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肾上腺髓质素通过受体介导的蛋白激酶 A 通路减轻肥胖大鼠白色脂肪组织炎症。

Adrenomedullin Attenuates Inflammation in White Adipose Tissue of Obese Rats Through Receptor-Mediated PKA Pathway.

机构信息

Department of Physiology, Nanjing Medical University, Nanjing, China.

Department of Cardiology, BenQ Medical Center, The Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China.

出版信息

Obesity (Silver Spring). 2021 Jan;29(1):86-97. doi: 10.1002/oby.23012. Epub 2020 Sep 28.

DOI:10.1002/oby.23012
PMID:32985779
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7821304/
Abstract

OBJECTIVE

Adrenomedullin (ADM) possesses therapeutic potential for inflammatory diseases. Consequently, the effects of ADM on inflammation in visceral white adipose tissue (vWAT) of obese rats or in adipocytes were explored in this study.

METHODS

Male rats were fed a high-fat diet for 12 weeks to induce obesity, and obese rats were implanted with osmotic minipumps providing constant infusion of ADM (300 ng/kg per hour) and continued to be fed a high-fat diet for 4 weeks.

RESULTS

When compared with the control group, endogenous protein expression of ADM and ADM receptors in vWAT and in lipopolysaccharide (LPS)-treated adipocytes was markedly increased. ADM significantly decreased the protein expression of the inflammatory mediators TNFα, IL-1β, cyclooxygenase-2, and inducible nitric oxide synthase in vWAT of obese rats and in adipocytes stimulated by LPS. It also inhibited the activation of the inflammatory signaling pathways MAPK and NF-κB induced by LPS in adipocytes. These effects of ADM in adipocytes were inhibited by the administration of ADM receptor antagonist and cAMP-dependent protein kinase (PKA) activation inhibitor.

CONCLUSIONS

ADM can inhibit inflammation in WAT in obesity, which may be mediated by the activation of ADM receptors and PKA.

摘要

目的

肾上腺髓质素 (ADM) 对炎症性疾病具有治疗潜力。因此，本研究探讨了 ADM 对肥胖大鼠内脏白色脂肪组织 (vWAT) 中炎症的影响及其对脂肪细胞炎症的影响。

方法

雄性大鼠喂食高脂肪饮食 12 周以诱导肥胖，然后给肥胖大鼠植入持续输注 ADM（300ng/kg/小时）的渗透微型泵，并继续喂食高脂肪饮食 4 周。

结果

与对照组相比，vWAT 中和脂多糖 (LPS) 处理的脂肪细胞中 ADM 和 ADM 受体的内源性蛋白表达明显增加。ADM 显著降低了肥胖大鼠 vWAT 中炎症介质 TNFα、IL-1β、环加氧酶-2 和诱导型一氧化氮合酶以及 LPS 刺激的脂肪细胞中的蛋白表达。它还抑制了 LPS 诱导的脂肪细胞中炎症信号通路 MAPK 和 NF-κB 的激活。ADM 在脂肪细胞中的这些作用被 ADM 受体拮抗剂和 cAMP 依赖性蛋白激酶 (PKA) 激活抑制剂的给药所抑制。

结论

ADM 可抑制肥胖时 WAT 中的炎症，这可能是通过 ADM 受体的激活和 PKA 介导的。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/516bc5b0cbd9/OBY-29-86-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/54cee519cd18/OBY-29-86-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/c2b4d07e799f/OBY-29-86-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/15a32805e99c/OBY-29-86-g003.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/85f4e4e0c035/OBY-29-86-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/3b0a01cb7bc5/OBY-29-86-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/54520df80fad/OBY-29-86-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/516bc5b0cbd9/OBY-29-86-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/54cee519cd18/OBY-29-86-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/c2b4d07e799f/OBY-29-86-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/15a32805e99c/OBY-29-86-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/8b3935402a06/OBY-29-86-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/85f4e4e0c035/OBY-29-86-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/3b0a01cb7bc5/OBY-29-86-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/54520df80fad/OBY-29-86-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3d35/7821304/516bc5b0cbd9/OBY-29-86-g008.jpg

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