Enzymatic Synthesis of a Novel Kaempferol-3-O-β-d-glucopyranosyl-(1→4)-O-α-d-glucopyranoside Using Cyclodextrin Glucanotransferase and Its Inhibitory Effects on Aldose Reductase, Inflammation, and Oxidative Stress

2017 ◽  
Vol 65 (13) ◽  
pp. 2760-2767 ◽  
Author(s):  
Woo-Jae Choung ◽  
Seung Hwan Hwang ◽  
Dam-Seul Ko ◽  
Set Byeol Kim ◽  
Seo Hyun Kim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aldose Reductase ◽  
Enzymatic Synthesis ◽  
Cyclodextrin Glucanotransferase ◽  
Inhibitory Effects ◽  
And Oxidative Stress

scholarly journals Enzymatic Synthesis and Anti-Allergic Activities of Curcumin Oligosaccharides

2010 ◽  
Vol 3 ◽  
pp. BCI.S2768 ◽  
Author(s):  
Kei Shimoda ◽  
Hiroki Hamada
Keyword(s):  
Mast Cells ◽  
Histamine Release ◽  
Enzymatic Synthesis ◽  
Antibody Formation ◽  
Cyclodextrin Glucanotransferase ◽  
Enzymatic Method ◽  
Inhibitory Effects ◽  
Peritoneal Mast Cells ◽  
Rat Peritoneal Mast Cells ◽  
Suppressive Action

Curcumin 4‘- O-glucooligosaccharides were synthesized by a two step-enzymatic method using almond β-glucosidase and cyclodextrin glucanotransferase (CGTase). Curcumin was glucosylated to curcumin 4‘- O-β-D-glucopyranoside by almond β-glucosidase in 19% yield. Curcumin 4‘- O-β-D-glucopyranoside was converted into curcumin 4‘- O-β-glucooligosaccharides, i.e. 4‘- O-β-maltoside (51%) and 4‘- O-β-maltotrioside (25%), by further CGTase-catalyzed glycosylation. Curcumin 4‘- O-β-glycosides showed suppressive action on IgE antibody formation and inhibitory effects on histamine release from rat peritoneal mast cells.

Berberine inhibits aldose reductase and oxidative stress in rat mesangial cells cultured under high glucose

2008 ◽  
Vol 475 (2) ◽  
pp. 128-134 ◽  
Author(s):  
Weihua Liu ◽  
Peiqinq Liu ◽  
Sha Tao ◽  
Yanhui Deng ◽  
Xuejuan Li ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Aldose Reductase ◽  
High Glucose ◽  
Mesangial Cells ◽  
And Oxidative Stress ◽  
Cells Cultured

scholarly journals Dihydromyricetin Attenuates Palmitate Acid-Induced Oxidative Stress by promoting Autophagy via SIRT3-ATG4B Signaling in Hepatocytes

2021 ◽  
Author(s):  
Mantian Mi ◽  
Li Huang ◽  
Xianglong Zeng ◽  
Bo Li ◽  
Cong Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepg2 Cells ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Inhibitory Effects ◽  
Potential Therapeutic Target ◽  
Mitochondrial Ros ◽  
Intracellular Ros ◽  
Protein Expressions ◽  
And Oxidative Stress

Abstract Background Oxidative stress in hepatocytes was an important pathogenesis of nonalcoholic steatohepatitis (NASH). Autophagy was a cellular process that can remove damaged organelles under oxidative stress, and thus presented a potential therapeutic target against NASH. The aim of this work was to investigate whether autophagy participated the protective effects of dihydromyricetin (DHM) on palmitic acid (PA)-induced oxidative stress in hepatocytes and the underlying mechanism. Methods HepG2 cells were pretreated with DHM (20 µM) for 2 h, followed by PA (0.2 mM) treatment for 16 h. The oxidative stress was assessed by the quantification of intracellular reactive oxygen species (ROS), mitochondrial ROS (mtROS), mitochondrial membrane potential (MMP) and mitochondrial ultrastructural analyses. The protein expressions of SIRT3, LC3I/II, P62 and ATG4B, as well as the acetylation of AGT4B were determined by western blotting using HepG2 and HepG2/ ATG4B+/− cells with heterozygous knockout of ATG4B. Results Exposure to PA resulted in increased intracellular ROS and mtROS, decreased MMP and aggravated mitochondrial injury in HepG2 cells, which were notably attenuated by DHM treatment. DHM-induced inhibition of oxidative stress was associated with the induction of autophagy, characterized by upregulated ATG4B and LC3 II as well as downregulated P62 levels. Furthermore, the inhibitory effects of DHM on PA-induced autophagy arrest and oxidative stress were eliminated when pretreated with a SIRT3 inhibitor 3-TYP or conducted in HepG2/ATG4B+/− cells, suggesting that SIRT3 and ATG4B were involved in DHM-induced benefits. Moreover, DHM treatment increased the protein expression of SIRT3 and SIRT3-dependent deacetylation of ATG4B in HepG2 cells. Conclusion Our results demonstrated that DHM attenuated PA-induced oxidative stress in hepatocytes through induction of autophagy, which was mediated through the increased expression of SIRT3 and SIRT3-mediated ATG4B deacetylation following DHM treatment.

scholarly journals Inhibitory effects of Anadenanthera colubrina (Vell.) Brenan stem bark extract on -glucosidase activity and oxidative stress

2020 ◽  
Vol 14 (11) ◽  
pp. 583-592
Author(s):  
Joaquim da Costa Odelio ◽  
dos Santos Barbosa Robson ◽  
Mendes Soares Ilsamar ◽  
Euripedes de Souza Eber ◽  
Fernando A. Gellen Luís ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Bark ◽  
Bark Extract ◽  
Inhibitory Effects ◽  
Glucosidase Activity ◽  
Stem Bark Extract ◽  
And Oxidative Stress

scholarly journals Activation of TGR5 Partially Alleviates High Glucose-Induced Cardiomyocyte Injury by Inhibition of Inflammatory Responses and Oxidative Stress

2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Li Deng ◽  
Xuxin Chen ◽  
Yi Zhong ◽  
Xing Wen ◽  
Ying Cai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Cardiomyopathy ◽  
High Glucose ◽  
Inflammatory Responses ◽  
Inhibitory Effects ◽  
Rt Pcr ◽  
Hoechst 33342 ◽  
Selective Agonist ◽  
Cardioprotective Effects ◽  
And Oxidative Stress

High glucose- (HG-) induced cardiomyocyte injury is the leading cause of diabetic cardiomyopathy, which is associated with the induction of inflammatory responses and oxidative stress. TGR5 plays an important role in the regulation of glucose metabolism. However, whether TGR5 has cardioprotective effects against HG-induced cardiomyocyte injury is unknown. Neonatal mouse cardiomyocytes were isolated and incubated in a HG medium. Protein and mRNA expression was detected by western blotting and RT-PCR, respectively. Cell apoptosis was determined by Hoechst 33342 staining and flow cytometry. After treatment of cells with HG, TGR5-selective agonist INT-777 reduced the increase in expression of proinflammatory cytokines and NF-κB, whereas pretreatment of cells with TGR5 shRNA significantly reduced the inhibitory effects of INT-777. We also found that INT-777 increased the protein expression of Nrf2 and HO-1. In the presence of TGR5 shRNA, the expression of Nrf2 and HO-1 was reduced, indicating that TGR5 may exert an antioxidant effect partially through the Nrf2/HO-1 pathway. Furthermore, INT-777 treatment inhibited HG-induced ROS production and apoptosis that were attenuated in the presence of TGR5 shRNA or ZnPP (HO-1 inhibitor). Activation of TGR5 has cardioprotective effects against HG-induced cardiomyocyte injury and could be a pharmacological target for the treatment of diabetic cardiomyopathy.

Inhibitory effects ofCynodon dactylonL. on inflammation and oxidative stress in adjuvant treated rats

2009 ◽  
Vol 00 (00) ◽  
pp. 090706062732049-7
Author(s):  
G. Sindhu ◽  
M. Ratheesh ◽  
G. L. Shyni ◽  
A. Helen
Keyword(s):  
Oxidative Stress ◽  
Inhibitory Effects ◽  
And Oxidative Stress
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