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Moreover, we showed that mediated by ERK, JNK, and PKC, signaling cascades mediate Nrf2 translocation. We confirmed this phenomenon by the suppressed nuclear Nrf2 activation in cells that were treated with respective inhibitors (PD98059, SP600125, and GF109203X). However, antioxidant protein expressions were impaired in Nrf2 knockdown cells to confirm that ARE/Nrf2 pathways and the inhibition of AP-1 had significant roles in EGT-mediated protective effects. We can conclude that ergothioneine ameliorated UVA-induced skin aging and is a useful food supplement for skin care products. Copyright © 2020 You-Cheng Hseu et al.Norepinephrine (NE) is the naturally occurring adrenergic agonist that is released in response to hypotension, and it is routinely administered in clinical settings to treat moderate to severe hypotension that may occur during general anesthesia and shock states. Although NE has incontestable beneficial effects on blood pressure maintenance during hypotensive conditions, deleterious effects of NE on endothelial cell function may occur. In particular, the role of reactive oxygen species (ROS) and NADPH oxidase (Nox) on the deleterious effects of NE on endothelial cell function have not been fully elucidated. Therefore, we investigated the effects of NE on ROS production in rat lung microvascular endothelial cells (RLMEC) and its contribution to cell death. RLMEC were treated with NE (5 ng/mL) for 24 hours and ROS production was assessed by CellROX and DCFDA fluorescence. Nox activity was assessed by NADPH-stimulated ROS production in isolated membranes and phosphorylation of p47phox; cell death was assessed by flow cytometry and DNA fragmentation. Caspase activation was assessed by fluorescent microscopy. Nox1, Nox2, and Nox4 mRNA expression was assessed by real-time PCR. NE increased ROS production, Nox activity, p47phox phosphorylation, Nox2 and Nox4 mRNA content, caspase-3 activation, and RLMEC death. Phentolamine, an α 1-adrenoreceptor antagonist, inhibited NE-induced ROS production and Nox activity and partly inhibited cell death while β-blockade had no effect. Apocynin and PEGSOD inhibited NE-induced caspase-3 activation and cell death while direct inhibition of caspase-3 abrogated NE-induced cell death. PEG-CAT inhibited NE-induced cell death but not caspase-3 activation. Collectively, these results indicate that NE induces RLMEC death via activation of Nox by α-adrenergic signaling and caspase-3-dependent pathways. NE has deleterious effects on RLMECs that may be important to its long-term therapeutic use. Copyright © 2020 Andreia Z. Chignalia et al.Mitochondrial dysfunction and oxidative stress play an important role in the pathogenesis of both atrial fibrillation (AF) and diabetes mellitus (DM). Wenxin Keli (WXKL), an antiarrhythmic traditional Chinese medicine, has been shown to prevent cardiac arrhythmias through modulation of cardiac ion channels. This study tested the hypothesis that WXKL can improve atrial remodeling in diabetic rats by restoring mitochondrial function. Primary atrial fibroblasts of neonatal SD rats were divided into four groups control, hydrogen peroxide (H2O2), H2O2+WXKL 1 g/L, and H2O2+WXKL 3 g/L groups. Intracellular mitochondrial membrane potential (MMP), reactive oxygen species (ROS), and mitochondrial oxygen consumption were measured. SD male rats were randomly divided into three groups control, DM, and DM+WXKL groups. Rats in the DM+WXKL group were treated with daily gavage of WXKL at 3 g/kg. After eight weeks, echocardiography, hemodynamic examination, histology, electrophysiology study, mitochondrial respiratory function, and western blots were assessed. H2O2 treatment led to increased ROS and decreased intracellular MMP and mitochondrial oxygen consumption in primary atrial fibroblasts. WXKL improved the above changes. DM rats showed increased atrial fibrosis, greater left atrial diameter, lower atrial conduction velocity, higher conduction heterogeneity, higher AF inducibility, and lower mitochondrial protein expression, and all these abnormal changes except for left atrial diameter were improved in the DM+WXKL group. WXKL improves atrial remodeling by regulating mitochondrial function and homeostasis and reducing mitochondrial ROS in diabetic rats. Copyright © 2020 Mengqi Gong et al.Objective Sepsis is a life-threatening organ dysfunction caused by dysregulation of a host's response to infections. Sepsis-one of the most common contributing factors to acute kidney injuries in critically ill patients-is caused by bacterial endotoxins that lead to excessive production of proinflammatory cytokines. This condition can be treated with few side-effects by using electroacupuncture (EA) to regulate the neuroendocrine immune system to control the production of these cytokines. A number of studies have proven that EA stimulates the vagus nerve to manage inflammatory responses through the cholinergic pathway, slowing sepsis. selleck products This study was conducted to investigate the effect of bilateral EA at ST 36 (Zusanli) on rats' renal function by measuring their levels of plasma urea and creatinine. Materials and Methods This study was a randomized, double-blinded, laboratory experimental post-test, with both subjects and laboratory investigators blinded. Twenty-eight male Wistar rats were divided randomly into 4 groups of 7 rats each (1) a control group; (2) a sepsis group; (3) an EA + group; and (4) a sham EA + group. EA and sham EA was applied once for 30 minutes before intraperitoneal administration of live Eschericia coli bacteria ATCC 25922. Six hours after administration of the bacteria the rats' plasma urea and creatinine levels were measured. Results There was a statistically significant difference in the mean levels of urea (P  less then  0.001, 95% confidence interval (CI) 57.1-76.6) and creatinine (P = 0.005, 95% CI 0.14-0.62) between the sepsis and control groups. Conclusions These findings suggest that EA pretreatment at ST 36 attenuated the induced inflammatory bacteria response and mitigated acute kidney injury. Copyright 2020, Mary Ann Liebert, Inc., publishers.