绿原酸可减轻链脲佐菌素诱导的糖尿病大鼠血液中的促炎反应。

IF 2.7 Q3 MEDICINE, RESEARCH & EXPERIMENTAL
Youngchan Lee, Chun-Sik Bae, Taeho Ahn
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引用次数: 0

摘要

背景:绿原酸(CGA)可清除活性氧(ROS)和活性氮,从而减轻炎症反应。本研究将 CGA 的抗炎作用扩大到链脲佐菌素(STZ)诱导的糖尿病大鼠。研究还调查了 STZ 糖尿病大鼠外周血单核细胞(PBMC)中氧化应激、促炎和细胞色素 P450(CYP)1A 酶之间的相互关系:结果:与正常大鼠相比,STZ 诱导的糖尿病大鼠血清中促炎性细胞因子白细胞介素-6 和肿瘤坏死因子-α 的水平分别升高了约 3.4 倍和 2.9 倍,白蛋白浓度降低。C反应蛋白(CRP)值也增加了约3.8倍,表明STZ诱导的糖尿病大鼠血液中存在炎症。在 STZ 处理的大鼠 PBMC 中,CYP1A 酶的表达水平和催化活性分别升高了约 2.2-2.5 倍和 4.3-6.7 倍。还观察到 PBMC 结合的白蛋白量减少。相反,经 CGA 处理的糖尿病大鼠血清中细胞因子和 CRP 的水平以及 PBMC 中 CYP1A 酶的活性均显著降低,且降低程度与 CGA 浓度相关。此外,CGA 还能降低 STZ 介导的血清和 PBMC 中 ROS 的升高。然而,CGA 处理并没有改变 STZ 导致的血糖水平升高和 CYP1A 酶的表达。STZ 导致的血清和 PBMC 结合白蛋白水平的下降也未因服用 CGA 而恢复:这些结果表明,CGA 可用于治疗 1 型糖尿病引发的炎症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Chlorogenic acid attenuates pro-inflammatory response in the blood of streptozotocin-induced diabetic rats.

Chlorogenic acid attenuates pro-inflammatory response in the blood of streptozotocin-induced diabetic rats.

Chlorogenic acid attenuates pro-inflammatory response in the blood of streptozotocin-induced diabetic rats.

Chlorogenic acid attenuates pro-inflammatory response in the blood of streptozotocin-induced diabetic rats.

Background: Chlorogenic acid (CGA) has been shown to reduce pro-inflammation by scavenging reactive oxygen species (ROS) and reactive nitrogen species. In this study, the anti-inflammatory effect of CGA was expanded to streptozotocin (STZ)-induced diabetic rats. The inter-relationships among oxidative stress, pro-inflammation, and cytochrome P450 (CYP) 1A enzymes were also investigated in peripheral blood mononuclear cells (PBMC) of STZ-diabetic rats.

Results: The levels of pro-inflammatory cytokines, interleukin-6 and tumor necrosis factor-alpha, increased by approximately 3.4- and 2.9-fold, respectively, and the albumin concentration decreased in the serum of STZ-induced diabetic rats compared to normal rats. The C-reactive protein (CRP) values also increased by about 3.8-fold higher, indicating that STZ induced an inflammation in the blood of STZ-diabetic rats. The expression levels and catalytic activities of CYP1A enzymes were elevated by approximately 2.2-2.5- and 4.3-6.7-fold, respectively, in the PBMC of STZ-treated rats. A decrease in the amount of PBMC-bound albumin was also observed. In contrast, the levels of cytokines and CRP in serum and the activities of CYP1A enzymes in PBMC were significantly reduced in CGA-treated diabetic rats in a CGA concentration-dependent manner. In addition, STZ-mediated elevation of ROS in serum and PBMC was decreased by the CGA administration. However, the CGA treatment did not change the enhanced blood glucose level and expression of CYP1A enzymes by STZ. STZ-mediated decrease in the levels of serum and PBMC-bound albumin was not also restored by the CGA administration.

Conclusions: These results suggest that CGA could be used to treat type 1 diabetes-induced inflammation.

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来源期刊
CiteScore
4.40
自引率
0.00%
发文量
32
审稿时长
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