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Tangshen Formula Alleviates Hepatic Steatosis by Inducing Autophagy Through the AMPK/SIRT1 Pathway
Conclusion In conclusion, the present study demonstrated that autophagy was involved in relieving the effects of TSF against NAFLD, which were mediated by the AMPK/SIRT1 pathway (Figure 7D). These findings may improve our current understanding of the role of TSF in treating hepatic steatosis and provide an experimental basis for the clinical application of TSF in NAFLD and its related metabolic syndrome. Ethics Statement This study was carried out in accordance with the recommendations in the Guide for the Care and Use of Laboratory Animals of the National Institutes of Health. The protocol was approved by the Ethics Co...
Source: Frontiers in Physiology - April 25, 2019 Category: Physiology Source Type: research

Resveratrol Promotes Diabetic Wound Healing via SIRT1-FOXO1-c-Myc Signaling Pathway-Mediated Angiogenesis
Conclusion: Our findings indicate that the positive role of RES in diabetic wound healing via its SIRT1-dependent endothelial protection and pro-angiogenic effects involves the inhibition of FOXO1 and the de-repression of c-Myc expression. Introduction Diabetes mellitus is a metabolic disease with an increasing incidence worldwide (Zimmet et al., 2014). The disease often leads to the development of serious complications such as microangiopathy, mainly including retinopathy, nephropathy, neuropathy, and diabetic non-healing skin ulcers (Zheng et al., 2018). Diabetic non-healing skin ulcers such as foot ulcers are ca...
Source: Frontiers in Pharmacology - April 23, 2019 Category: Drugs & Pharmacology Source Type: research

TonEBP Suppresses the HO-1 Gene by Blocking Recruitment of Nrf2 to Its Promoter
Discussion Dynamic changes in the functional phenotype of macrophages are associated with pathogenesis of inflammatory diseases (5–7). TonEBP primes macrophages toward an M1 phenotype, which has pro-inflammatory properties. TonEBP does this by promoting expression of pro-inflammatory genes via interaction with NF-κB (36) and by binding directly to the promoter (37, 64). In addition, TonEBP suppresses expression of the anti-inflammatory cytokine IL-10 by limiting chromatin access to the promoter (37). The pro-inflammatory function of TonEBP suggests that inhibiting its expression or activation could suppres...
Source: Frontiers in Immunology - April 17, 2019 Category: Allergy & Immunology Source Type: research

Pancreatic {beta}-cells detoxify H2O2 through the peroxiredoxin/thioredoxin antioxidant system Metabolism
Oxidative stress is thought to promote pancreatic β-cell dysfunction and contribute to both type 1 and type 2 diabetes. Reactive oxygen species (ROS), such as superoxide and hydrogen peroxide, are mediators of oxidative stress that arise largely from electron leakage during oxidative phosphorylation. Reports that β-cells express low levels of antioxidant enzymes, including catalase and GSH peroxidases, have supported a model in which β-cells are ill-equipped to detoxify ROS. This hypothesis seems at odds with the essential role of β-cells in the control of metabolic homeostasis and organismal survival through exquisite...
Source: Journal of Biological Chemistry - March 28, 2019 Category: Chemistry Authors: Jennifer S. Stancill, Katarzyna A. Broniowska, Bryndon J. Oleson, Aaron Naatz, John A. Corbett Tags: Signal Transduction Source Type: research

Quercetin and Allopurinol Reduce Liver Thioredoxin‐Interacting Protein to Improve Inflammation and Lipid Accumulation in Diabetic Rats
Conclusions and ImplicationsThese results demonstrate that hepatic TXNIP inhibition by quercetin and allopurinol contributes to the improvement of liver inflammation and lipid accumulation under hyperglycemia condition. Therefore, quercetin and allopurinol targeting hepatic TXNIP may have therapeutic application to prevent type 1 diabetes‐associated NAFLD.
Source: British Journal of Pharmacology - May 3, 2013 Category: Drugs & Pharmacology Authors: Wei Wang, Chuang Wang, Xiao‐Qin Ding, Ying Pan, Ting‐Ting Gu, Ming‐Xing Wang, Yang‐Liu Liu, Fu‐Meng Wang, Shui‐Juan Wang, Ling‐Dong Kong Tags: Research Paper Source Type: research