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Yoko Yagishita, Akira Uruno, Dionysios V Chartoumpekis, Thomas W Kensler, and Masayuki Yamamoto

Nrf2 (NF-E2-related factor 2) plays a critical role in cellular responses to oxidative and electrophilic stresses ( Itoh et al . 1995 ). In quiescent conditions, Keap1 (Kelch-like ECH-associated protein 1) suppresses Nrf2 activity by serving as a

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Bo Chen, Yanrong Lu, Younan Chen, and Jingqiu Cheng

activity is disrupted, it is no longer possible to maintain appropriate redox balance. Nuclear factor-E2-related factor 2 (Nrf2), a transcription factor with a high sensitivity to oxidative stress, binds to antioxidant response elements (AREs) in the

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Gen Chen, Xiangjuan Chen, Chao Niu, Xiaozhong Huang, Ning An, Jia Sun, Shuai Huang, Weijian Ye, Santie Li, Yingjie Shen, Jiaojiao Liang, Weitao Cong, and Litai Jin

-inflammatory cytokines such as IL6 , IL8 and TNFa ( Tang et al. 2017 ). Therefore, protecting vascular cells from oxidative stress injury is a major approach in the treatment of diabetic complications ( Rask-Madsen & King 2013 ). Nrf2 is one of the most

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Wenpeng Dong, Ye Jia, Xiuxia Liu, Huan Zhang, Tie Li, Wenlin Huang, Xudong Chen, Fuchun Wang, Weixia Sun, and Hao Wu

2-related factor 2 (NRF2) has been identified as a governor of antioxidant and redox signaling. NRF2 activates the transcription of downstream antioxidant genes such as heme oxygenase-1 ( Ho1 ) and NAD(P)H dehydrogenase quinone 1 ( Nqo1 ) ( Ruiz et

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Ziping Jiang, Junduo Wu, Fuzhe Ma, Jun Jiang, Linlin Xu, Lei Du, Wenlin Huang, Zhaohui Wang, Ye Jia, Laijin Lu, and Hao Wu

, enhancing OS ( Betteridge 2000 , Incalza et al . 2018 ). This has brought to light the activation of the antioxidant defense system as a viable strategy to improve diabetic ED ( Laight et al . 2000 ). Nuclear factor erythroid 2-related factor 2 (NRF2

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Jia Sun, Haiping Zhu, Xiaorong Wang, Qiuqi Gao, Zhuoying Li, and Huiya Huang

that CoQ10, as an effective antioxidant in mitochondria, exerts beneficial effects in DN via mitophagy through restoration of Nrf2/ARE signaling. Thus, a novel role of CoQ10 in alleviating DN-induced mitochondrial dysfunction by modulating mitophagy is

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Wailan Shan, Shiyin Lu, Biqian Ou, Jia Feng, Zixian Wang, Huixian Li, Xiaohua Lu, and Ma Yi

Obesity is strongly linked to male infertility. Apoptotic inflammatory response caused by oxidative stress in testicular spermatogenic cells is one of the important causes of obesity-related male infertility. Pituitary adenylate cyclase activating polypeptide (PACAP) as a bioactive peptide secreted by the pituitary gland, has a powerful triple role of anti-oxidation, anti-apoptosis and anti-inflammation, and is involved in male reproduction regulation, but the specific mechanism remains unknown. The purpose of the current study is to explore the role of PACAP in obesity-related male infertility. In cell-level experiments, Mouse spermatocytes (GC-2) were treated with palmitate (PA) to establish an high-fat injury cell model in vitro and then treated with PACAP. In animal-level experiments, C57BL/6 male mice were fed with a high-fat diet (HFD) to induce obesity and then treated with PACAP. The cell mechanism studies showed that PACAP selectively binds to the PAC1 receptor to attenuate palmitic acid-induced mouse spermatogenic cell (GC-2) oxidative damage and apoptotic inflammatory response via the PKA/ERK/Nrf2 signaling axis. However, this mechanism was inhibited in GC-2 cells inhibiting the activity of Nrf2. The animal experiment studies showed that PACAP treatment ameliorated obesity characteristics, including body weight, epididymal adipose weight, testes/body weight, serum lipids levels, and reproductive hormone levels in vivo. Additionally, PACAP was shown to improve the reproductive function of the obese mice, which was characterized by improved testis morphology and sperm parameters via Keap1/Nrf2/ARE pathway. These beneficial effects of PACAP were abolished in obese mice with testis-specific knockdown of Nrf2.

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Anna E Bollag, Tianyang Guo, Ke-Hong Ding, Vivek Choudhary, Xunsheng Chen, Qing Zhong, Jianrui Xu, Kanglun Yu, Mohamed E Awad, Mohammed Elsalanty, Maribeth H Johnson, Meghan E McGee-Lawrence, Wendy B Bollag, and Carlos M Isales

the effects of various endogenous antioxidant systems upregulated by the activation of nuclear factor erythroid 2-related factor (NRF2), which is known to induce the expression of various endogenous antioxidant pathways ( de Figueiredo et al. 2015

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Chao Li, Bin Yang, Zhihao Xu, Eric Boivin, Mazzen Black, Wenlong Huang, Baoyou Xu, Ping Wu, Bo Zhang, Xian Li, Kunsong Chen, Yulian Wu, and Gina R Rayat

factor NRF2 and the subsequent NRF2/HO1 signaling pathway ( Zhang et al . 2013 ). In vivo study also demonstrated that C3G protected β cells against oxidative stress-mediated injury in streptozotocin-induced diabetic mice ( Sun et al . 2012

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Wanbao Yang, Hui Yan, Quan Pan, James Zheng Shen, Fenghua Zhou, Chaodong Wu, Yuxiang Sun, and Shaodong Guo

hyperglucagonemia results in excess hepatic glucose production, enhancing blood glucose in patients with type 2 diabetes (T2D) ( Consoli 1992 ). Inactivation of glucagon receptor is associated with significant improvement of blood glucose in diabetic mice ( Lee et