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首页> 外文期刊>Journal of cellular biochemistry. >Cinnamaldehyde and Nitric Oxide Attenuate Advanced Glycation End Products-Induced the JAK/STAT Signaling in Human Renal Tubular Cells
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Cinnamaldehyde and Nitric Oxide Attenuate Advanced Glycation End Products-Induced the JAK/STAT Signaling in Human Renal Tubular Cells

机译：肉桂醛和一氧化氮减弱高级糖基化终产物诱导的人类肾小管细胞的JAK / STAT信号传导。

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摘要

Cinnamaldehyde is a major and a bioactive compound isolated from the leaves of Cinnamomum osmophloeum kaneh. It possesses anti-diabetic properties in vitro and in vivo and has anti-inflammatory and anti-cancer effects. To explore whether cinnamaldehyde was linked to altered advanced glycation end products (AGE)-mediated diabetic nephropathy, the molecular mechanisms of cinnamaldehyde responsible for inhibition of AGE-reduced nitric oxide (NO) bioactivity in human renal proximal tubular cells were examined. We found that raising the ambient AGE concentration causes a dose-dependent decrease in NO generation. Cinnamaldehyde significantly reverses AGE-inhibited NO generation and induces high levels of cGMP synthesis and PKG activation. Treatments with cinnamaldehyde, the NO donor S-nitroso-N-acetylpenicillamine, and the JAK2 inhibitor AG490 markedly attenuated AGE-inhibited NOS protein levels and NO generation. Moreover, AGE-induced the JAK2-STAT1/STAT3 activation, RAGE/p27(Kip1)/collagen IV protein levels, and cellular hypertrophy were reversed by cinnamaldehyde. The ability of cinnamaldehyde to suppress STAT activation was also verified by the observation that it significantly increased SCOS-3 protein level. These findings indicate for the first time that in the presence of cinnamaldehyde, the suppression of AGE-induced biological responses is probably mediated by inactivating the JAK2-STAT1/STAT3 cascade or activating the NO pathway. (C) 2015 Wiley Periodicals, Inc.
机译：肉桂醛是从桂皮的叶子中分离出的主要和生物活性化合物。它具有体外和体内抗糖尿病的特性，并具有抗炎和抗癌作用。为了探讨肉桂醛是否与改变的晚期糖基化终产物（AGE）介导的糖尿病性肾病相关，研究了肉桂醛在人肾近端肾小管细胞中抑制AGE还原一氧化氮（NO）生物活性的分子机制。我们发现提高环境AGE浓度会导致NO生成的剂量依赖性降低。肉桂醛可显着逆转AGE抑制型NO的产生，并诱导高水平的cGMP合成和PKG活化。用肉桂醛，NO供体S-亚硝基-N-乙酰青霉胺和JAK2抑制剂AG490处理可显着减弱AGE抑制的NOS蛋白水平和NO生成。此外，肉桂醛逆转了AGE诱导的JAK2-STAT1 / STAT3活化，RAGE / p27（Kip1）/胶原IV蛋白水平和细胞肥大。肉桂醛抑制STAT活化的能力还通过观察到它显着增加SCOS-3蛋白水平的观察得到了证实。这些发现首次表明，在存在肉桂醛的情况下，AGE诱导的生物反应的抑制可能是通过失活JAK2-STAT1 / STAT3级联反应或激活NO途径来介导的。 （C）2015威利期刊公司

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