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Activated pathogenic Th17 lymphocytes induce hypertension following high-fructose intake in Dahl salt-sensitive but not Dahl salt-resistant rats

机译:在DAHL盐敏感但不是DAHL耐盐大鼠的高果糖摄入后,活化致病性TH17淋巴细胞诱导高血压

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Objectives: High-salt or high-fructose intakes are risk factors for hypertension via oxidative stress and inflammation. T helper (Th)17 lymphocytes play an important role in the development of hypertension. We tested the hypothesis that activation of pathogenic Th17 lymphocytes induces hypertension after high-fructose intake in Dahl salt-sensitive (SS) but not Dahl salt-resistant (SR) rats.Methods: Eight-week-old male SS and SR rats were offered 20% fructose solution or tap water only for 4 weeks. Systolic blood pressure was measured by the tail-cuff method. T lymphocytes (Th17 and T regulatory (Treg)) profiling was determined via flow cytometry. The expression of Th17 -related (interleukin (IL)-17A, IL-17RA,IL-23R and retinoic acid receptor-related orphan receptor (ROR) γt) and Treg-related (IL-10, CD25, forkhead box (Fox)P3, and TGF-?) factors were measured via ELISA or qRT-PCR. Th17 lymphocytes isolated from high fructose-fed SS rats were intraperitoneally injected into recipient SS and SR rats. Moreover, recombinant IL-23 protein was subcutaneously injected into SS and SR rats to induce hypertension.Results: High-fructose intake induced hypertension via the activation of pathogenic Th17 lymphocytes in SS but not SR rats. Injection of activated Th17 lymphocytes isolated from fructose-fed SS rats induced hypertension via increase of serum IL-17A in only recipient SS rat. In addition, injection of IL-23 induced hypertension via activation of pathogenic Th17 lymphocytes in only SS rats.Conclusion: Activation of pathogenic Th17 lymphocytes induces hypertension after high-fructose intake in SS but not SR rats. These results implicate that immunologic tolerance plays an important role in the protection against hypertension in SR.? 2020. Published by The Company of Biologists Ltd.
机译:目的:高盐或高果糖摄入量是通过氧化应激和炎症的高血压的危险因素。 T Helper(Th)17淋巴细胞在高血压的发展中发挥着重要作用。我们测试了致病性Th17淋巴细胞激活的假设诱导高果糖摄入量诱导高果糖(SS)但不是DAHL耐盐(SR)大鼠的高血压。提供:八周龄雄性SS和SR大鼠。 20%果糖溶液或仅自来水4周。通过尾袖法测量收缩压。通过流式细胞术确定T淋巴细胞(TH17和T调节(THREG))分析。 Th17-相关(白细胞介素(IL)-17A,IL-17RA,IL-23R和视黄酸受体相关的孤儿(ROR)γT)和Treg相关(IL-10,CD25,FORKHEAD盒(FOX)的表达通过ELISA或QRT-PCR测量P3和TGF-α)因子。从高果糖喂养SS大鼠分离的淋巴细胞腹膜内注射到受体SS和SR大鼠中。此外,将重组IL-23蛋白皮下注射到SS和SR大鼠中以诱导高血压。结果:高果糖摄入量通过在SS中的致病性Th17淋巴细胞活化而不是SR大鼠的激活。通过仅通过受体SS大鼠增加血清IL-17A的血清IL-17a分离的活化Th17淋巴细胞诱导高血压。此外,仅通过SS大鼠激活致病性Th17淋巴细胞的激活注射IL-23诱导的高血压。结论:致病性Th17淋巴细胞的激活诱导高果糖摄入后的高血压,但不是SR大鼠。这些结果暗示免疫耐受在SR中的高血压保护中起着重要作用。 2020年。由Biologury Ltd.公司发布

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