Fortunellin通过通过AMPK / Nrf-2途径调节来抑制炎症和氧化应激，从而保护小鼠免受果糖引起的糖尿病性心脏病的伤害。,Biochemical and Biophysical Research Communications

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Fortunellin通过通过AMPK / Nrf-2途径调节来抑制炎症和氧化应激，从而保护小鼠免受果糖引起的糖尿病性心脏病的伤害。
Biochemical and Biophysical Research Communications ( IF 2.5 ) Pub Date : 2017-06-19 , DOI: 10.1016/j.bbrc.2017.06.076
Cuihua Zhao ₁ , Yuan Zhang ₁ , Hongyang Liu ₁ , Peng Li ₁ , Han Zhang ₁ , Guanchang Cheng ₁

Affiliation

炎症和氧化应激有助于糖尿病性心肌病（DCM）的发展。该研究最初旨在计算消炎和抗氧化剂福尔霉素（Fortunellin）在高果糖诱导的糖尿病小鼠心脏损伤中的作用。使用各种测定法发现福尔青霉素对小鼠和细胞无毒性。高果糖用于诱导糖尿病小鼠。测量心脏组织病理学变化和心脏功能。Fortunellin大大减轻了组织病理学改变的评分并减轻了心脏功能，并伴有炎症和氧化应激降低。Fortunellin可显着降低促炎细胞因子和p-IκB激酶α（IKKα），p-IκBα和p-核因子-κB（NF-κB）的表达，而超氧化物歧化酶（SOD），过氧化氢酶（CAT）），血红素加氧酶-1（HO-1）和p-AMP激活的蛋白激酶（AMPK）显着增强。此外，在具有核因子红系2相关因子2（Nrf2）的H9C2细胞中，敲除消除了Fortunellin对心脏损伤的预防作用，这一点已通过炎症反应和氧化应激的升高得以证明。对p-AMPK的抑制作用降低了Fortunellin诱导的Nrf2和HO-1的水平，从而消除了Fortunellin的保护作用。我们的研究首次提出，用果糖处理可增强糖尿病小鼠和心肌细胞中的AMPK / Nrf2途径，从而保护福尔青林免受果糖诱导的炎症和氧化应激的侵害。在H9C2细胞中，具有核因子红系2相关因子2（Nrf2）的敲除取消了Fortunellin对心脏损伤的预防作用，这一点已通过炎症反应和氧化应激的升高得以证明。对p-AMPK的抑制降低了由Fortunellin诱导的Nrf2和HO-1的水平，从而消除了Fortunellin的保护作用。我们的研究首次提出，用果糖处理可增强糖尿病小鼠和心肌细胞中的AMPK / Nrf2途径，从而保护福尔青林免受果糖诱导的炎症和氧化应激的侵害。在H9C2细胞中，具有核因子红系2相关因子2（Nrf2）的敲低取消了Fortunellin对心脏损伤的预防作用，这一点已通过炎症反应和氧化应激的升高得以证明。对p-AMPK的抑制降低了由Fortunellin诱导的Nrf2和HO-1的水平，从而消除了Fortunellin的保护作用。我们的研究首次提出，用果糖处理可增强糖尿病小鼠和心肌细胞中的AMPK / Nrf2途径，从而保护福尔青林免受果糖诱导的炎症和氧化应激的侵害。

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Fortunellin protects against high fructose-induced diabetic heart injury in mice by suppressing inflammation and oxidative stress via AMPK/Nrf-2 pathway regulation.

Inflammation and oxidative stress contribute to the progression of diabetic cardiomyopathy (DCM). The study was first designed to calculate the role of an anti-inflammatory and anti-oxidant Fortunellin (For) in high fructose-induced cardiac injury in diabetic mice. Fortunellin was found to be none of toxicity to mice and cells using various assays. High fructose was used to induce mice with diabetes. The heart histopathological changes and cardiac function were measured. Fortunellin significantly attenuated the score of histopathological alterations and alleviated heart function, accompanied with reduced inflammation and oxidative stress. The pro-inflammatory cytokines and the expression of p-IκB kinase α (IKKα), p-IκBα, and p-nuclear factor-κB (NF-κB) were dramatically reduced by Fortunellin, while superoxide dismutase (SOD), catalase (CAT), heme oxygenase-1 (HO-1) and p-AMP-activated protein kinase (AMPK) were significantly enhanced. Moreover, in H9C2 cells with nuclear factor erythroid 2-related factor 2 (Nrf2) knock-down abolished the prevention of Fortunellin against cardiac injury, proved by elevated inflammatory response and oxidative stress. Suppression of p-AMPK reduced the level of Nrf2 and HO-1 induced by Fortunellin, eliminating the protective role of Fortunellin. For the first time, our study suggested that Fortunellin protected against fructose-induced inflammation and oxidative stress by enhancing AMPK/Nrf2 pathway in diabetic mice and cardiomyocytes with fructose treatment.

更新日期：2019-11-01

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