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Optical Angiography at Diabetes
Published in Andrey V. Dunaev, Valery V. Tuchin, Biomedical Photonics for Diabetes Research, 2023
Dan Zhu, Jingtan Zhu, Dongyu Li, Tingting Yu, Wei Feng, Rui Shi
Zhanyang et al. [88] tested the hypothesis that recombinant FGF21 (rFGF21) administration may reduce T2D-induced BBB disruption via NF-E2-related factor-2 (Nrf2) upregulation. They studied a series of BBB-related tight junction proteins, including ZO1, VE-cadherin, and occludin with immunofluorescence and immunocytochemistry in diabetic mice, and found that in db/db mice, the staining is fragmented, losing continuity. rFGF21 treatment reversed this process, making occludin and VE-cadherin staining more integral and continuous compared to untreated db/db group. rFGF21 administration may decrease T2D-induced BBB permeability.
Therapeutics in pulmonary hypertension
Published in Anthony J. Hickey, Heidi M. Mansour, Inhalation Aerosols, 2019
Maria F. Acosta, Don Hayes, Jeffrey R. Fineman, Jason X.-J. Yuan, Stephen M. Black, Heidi M. Mansour
NRF2 activators: The NF-κB pathway can be activated by oxidants and the subsequently produced inflammatory cytokines have been shown to be stimulators of an endothelial-mesenchymal transition (EndMT) (50). NF-E2-related factor 2 (Nrf2), is the main regulatory factor of the antioxidant response through regulating expression of a series of antioxidant enzymes, including heme oxygenase-1 (HO-1). In response to oxidative stress or electrophiles, Nrf2 separates from Kelch-like ECH-associated protein 1 (Keap1), a key Nrf2 inhibitory factor of Nrf2/HO-1 pathway, translocates into the nucleus, and induces the expression of antioxidant proteins (50). Nrf2 activators could be used to bind cysteine residue of Keap1 and promote de-methylation of Nrf2 promoter, giving pharmacological activities in the cardiovascular system, including adjunctive treatment of microcirculation protection, endothelial protection, myocardial preservation, and antioxidation (50).
Impact of Dietary Polyphenols on Arterial Stiffness
Published in Catherina Caballero-George, Natural Products and Cardiovascular Health, 2018
Tess De Bruyne, Lynn Roth, Harry Robberecht, Luc Pieters, Guido De Meyer, Nina Hermans
A proposed mechanism for ‘nutritional antioxidants,’ like polyphenols, involves the paradoxical oxidative activation of the NFE2-related factor 2 (Nrf2) signaling pathway. Nrf2 can be activated by ROS in the cytoplasm, after which it translocates to the nucleus and regulates ARE-mediated transcriptions of various genes encoding the above-mentioned antioxidant enzymes (Goszcz et al., 2017; Zhang and Tsao, 2016). Nrf2 is under constant control of the redox-sensitive repressor protein Keap1 (Zenkov et al., 2016).
Bone marrow mesenchymal stem cells inhibit ferroptosis via regulating the Nrf2-keap1/p53 pathway to ameliorate chronic kidney disease injury in the rats
Published in Journal of Receptors and Signal Transduction, 2023
Lishi Shao, Qixiang Fang, Chen Shi, Ya Zhang, Chunjuan Xia, Yifan Zhang, Jiaping Wang, Fukun Chen
The NF-E2-related factor 2 (Nrf2) is a transcriptional regulator assumed to be the most prominent active component involved in antioxidant response regulation, given that several of its targets are associated with the prevention or correction of intracellular redox imbalance [12]. It plays a pivotal role in mediating iron/heme metabolism [13]. Ferroportin (SLC40A1) is a critical protein for iron storage, as are the light and heavy ferritin chains (FTL/FTH1), which are responsible for the cell iron efflux, all of which are controlled by Nrf2 [14,15]. A recent study demonstrated the role of the Kelch-like ECH-associated protein 1 (Keap1)–Nrf2 pathway in the regulation of cancer cell responses to ferroptosis-inducing therapeutics [16]. The p53 tumor suppressor can induce apoptosis and ferroptosis in response to damage to the genome [17]. In addition, studies have reported that p53 antagonizes erastin-induced ferroptosis by accelerating intranuclear dipeptidyl-peptidase-4 (DPP4) localization [18], highlighting the need to further study whether MSCs can alleviate CKD by regulating ferroptosis via Nrf2–Keap1/p53 activation.
Dexmedetomidine provides protection to neurons against OGD/R-induced oxidative stress and neuronal apoptosis
Published in Toxicology Mechanisms and Methods, 2021
Deming Xu, Changbi Zhou, Juanyun Lin, Wenhui Cai, Wei Lin
NF-E2-related factor 2 (Nrf2) is a pivotal modulator of antioxidants and can balance oxygen free radicals and inflammation within cells (Sandberg et al. 2014). Under conditions involving inflammation and oxidative stress, the levels of reactive oxygen species (ROS) begin to increase. In turn, this causes increased oxidation of Keap1, thus leading to the release of Nrf2. Following translocation to the nucleus, Nrf2 is capable of binding to the antioxidant response element (ARE) in order to activate the expression of antioxidant genes, including superoxide dismutase (SOD), heme oxygenase-1 (HO-1), and NAD(P)H: quinone oxidoreductase-1 (NQO-1), so as to eliminate excessive ROS (Xue et al. 2016; Wasik et al. 2017). As oxidative stress can be induced by OGD/R treatment, and can therefore result in neuronal injury, studies have begun to focus on biological molecules that can reduce oxidative stress in OGD/R-treated neurons. Interestingly, a significant body of evidence now indicates that the Nrf2/ARE signaling pathway is a vital regulator of oxidative stress in a variety of diseases. For instance, the upregulation of CKIP-1 attenuates high-glucose triggered oxidative stress in human retinal endothelial cells by regulating the Nrf2/ARE signaling pathway (Zhang et al. 2019). Another study demonstrated that the activation of the Nrf2/ARE pathway suppressed cognitive deficits in a mouse model of Alzheimer's disease by modulating oxidative stress (Tian et al. 2019). Other research has indicated that the Nrf2/ARE pathway plays a pivotal role in Parkinson’s disease and could therefore represent a promising target for the development of new therapeutic options for Parkinson’s disease (Gureev and Popov 2019). However, the regulatory mechanisms associated with Nrf2/ARE pathway activation in OGD/R-treated neurons has not been investigated specifically.
Hydrogen gas protects against delayed encephalopathy after acute carbon monoxide poisoning in a rat model
Published in Neurological Research, 2020
Meihua Shen, Yijun Zheng, Kaimin Zhu, Zhonghai Cai, Wenwu Liu, Xuejun Sun, Jiankang Liu, Duming Zhu
NRF2 (NF-E2-related factor 2, NFE2L2) is a transcription factor related to oxidative stress, and mediates a broad-range of adaptive responses to environmental and endogenous stresses [29]. As an important transcription factor, it may induce the expression of a variety of anti-oxidases (such as SOD-1, CAT, HO-1, GST and GP1), indirectly exerting anti-oxidative effects. Several studies have revealed that hydrogen treatment affects Nrf2 expression and/or DNA binding activity. It has been reported that hydrogen gas is able to attenuate hyperoxia induced lung injury and ovalbumin-induced asthma via the Nrf2 pathway [30,31]. Their findings were further confirmed in Nrf2-deficient mice. In H9c2 cells, serum and glucose deprivation was employed to induce myocardial injury, and Xie et al. found hydrogen gas rich medium further upregulates HO-1 expression and nuclear Nrf2 levels in injured H9c2 cells and reduces hydroxyl radicals, and these effects were significantly reduced after genetic silencing of Nrf2 by RNA interference [32], and the protective effects of hydrogen gas were also absent in NRF2 knockout mice [33] In seawater instillation-induced acute lung injury, Diao et al. found hydrogen gas (2%) markedly improves lung endothelial permeability, in association with the inhibition of inflammation (lung MPO activity, and BALF TNF-α, IL-1β and IL-6 contents), oxidative stress (lung MDA content; upregulation of Nrf2 and HO-1 expression) and apoptosis (caspase-3 expression) [34]. More recently, Yu et al. found hydrogen gas (2%) increases the survival rate and attenuated intestinal injury in wild type (but not Nrf2 knockout) mice with severe sepsis, in association with reduced HMGB1 release and increased HO-1 expression [33]. In this study, the mRNA expression levels of Nrf2, HO-1, SOD and CAT as well as Nrf2, GST and GP1 protein amounts were detected in the hippocampus and cortex. As shown above, CO exposure induced the expression of Nrf2 and downstream genes (Nrf2, HO-1, SOD, CAT, GST and GP1), and HCH further upregulated these anti-oxidases as shown by both RT-PCR and Western blotting. Xie et al. [31] also showed serum and glucose deprivation (SGD) – induced myocardial injury in H9c2 cells could significantly increase HO-1 expression and nuclear Nrf2 levels, with hydrogen rich medium further enhancing SGD induced upregulation of HO-1 and Nrf2.