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Naringenin Produces Neuroprotection Against LPS-Induced Dopamine Neurotoxicity via the Inhibition of Microglial NLRP3 Inflammasome Activation
Conclusions: This study demonstrated that NAR targeted microglial NLRP3 inflammasome to protect DA neurons against LPS-induced neurotoxicity. These findings suggest NAR might hold a promising therapeutic potential for PD. Background Parkinson's disease (PD) is the second most prevalent central nervous system (CNS) degenerative disease. It is characterized by slow and progressive loss of dopamine (DA) neurons in the midbrain substantia nigra (SN) with the accumulation of α-synuclein in Lewy bodies and neuritis (1). Although the etiology of PD remains unclear, amounts of studies have suggested that ne...
Source: Frontiers in Immunology - April 30, 2019 Category: Allergy & Immunology Source Type: research

FKN Facilitates HK-2 Cell EMT and Tubulointerstitial Lesions via the Wnt/ β-Catenin Pathway in a Murine Model of Lupus Nephritis
In this study, we therefore examined whether FKN could stimulate the process of EMT, NF-kB, TGFβ, CCL22, F4/80, inflammation, and tubulointerstitial fibrosis in a murine model of LN. We also determined whether FKN was involved in the EMT process of Wnt/β-catenin-expressing HK-2 cells. Mechanistically, we ascertained, for the first time, whether FKN up-regulated EMT-related gene signatures (e.g., vimentin, α-SMA), and hence, renal tubulointerstitial fibrogenesis, and the role of the Wnt/β-catenin signaling pathway in this process. Materials and Methods Cell Culture, Stable Infection, and Gr...
Source: Frontiers in Immunology - April 29, 2019 Category: Allergy & Immunology Source Type: research

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

lncRNA ZEB1-AS1 Mediates Oxidative Low-Density Lipoprotein-Mediated Endothelial Cells Injury by Post-transcriptional Stabilization of NOD2
Conclusion We report the discovery that ZEB1-AS1 functionally participates in ox-LDL-induced ECs injury via LRPPRC-mediated stabilization of NOD2. Uncovering the precise role of ZEB1-AS1/LRPPRC/NOD2 pathway in the progression of ox-LDL-induced ECs death and AS will not only increase our knowledge of ox-LDL-induced AS, but also enable the development of novel therapeutic strategies to overcome oxidation product-induced diseases. Author Contributions XX and CL designed and mainly did the study. CM, ZD, and YD helped and did the study. Conflict of Interest Statement The authors declare that the research was conducted in ...
Source: Frontiers in Pharmacology - April 15, 2019 Category: Drugs & Pharmacology Source Type: research

Mitochondrial respiratory chain deficiency inhibits lysosomal hydrolysis.
Abstract Mitochondria are key organelles for cellular metabolism, and regulate several processes including cell death and macroautophagy/autophagy. Here, we show that mitochondrial respiratory chain (RC) deficiency deactivates AMP-activated protein kinase (AMPK, a key regulator of energy homeostasis) signaling in tissue and in cultured cells. The deactivation of AMPK in RC-deficiency is due to increased expression of the AMPK-inhibiting protein FLCN (folliculin). AMPK is found to be necessary for basal lysosomal function, and AMPK deactivation in RC-deficiency inhibits lysosomal function by decreasing the activity...
Source: Autophagy - March 26, 2019 Category: Cytology Authors: Fernandez-Mosquera L, Yambire KF, Couto R, Pereyra L, Pabis K, Ponsford AH, Diogo CV, Stagi M, Milosevic I, Raimundo N Tags: Autophagy Source Type: research

Coagulation factor XI induces Ca2+ response and accelerates cell migration in vascular smooth muscle cells via proteinase-activated receptor 1.
In conclusion, FXIa mainly elicits Ca2+ signal via the PAR1/CaV1.2-mediated Ca2+ influx and accelerates the migration in vascular smooth muscle cells. The present study provides the first evidence that FXIa exerts a direct cellular effect on vascular smooth muscle. PMID: 30566391 [PubMed - as supplied by publisher]
Source: Am J Physiol Cell Ph... - December 19, 2018 Category: Cytology Authors: Liu W, Hashimoto T, Yamashita T, Hirano K Tags: Am J Physiol Cell Physiol Source Type: research

TGF- β1 acts as mediator in fluoride-induced autophagy in the mouse osteoblast cells.
TGF-β1 acts as mediator in fluoride-induced autophagy in the mouse osteoblast cells. Food Chem Toxicol. 2018 Mar 02;: Authors: Zhao Y, Li Y, Gao Y, Yuan M, Manthari RK, Wang J, Wang J Abstract It is well known that excess fluoride intake can result in fluorosis, which is a serious public health problem. TGF-β1 affects a wide variety of cellular activities and plays an important role in fluorosis. Recent literature proved that fluoride induces autophagy, however, the mechanism is still unclear, and the role of TGF-β1 in the fluoride-induced autophagy should be further illustrated. Therefore, in this...
Source: Food and Chemical Toxicology - March 2, 2018 Category: Food Science Authors: Zhao Y, Li Y, Gao Y, Yuan M, Manthari RK, Wang J, Wang J Tags: Food Chem Toxicol Source Type: research

Analysis of the Role of Insulin Signaling in Bone Turnover Induced by Fluoride.
In conclusion, insulin played the important role in bone lesion induced by excessive amount of fluoride through mediating InR receptor signaling, and IGF1 signaling probably exerted action on bone turnover caused by overdose of fluoride. PMID: 26521058 [PubMed - as supplied by publisher]
Source: Biological Trace Element Research - October 31, 2015 Category: Biology Authors: Liu Q, Liu H, Yu X, Wang Y, Yang C, Xu H Tags: Biol Trace Elem Res Source Type: research

Wnt-RhoA Signaling Pathways in Fluoride-Treated Ameloblast-Lineage Cells
This study examined the effect of sodium fluoride (NaF) on the Wnt and RhoA signaling pathways in murine ameloblast-lineage cells (ALCs) to better understand the developmental mechanisms of dental fluorosis. Wnt and Rho pathway activities were investigated when ALCs were treated with 1.5 mM NaF, dickkopf-related protein-1 (Dkk-1), secreted frizzled related-protein-2 (sFRP-2), β-catenin siRNA dominant negative RhoA (RhoADN) plasmid and Y-27632. Wnt pathway activity was investigated via RT-PCR, Western blot and Topflash luciferase assay. The activity of the RhoA pathway was analyzed via Rho pull-down assay and immunoprecipi...
Source: Cells Tissues Organs - November 14, 2014 Category: Cytology Source Type: research

A role for PERK in the mechanism underlying fluoride-induced bone turnover.
In conclusion these findings underscore the importance of PERK in modulating fluoride induced bone formation and bone resorption. Understanding the link between PERK and bone turnover could probe into the mechanism underlying different bone lesion of skeletal fluorosis. PMID: 25132241 [PubMed - as supplied by publisher]
Source: Toxicology - August 15, 2014 Category: Toxicology Authors: Sun F, Li X, Yang C, Lv P, Li G, Xu H Tags: Toxicology Source Type: research

Effect of siRNA PERK on Fluoride-Induced Osteoblastic Differentiation in OS732 Cells.
This study proved that the mechanism underlying fluoride induced osteoblastic and osteoclastic differentiation possible was due to activation of ALP and RANKL mediated by PERK in OS732 cells. PMID: 24838929 [PubMed - as supplied by publisher]
Source: Biological Trace Element Research - May 18, 2014 Category: Biology Authors: Lü P, Li X, Ruan L, Xu H, Liu Q Tags: Biol Trace Elem Res Source Type: research

Role of Unfolded Protein Response in Affecting Osteoblast Differentiation Induced by Fluoride.
In conclusion, fluoride had dual effect on osteogenic action. The UPR possibly involved in the mechanism of osteoblasts differentiation induced by fluoride. PMID: 24522478 [PubMed - as supplied by publisher]
Source: Biological Trace Element Research - February 13, 2014 Category: Biology Authors: Li XN, Lv P, Sun Z, Li GS, Xu H Tags: Biol Trace Elem Res Source Type: research

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