Protective effects of sesamol on systemic oxidative stress-induced cognitive impairments <i>via</i> regulation of Nrf2/Keap1 pathway

Ren, Bo; Tian, Yuan; Diao, Zhijun; Zhang, Chenxi; Liu, Zhigang; Liu, Xuebo

doi:10.1039/c8fo01436a

Cited by 63 publications

(50 citation statements)

References 48 publications

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“…These findings were consistent with previous studies, which showed that sesamol increased GSH and decreased MDA levels in rat ischemic cortex tissues [24]. Sesamol regulation of GSH and MDA levels also reduced oxidative stress and improved cognitive impairments in mouse brains [54]. Hence, sesamol had a protective effect against oxidative stress, and thus maintained lung function in asthmatic mice.…”

Section: Discussionsupporting

confidence: 92%

Sesamol Alleviates Airway Hyperresponsiveness and Oxidative Stress in Asthmatic Mice

Liou

Chen

et al. 2020

Antioxidants

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Sesamol, isolated from sesame seeds (Sesamum indicum), was previously shown to have antioxidative, anti-inflammatory, and anti-tumor effects. Sesamol also inhibited lipopolysaccharide (LPS)-induced pulmonary inflammatory response in rats. However, it remains unclear how sesamol regulates airway inflammation and oxidative stress in asthmatic mice. This study aimed to investigate the efficacy of sesamol on oxidative stress and airway inflammation in asthmatic mice and tracheal epithelial cells. BALB/c mice were sensitized with ovalbumin, and received oral sesamol on days 14 to 27. Furthermore, BEAS-2B human bronchial epithelial cells were treated with sesamol to investigate inflammatory cytokine levels and oxidative responses in vitro. Our results demonstrated that oral sesamol administration significantly suppressed eosinophil infiltration in the lung, airway hyperresponsiveness, and T helper 2 cell-associated (Th2) cytokine expressions in bronchoalveolar lavage fluid and the lungs. Sesamol also significantly increased glutathione expression and reduced malondialdehyde levels in the lungs of asthmatic mice. We also found that sesamol significantly reduced proinflammatory cytokine levels and eotaxin in inflammatory BEAS-2B cells. Moreover, sesamol alleviated reactive oxygen species formation, and suppressed intercellular cell adhesion molecule-1 (ICAM-1) expression, which reduced monocyte cell adherence. We demonstrated that sesamol showed potential as a therapeutic agent for improving asthma.

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Section: Discussionsupporting

confidence: 92%

Sesamol Alleviates Airway Hyperresponsiveness and Oxidative Stress in Asthmatic Mice

Liou

Chen

et al. 2020

Antioxidants

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“…Reactive oxygen species (ROS), the most important oxygen free radical, is closely related to the pathology and development of various neurodegenerative diseases (Deshmukh, Unni, Krishnappa, & Padmanabhan, 2017). Excessive ROS production disrupts the balance between cellular oxidation and antioxidant defense systems, induces lipid peroxidation, DNA fragmentation, cellular integrity, and functional impairment, and ultimately leads to neuronal function disruption and apoptosis (Finkel & Holbrook, 2000; Ren et al, 2018).…”

Section: Introductionmentioning

confidence: 99%

Icaritin activates Nrf2/Keap1 signaling to protect neuronal cells from oxidative stress

Zhang

et al. 2020

Chem Biol Drug Des

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Oxidative stress is closely related to brain aging and development of various neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, and brain stroke (Allen & Bayraktutan, 2009; Okazawa, Ikawa, Tsujikawa, Kiyono, & Yoneda, 2014). The brain is extremely intolerant to oxidative stress because of its high demand for oxygen and the presence of large amounts of unsaturated lipids (Cutler et al., 2004). Reactive oxygen species (ROS), the most important oxygen free radical, is closely related to the pathology and development of various neurodegenerative diseases (Deshmukh, Unni, Krishnappa, & Padmanabhan, 2017). Excessive ROS production disrupts the balance between cellular oxidation and antioxidant defense systems, induces lipid peroxidation, DNA fragmentation, cellular integrity, and functional impairment, and ultimately leads to neuronal function disruption and apoptosis (Finkel & Holbrook, 2000; Ren et al., 2018).

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“…Similarly, the Keap1-hypo allele (Nrf2 activation) mice were partially protected from obesity, had lower fasting glucose and insulin levels, and developed less liver steatosis [40]. In addition, sesamol has been shown to protect cognitive impairments by activating the Nrf2 transcriptional pathway [41]. Therefore, the identification of a potent Nrf2 activator may provide another tool to prevent obesity and its associated metabolic diseases by enhancing energy expenditure.…”

Section: Discussionmentioning

confidence: 99%

Sesamol Increases Ucp1 Expression in White Adipose Tissues and Stimulates Energy Expenditure in High-Fat Diet-Fed Obese Mice

et al. 2020

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Sesamol found in sesame oil has been shown to ameliorate obesity by regulating lipid metabolism. However, its effects on energy expenditure and the underlying molecular mechanism have not been clearly elucidated. In this study, we show that sesamol increased the uncoupling protein 1 (Ucp1) expression in adipocytes. The administration of sesamol in high-fat diet (HFD)-fed mice prevented weight gain and improved metabolic derangements. The three-week sesamol treatment of HFD-fed mice, when the body weights were not different between the sesamol and control groups, increased energy expenditure, suggesting that an induced energy expenditure is a primary contributing factor for sesamol’s anti-obese effects. Consistently, sesamol induced the expression of energy-dissipating thermogenic genes, including Ucp1, in white adipose tissues. The microarray analysis showed that sesamol dramatically increased the Nrf2 target genes such as Hmox1 and Atf3 in adipocytes. Moreover, 76% (60/79 genes) of the sesamol-induced genes were also regulated by tert-butylhydroquinone (tBHQ), a known Nrf2 activator. We further verified that sesamol directly activated the Nrf2-mediated transcription. In addition, the Hmox1 and Ucp1 induction by sesamol was compromised in Nrf2-deleted cells, indicating the necessity of Nrf2 in the sesamol-mediated Ucp1 induction. Together, these findings demonstrate the effects of sesamol in inducing Ucp1 and in increasing energy expenditure, further highlighting the use of the Nrf2 activation in stimulating thermogenic adipocytes and in increasing energy expenditure in obesity and its related metabolic diseases.

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Protective effects of sesamol on systemic oxidative stress-induced cognitive impairments via regulation of Nrf2/Keap1 pathway

Abstract: Sesamol treatment alleviated systemic oxidative stress induced cognitive deficits via improving neuronal impairments, restoring antioxidant activities and up-regulating antioxidative signaling pathway.

Cited by 63 publications

References 48 publications

Sesamol Alleviates Airway Hyperresponsiveness and Oxidative Stress in Asthmatic Mice

Sesamol Alleviates Airway Hyperresponsiveness and Oxidative Stress in Asthmatic Mice

Icaritin activates Nrf2/Keap1 signaling to protect neuronal cells from oxidative stress

Sesamol Increases Ucp1 Expression in White Adipose Tissues and Stimulates Energy Expenditure in High-Fat Diet-Fed Obese Mice

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