盐敏感性高血压终末器官免疫细胞和炎症的不同变化:增加 M2 巨噬细胞的影响。

IF 6.7 2区 医学 Q1 MEDICINE, RESEARCH & EXPERIMENTAL
Shobana Navaneethabalakrishnan, Bethany L Goodlett, Hannah L Smith, Robert A Montalvo, Alyssa Cardenas, Brett M Mitchell
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引用次数: 0

摘要

盐敏感性高血压(SSHTN)与M1巨噬细胞极化和炎症反应有关,导致炎症相关的淋巴管生成和包括肾脏和性腺在内的多个器官的功能损伤。 然而,促进M2巨噬细胞极化是否能缓解盐敏感性高血压(SSHTN)小鼠的高血压、炎症和终末器官损伤仍不清楚。 通过在饮用水中添加硝基-L-精氨酸甲酯盐酸盐(L-NAME;0.5 毫克/毫升)使雌雄小鼠患高血压 2 周,然后间隔 2 周不加任何处理,再用高盐饮食治疗 3 周(SSHTN)。 在高盐饮食的同时腹腔注射 AVE0991(AVE)。 给对照组小鼠提供标准饮食和自来水。 AVE 治疗可明显降低 SSHTN 小鼠的血压和炎症反应。 值得注意的是,AVE 促进了 M2 巨噬细胞的极化,减少了促炎免疫细胞群,并改善了 SSHTN 小鼠肾脏和性腺组织的功能。 此外,AVE 还能减少雄性 SSHTN 小鼠肾脏和睾丸以及雌性 SSHTN 小鼠卵巢中的淋巴管生成。 这些发现凸显了 AVE 通过促进 M2 巨噬细胞极化和抑制促炎免疫反应,在减轻 SSHTN 引起的血压升高、炎症和终末器官损伤方面的有效性。 以巨噬细胞极化为靶点是缓解 SSHTN 炎症和器官损伤的一种有前景的治疗方法。 我们有必要开展进一步的研究,以阐明 AVE 介导效应的确切机制,并评估其在治疗 SSHTN 方面的临床潜力。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Differential changes in end organ immune cells and inflammation in salt-sensitive hypertension: effects of increasing M2 macrophages.

Salt-sensitive hypertension (SSHTN) is associated with M1 macrophage polarization and inflammatory responses, leading to inflammation-associated lymphangiogenesis and functional impairment across multiple organs, including kidneys and gonads. However, it remains unclear whether promoting M2 macrophage polarization can alleviate the hypertension, inflammation, and end organ damage in mice with salt sensitive hypertension (SSHTN). Male and female mice were made hypertensive by administering nitro-L-arginine methyl ester hydrochloride (L-NAME; 0.5 mg/ml) for 2 weeks in the drinking water, followed by a 2-week interval without any treatments, and a subsequent high salt diet for 3 weeks (SSHTN). AVE0991 (AVE) was intraperitoneally administered concurrently with the high salt diet. Control mice were provided standard diet and tap water. AVE treatment significantly attenuated BP and inflammation in mice with SSHTN. Notably, AVE promoted M2 macrophage polarization, decreased pro-inflammatory immune cell populations, and improved function in renal and gonadal tissues of mice with SSHTN. Additionally, AVE decreased lymphangiogenesis in the kidneys and testes of male SSHTN mice and the ovaries of female SSHTN mice. These findings highlight the effectiveness of AVE in mitigating SSHTN-induced elevated BP, inflammation, and end organ damage by promoting M2 macrophage polarization and suppressing pro-inflammatory immune responses. Targeting macrophage polarization emerges as a promising therapeutic approach for alleviating inflammation and organ damage in SSHTN. Further studies are warranted to elucidate the precise mechanisms underlying AVE-mediated effects and to assess its clinical potential in managing SSHTN.

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来源期刊
Clinical science
Clinical science 医学-医学:研究与实验
CiteScore
11.40
自引率
0.00%
发文量
189
审稿时长
4-8 weeks
期刊介绍: Translating molecular bioscience and experimental research into medical insights, Clinical Science offers multi-disciplinary coverage and clinical perspectives to advance human health. Its international Editorial Board is charged with selecting peer-reviewed original papers of the highest scientific merit covering the broad spectrum of biomedical specialities including, although not exclusively: Cardiovascular system Cerebrovascular system Gastrointestinal tract and liver Genomic medicine Infection and immunity Inflammation Oncology Metabolism Endocrinology and nutrition Nephrology Circulation Respiratory system Vascular biology Molecular pathology.
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