Astaxanthin Suppresses Cigarette Smoke-Induced Emphysema through Nrf2 Activation in Mice

Kubo, Hiroaki; Asai, Kuniya; Kojima, Kazuyuki; Sugitani, A.; Kyomoto, Yohkoh; Okamoto, Atsuko; Yamada, Kazuhiro; Ijiri, Naoki; Watanabe, Tetsuya; Hirata, Kazuto; Kawaguchi, Tomoya

doi:10.3390/md17120673

Cited by 45 publications

(40 citation statements)

References 51 publications

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“…The cigarette smoke-exposed mice showed less weight gain, increased inflammatory cell infiltration in BALF, and development of emphysema characterized by alveolar enlargement and greater destruction of alveoli, similar to mice in a previous report. 23 , 33 , 34 Our results showed a discrepancy regarding the effect of NYT on smoking-induced change in pulmonary morphology: NYT induced partial recovery of alveolar damage as indicated by the DI; however, NYT did not reduce air space enlargement as indicated by the MLI. Some reports showed that the DI is a more sensitive parameter of pulmonary destruction than the MLI, 30 , 35 whereas others revealed a correlation between the MLI and loss of elastic recoil.…”

Section: Discussioncontrasting

confidence: 61%

<p>Ninjin’yoeito Ameliorates Skeletal Muscle Complications in COPD Model Mice by Upregulating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α Expression</p>

Miyamoto¹,

Asai²,

Kadotani³

et al. 2020

COPD

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Purpose: Sarcopenia, the loss of skeletal muscle mass and strength, is a common systemic consequence of chronic obstructive pulmonary disease (COPD) and is correlated with higher mortality. Ninjin'yoeito (NYT) is a Japanese herbal medicine used to treat athrepsia and anorexia and is reported to ameliorate weight loss and muscular dysfunction. Recent studies have shown that its crude components upregulate the peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α)-related pathway, which is involved in skeletal muscle functions. Here, we examined whether NYT improves skeletal muscle complications by upregulating PGC-1α in COPD model mice. Materials and Methods: Mice were divided into four groups: control, NYT, smoking, and smoking + NYT. The smoking and smoking + NYT groups were exposed to cigarette smoke for 60 min once daily. The mice in the NYT and smoking + NYT groups were fed an NYT-containing diet (3% w/w). We performed cellular analysis of bronchoalveolar lavage fluid, assessed pulmonary morphological changes, examined the expression of PGC-1α mRNA and protein in the gastrocnemius and soleus muscle, measured the hindlimb muscle volume with micro-computed tomography, and determined the myofiber proportion in soleus muscle after 12 weeks. Results: Cigarette smoke exposure resulted in reduced skeletal muscle volume and slowtwitch muscle fibers and development of pulmonary emphysema. NYT feeding induced partial recovery of the damaged alveolar wall; however, NYT did not ameliorate smokeinduced alveolar enlargement. These findings revealed that NYT did not have sufficient efficacy in suppressing pulmonary emphysema. On the other hand, PGC-1α expression in muscle tissue of the NYT-fed mice increased significantly, resulting in suppression of smokeinduced loss of muscle mass and alteration in the muscle fiber distribution. Conclusion: NYT increases PGC-1α expression in the muscle of COPD model mice and is involved in suppressing cigarette smoke-induced muscle complications. NYT may be a novel preventive and therapeutic medication for muscular dysfunctions in COPD.

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Section: Discussioncontrasting

confidence: 61%

<p>Ninjin’yoeito Ameliorates Skeletal Muscle Complications in COPD Model Mice by Upregulating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α Expression</p>

Miyamoto¹,

Asai²,

Kadotani³

et al. 2020

COPD

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“…In addition, the number of inflammatory cells in the bronchoalveolar lavage fluid was significantly reduced and emphysema was significantly suppressed in the ASX groups. In conclusion, ASX protects against oxidative stress by activating the Nrf2 pathway and improves cigarette smoke-induced emphysema [ 61 ].…”

Section: Major Biochemical Pathways Involved In Astaxanthin Pro-lomentioning

confidence: 99%

Astaxanthin as a Putative Geroprotector: Molecular Basis and Focus on Brain Aging

et al. 2020

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In recent years, the scientific interest in natural compounds with geroprotective activities has grown exponentially. Among the various naturally derived molecules, astaxanthin (ASX) represents a highly promising candidate geroprotector. By virtue of the central polyene chain, ASX acts as a scavenger of free radicals in the internal membrane layer and simultaneously controls oxidation on the membrane surface. Moreover, several studies have highlighted ASX’s ability to modulate numerous biological mechanisms at the cellular level, including the modulation of transcription factors and genes directly linked to longevity-related pathways. One of the main relevant evolutionarily-conserved transcription factors modulated by astaxanthin is the forkhead box O3 gene (FOXO3), which has been recognized as a critical controller of cell fate and function. Moreover, FOXO3 is one of only two genes shown to robustly affect human longevity. Due to its tropism in the brain, ASX has recently been studied as a putative neuroprotective molecule capable of delaying or preventing brain aging in different experimental models of brain damage or neurodegenerative diseases. Astaxanthin has been observed to slow down brain aging by increasing brain-derived neurotrophic factor (BDNF) levels in the brain, attenuating oxidative damage to lipids, protein, and DNA and protecting mitochondrial functions. Emerging data now suggest that ASX can modulate Nrf2, FOXO3, Sirt1, and Klotho proteins that are linked to longevity. Together, these mechanisms provide support for a role of ASX as a potential geroneuroprotector.

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“…Astaxanthin is a carotenoid, widely distributed in marine life such as shrimp and crab. It has been reported to improve smoking-induced emphysema and inhibit oxidative stress by activating Nrf2 and HO-1, providing a new treatment option for COPD [ 79 ]. Moreover, sulforaphane can protect lung epithelial cells by decreasing ROS levels and upregulating the expression of Nrf2 [ 57 , 58 ].…”

Section: Bioactive Compounds In Food In Chronic Diseasesmentioning

confidence: 99%

Food-Derived Pharmacological Modulators of the Nrf2/ARE Pathway: Their Role in the Treatment of Diseases

Zhao

Man

et al. 2021

Molecules

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Oxidative stress, which refers to unbalanced accumulation of reactive oxygen species (ROS) levels in cells, has been linked to acute and chronic diseases. Nuclear factor erythroid 2-related factor 2/antioxidant response element (Nrf2/ARE) pathway plays a vital role in regulating cytoprotective genes and enzymes in response to oxidative stress. Therefore, pharmacological regulation of Nrf2/ARE pathway is an effective method to treat several diseases that are mainly characterized by oxidative stress and inflammation. Natural products that counteract oxidative stress by modulating Nrf2 have contributed significantly to disease treatment. In this review, we focus on bioactive compounds derived from food that are Nrf2/ARE pathway regulators and describe the molecular mechanisms for regulating Nrf2 to exert favorable effects in experimental models of diseases.

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Astaxanthin Suppresses Cigarette Smoke-Induced Emphysema through Nrf2 Activation in Mice

Cited by 45 publications

References 51 publications

<p>Ninjin’yoeito Ameliorates Skeletal Muscle Complications in COPD Model Mice by Upregulating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α Expression</p>

<p>Ninjin’yoeito Ameliorates Skeletal Muscle Complications in COPD Model Mice by Upregulating Peroxisome Proliferator-Activated Receptor γ Coactivator-1α Expression</p>

Astaxanthin as a Putative Geroprotector: Molecular Basis and Focus on Brain Aging

Food-Derived Pharmacological Modulators of the Nrf2/ARE Pathway: Their Role in the Treatment of Diseases

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