrosis factor-alpha, and IL-6) are critically involved in inflammation, steatosis, fibrosis, and cancer development. NLRP3 inflammasome gain of function aggravates liver disease, resulting in severe liver fibrosis and highlighting this pathway in the pathogenesis of non-alcoholic fatty liver disease. On the other hand, HCV infection is the primary catalyst for progressive liver disease and development of liver cancer. It is well established that HCV-induced IL-1β production by hepatic macrophages plays a critical and central process that promotes liver inflammation and disease. In this review, we aim to clarify the role of the inflammasome in the aggravation of liver disease, and how selective blockade of this main pathway may be a useful strategy to delay fibrosis progression in liver diseases.

关键词： Caspase-1 Fibrosis Hepatitis C virus Inflammasome interleukin-1α interleukin-1β Liver disease Non-alcoholic fatty liver disease NLRP3 Tumor necrosis factor-alpha

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Expression Changes of Serum IL-1α,CCL2,and CXCL2 in Patients With Pemphigus

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International Journal of Dermatology and Venereology 2023年第2期6卷 102-106页

作者： Li-Dan Mao Yu Zhang Jun-Qin Liang Xiao-Jing Kang Feng-Xia Hu Fan-He Jiang Department of Dermatology and Venereology People’s Hospital of Xinjiang Uygur Autonomous RegionXinjiang Clinical Research Center for Dermatologic DiseasesXinjiang Key Laboratory of Dermatology ResearchUrumqiXinjiang 830001China Department of Dermatology People’s Hospital of Xinjiang Bayingol Mongolian Autonomous PrefectureBayingol Mongolian Autonomous PrefectureXinjiang 841000China

Objective:This study was performed to explore the possible changes of the serum levels of the cytokines including interleukin 1α(IL-1α),chemokine monocyte chemotactic protein 1(also known as chemokine[C-C motif]ligand 2[CCL2]),and C-X-C motif chemokine ligand 2(CXCL2)in patients with ***:The expression levels of IL-1α,CCL2,and CXCL2 in the serum of 57 patients with pemphigus PV(including 42 patients in progressive stage and 15 patients in remission stage)and 31 healthy controls were examined by enzyme-linked immunosorbent *** indepent-samples t-test was used to compare the two *** analysis of variance was used for multiple-group comparisons,and the post-hoc least significant difference test was used to detect differences among multiple ***:The serum expression levels of CCL2 and IL-1a were all significantly higher in the patients in progressive stage than in the controls([2.69±0.23]ng/mL vs.[2.55±0.28]ng/mL,P=0.043;[0.62±0.27]ng/mL vs.[0.48±0.23]ng/mL,P=0.038,respectively).In addition,the serum expression level of CXCL2 was significantly higher in patients in progressive stage than in in the remission stage([61.70±46.38]ng/mL vs.[24.97±18.46]ng/mL,P=0.037).Sex,disease classification,disease severity,treatment,and mucosal involvement had no significant influence on the expression of IL-1α,CCL2,or CXCL2 in the serum of patients groups and controls(all P>0.05).Conclusion:IL-1α,CCL2,and CXCL2 are heavily involved in the occurrence and development of pemphigus and may be related to the activity of the disease.

关键词： pemphigus cytokines chemokine interleukin-1α chemokine(C-C motif)ligand 2 C-X-C motif chemokine ligand 2

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The Effect Of Bifid Triple Viable To Endotoxemia And Some Cytokines Of Liver Cirrhosis Patients

The Effect Of Bifid Triple Viable To Endotoxemia And Some Cy...

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第十五届国际药理学大会

作者： mei ai - min wang rui - ting zhang hong - bo song li - gang. Department of Pharmacology Chengde Medical college Chengde Hebei Province China

＜正＞ Objective: The study is conducted to investigate the clinical significance of Bifid Triple Viable that was used to treat endotoxemia of Liver cirrhosis on the base of general therapy, and to observe the change of endotoxin and some cytokines （IL -1α,IL-6. TNFα） in plasma during the treatment. Methods: 60 hospitalizing patients with liver cirrhosis in the uncompensated period were included in present study. The patients satisfied the conditions were separated into two groups at random. One is control group, another is BTV group. Results: The level of endotoxin. IL - 1α, IL-6. TNFα in BTV group after therapy were lower than that before therapy, the differences were significant （p＜0.05）;The level of endotoxin. IL - 1α,IL-6 TNFα. in BTV group after therapy were lower than that in control group. The differences were significant （p＜0.05）. Conclusions: Applied Bifid Triple Viable to treat endotoxemia of Liver cirrhosis can sharply decrease the endotoxin level, and can down - regulate some cytokines （IL - 1α,IL - 6, TNFα） in plasma, and also can improve the liver function.

关键词： Bifid Triple Viable Endotoxemia interleukin-1α

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