Ruhee Ruheea Taskin, Ma Sihui, Suzuki Katsuhiko
Graduate School of Sport Sciences, Waseda University, Tokorozawa 359-1192, Japan.
Faculty of Sport Sciences, Waseda University, Tokorozawa 359-1192, Japan.
Antioxidants (Basel). 2020 Feb 4;9(2):136. doi: 10.3390/antiox9020136.
Regular exercise is beneficial to maintain a healthy lifestyle, but the beneficial effects are lost in the case of acute exhaustive exercise; this causes significant inflammation, oxidative stress along with organ damage. Recently, sulforaphane (SFN), an indirect antioxidant, has drawn special attention for its potential protective effect against inflammation and oxidative stress. However, no studies have been performed regarding acute exhaustive exercise-induced organ damage in association with SFN administration. Therefore, the aim of this study was to investigate the effects of SFN on acute exhaustive exercise-induced organ damage and the mechanisms involved. To perform the study, we divided mice into four groups: Control, SFN, exercise, and SFN plus exercise. The SFN group was administered orally (50 mg/kg body wt) 2 h before the running test. We measured plasma levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH), and acute exhaustive exercise significantly increased these biomarkers. In addition, the mRNA expression of pro-inflammatory cytokines, IL-6, IL-1β, and TNF-α, were significantly increased in the liver of exercise group. However, the SFN plus exercise group showed a significant reduction in the expression of cytokines and blood biomarkers of tissue damage or cell death. Furthermore, we measured mRNA expression of Nrf2, heme oxygenase (HO)-1, and antioxidant defense enzymes expression, i.e., superoxide dismutase (SOD1), catalase (CAT), and glutathione peroxidase (GPx1) in the liver. The expression of all these biomarkers was significantly upregulated in the SFN plus exercise group. Collectively, SFN may protect the liver from exhaustive exercise-induced inflammation via inducing antioxidant defense response through the activation of Nrf2/HO-1 signal transduction pathway.
规律运动有益于维持健康的生活方式，但在急性力竭运动的情况下，这些有益效果会丧失；这会导致显著的炎症、氧化应激以及器官损伤。近来，萝卜硫素（SFN）作为一种间接抗氧化剂，因其对炎症和氧化应激的潜在保护作用而备受关注。然而，尚未有关于与SFN给药相关的急性力竭运动诱导的器官损伤的研究。因此，本研究的目的是探究SFN对急性力竭运动诱导的器官损伤的影响及其相关机制。为进行该研究，我们将小鼠分为四组：对照组、SFN组、运动组和SFN加运动组。SFN组在跑步测试前2小时口服给药（50毫克/千克体重）。我们测量了血浆中丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）和乳酸脱氢酶（LDH）的水平，急性力竭运动显著升高了这些生物标志物。此外，运动组肝脏中促炎细胞因子IL-6、IL-1β和TNF-α的mRNA表达显著增加。然而，SFN加运动组细胞因子的表达以及组织损伤或细胞死亡的血液生物标志物显著降低。此外，我们测量了肝脏中Nrf2、血红素加氧酶（HO）-1的mRNA表达以及抗氧化防御酶的表达，即超氧化物歧化酶（SOD1）、过氧化氢酶（CAT）和谷胱甘肽过氧化物酶（GPx1）。在SFN加运动组中，所有这些生物标志物的表达均显著上调。总体而言，SFN可能通过激活Nrf2/HO-1信号转导通路诱导抗氧化防御反应，从而保护肝脏免受力竭运动诱导的炎症。
