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中国患者、大鼠、淋巴细胞和内皮细胞慢性间歇性低氧相关的炎症和氧化应激因素。

Inflammatory and oxidative stress‑associated factors in chronic intermittent hypoxia in Chinese patients, rats, lymphocytes and endotheliocytes.

机构信息

Division of Respiratory Disease, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

出版信息

Mol Med Rep. 2017 Dec;16(6):8092-8102. doi: 10.3892/mmr.2017.7632. Epub 2017 Sep 26.


DOI:10.3892/mmr.2017.7632
PMID:28983603
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5779894/
Abstract

In order to investigate the association between inflammatory and oxidative stress (OS)‑associated factors in chronic intermittent hypoxia (CIH), 238 CIH patients and 156 healthy volunteers were included. CIH rat and lymphocytes were used as experimental models. Interleukin (IL)‑6, tumor necrosis factor‑α (TNF‑α), C‑reactive protein (CRP), nitric oxide (NO) and nitric oxide synthase (NOS) were analyzed. Patients with CIH were older, with hypertension, increased heart rate (HR) and body mass index (BMI), and there were more males than females. Those with a history of smoking or type 2 diabetes (T2DM) history exhibited an increased risk of CIH. Serum IL‑6, TNF‑α and CRP in patients with CIH were increased, while NO and NOS were decreased. Hakka patients exhibited increased BMI measurements and NO expression, and decreased systolic arterial pressure, IL‑6 and TNF‑α compared with non‑Hakka patients. Rats with CIH exhibited hypertension and stable weight, less activity and decreased appetite, increased HR and serum IL‑6, TNF‑α and CRP, and decreased NO and NOS. IL‑6, TNF‑α, CRP, NO and induced‑NOS (iNOS) were increased in the lymphocytes of CIH rats compared with healthy ones. In rat endotheliocytes induced by CIH, IL‑6, TNF‑α, CRP and iNOS increased, while NO and endothelial‑NOS (eNOS) decreased. In the supernatant of co‑cultured lymphocytes and endotheliocytes, IL‑6, TNF‑α and CRP increased, although NO and NOS decreased. In conclusion, age, male gender, BMI, smoking and T2DM history, serum IL‑6, TNF‑α and CRP were positively correlated with CIH combined with hypertension, while NO and NOS were negatively correlated with CIH. Serum NO was predominantly synthesized and released by eNOS. Hakka patients exhibited decreased inflammation and OS with CIH. Increasing IL‑6, TNF‑α and CRP, and decreasing NO and NOS are biomarkers of CIH, which could be targets in diagnosis, treatment and prevention of CIH.

摘要

为了研究慢性间歇性低氧(CIH)相关的炎症和氧化应激(OS)相关因素之间的关联,纳入了 238 例 CIH 患者和 156 名健康志愿者。CIH 大鼠和淋巴细胞被用作实验模型。分析了白细胞介素(IL)-6、肿瘤坏死因子-α(TNF-α)、C 反应蛋白(CRP)、一氧化氮(NO)和一氧化氮合酶(NOS)。CIH 患者年龄较大,伴有高血压、心率(HR)和体重指数(BMI)增加,且男性多于女性。有吸烟史或 2 型糖尿病(T2DM)病史的患者患 CIH 的风险增加。CIH 患者的血清 IL-6、TNF-α 和 CRP 升高,而 NO 和 NOS 降低。与非客家人相比,客家人的 BMI 测量值和 NO 表达增加,收缩压、IL-6 和 TNF-α 降低。CIH 大鼠表现出高血压和稳定体重、较少的活动和食欲减退、HR 和血清 IL-6、TNF-α 和 CRP 增加以及 NO 和 NOS 减少。与健康大鼠相比,CIH 大鼠的淋巴细胞中 IL-6、TNF-α、CRP、诱导型-NOS(iNOS)增加。在 CIH 诱导的大鼠内皮细胞中,IL-6、TNF-α、CRP 和 iNOS 增加,而 NO 和内皮型-NOS(eNOS)减少。在共培养的淋巴细胞和内皮细胞的上清液中,IL-6、TNF-α 和 CRP 增加,而 NO 和 NOS 减少。总之,年龄、男性、BMI、吸烟和 T2DM 病史、血清 IL-6、TNF-α 和 CRP 与 CIH 合并高血压呈正相关,而 NO 和 NOS 与 CIH 呈负相关。血清 NO 主要由 eNOS 合成和释放。客家人在 CIH 时表现出炎症和 OS 减轻。增加 IL-6、TNF-α 和 CRP,减少 NO 和 NOS 是 CIH 的生物标志物,可能成为 CIH 的诊断、治疗和预防靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/43c723229b0c/MMR-16-06-8092-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/1d089aeb155c/MMR-16-06-8092-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/f0e121668c2f/MMR-16-06-8092-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/b8f1706c0733/MMR-16-06-8092-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/b07cdd6b7e6d/MMR-16-06-8092-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/39a4461b3e35/MMR-16-06-8092-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/338f202aff8c/MMR-16-06-8092-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/43c723229b0c/MMR-16-06-8092-g06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/1d089aeb155c/MMR-16-06-8092-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/f0e121668c2f/MMR-16-06-8092-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/b8f1706c0733/MMR-16-06-8092-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/b07cdd6b7e6d/MMR-16-06-8092-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/39a4461b3e35/MMR-16-06-8092-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/338f202aff8c/MMR-16-06-8092-g05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/208d/5779894/43c723229b0c/MMR-16-06-8092-g06.jpg

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