Abstract
Luteolin-6-C-neohesperidoside (LN) is a flavonoid isolated from moso bamboo leaf. This study was performed to evaluate the antifatigue effect of LN on a rat model undergoing the weight-loaded forced swimming test (FST). Briefly, male Sprague-Dawley rats (20–22 weeks old) were forced to undertake exhaustive swimming every other day for 3 weeks. Each swimming session was followed by the administration of distilled water, LN (25–75 mg/kg), or ascorbic acid (100 mg/kg) 1 h later. Oral administration of LN significantly improved exercise endurance; normalized alterations in energy metabolic markers; and decreased serum lactic acid, lactate dehydrogenase, and blood urea nitrogen levels of rats that underwent FST. Moreover, LN enhanced the activities of antioxidant enzymes and antioxidant capacity, as measured by enzyme activity assays, RT-PCR, and Western blotting, as well as decreasing the levels of proinflammatory cytokines such as tumor necrosis factor-α, interleukin-1β (IL-1β), and IL-6 and increasing the level of anti-inflammatory (IL-10) in the liver and skeletal muscle. These results suggested that LN reduces both physical and mental effects of chronic fatigue, probably by attenuating oxidative stress injury and inflammatory responses in the liver and skeletal muscle. This study thus supports the use of LN in functional foods for antifatigue and antioxidant effects.
Highlights
Chronic fatigue is characterized by persistent tiredness that is not relieved by rest and that is always worsened by physical or mental activity [1]
Oxidative stress was shown to stimulate the inflammatory response by increasing the release of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β in patients with chronic fatigue [10]
To clarify the molecular mechanism by which LN is involved in the fatigue and fatigue-related organ dysfunction induced by exhaustive exercise, we evaluated the expression of oxidative stress-related signaling genes in liver and skeletal muscle tissues
Summary
Chronic fatigue is characterized by persistent tiredness that is not relieved by rest and that is always worsened by physical or mental activity [1]. In view of ongoing research on chronic fatigue, it is emphasized that the pathogenesis of fatigue is associated with energy metabolism and immune and endocrine systems, as well as inflammatory response and dysfunction of the antioxidant defense system [5,6,7]. Among these potential factors, oxidative stress plays the most important role in the etiology of fatigue. Oxidative stress was shown to stimulate the inflammatory response by increasing the release of proinflammatory cytokines such as tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and IL-1β in patients with chronic fatigue [10]
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