ArticleLaboratory investigation; a journal of technical methods and pathology2012
Curcumin eliminates the inhibitory effect of advanced glycation end-products (AGEs) on gene expression of AGE receptor-1 in hepatic stellate cells in vitro.
Article in Laboratory investigation; a journal of technical methods and pathology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 50 citations in OpenAlex.
- Curcumin in Fibrosis Treatment: A Review.Drug design, development and therapy · 2026Review
- Curcumin Modulates NOX Gene Expression and ROS Production via P-Smad3C in TGF-β-Activated Hepatic Stellate Cells.Iranian biomedical journal · 2024Article
- AGER1 deficiency-triggered ferroptosis drives fibrosis progression in nonalcoholic steatohepatitis with type 2 diabetes mellitus.Cell death discovery · 2023Article
- Investigating Polyphenol Nanoformulations for Therapeutic Targets against Diabetes Mellitus.Evidence-based complementary and alternative medicine : eCAM · 2022Review
- Advanced Glycation End Products in the Skin: Molecular Mechanisms, Methods of Measurement, and Inhibitory Pathways.Frontiers in medicine · 2022Review
- Iron and Advanced Glycation End Products: Emerging Role of Iron in Androgen Deficiency in Obesity.Antioxidants (Basel, Switzerland) · 2020Article
- Curcumin, Alone or in Combination with Aminoguanidine, Increases Antioxidant Defenses and Glycation Product Detoxification in Streptozotocin-Diabetic Rats: A Therapeutic Strategy to Mitigate Glycoxidative Stress.Oxidative medicine and cellular longevity · 2020Article
- The role of curcumin in liver diseases.Archives of medical science : AMS · 2019Article
- Advanced Glycated End Products Alter Neutrophil Effect on Regulation of CDInflammation · 2019Article
- Effects and Underlying Mechanisms of Bioactive Compounds on Type 2 Diabetes Mellitus and Alzheimer's Disease.Oxidative medicine and cellular longevity · 2019Review
- GanDouLing combined with Penicillamine improves cerebrovascular injury via PERK/eIF2α/CHOP endoplasmic reticulum stress pathway in the mouse model of Wilson's disease.Bioscience reports · 2018Article
- Perilipin 5 and liver fatty acid binding protein function to restore quiescence in mouse hepatic stellate cells.Journal of lipid research · 2018Article
- Role of advanced glycation end products in mobility and considerations in possible dietary and nutritional intervention strategies.Nutrition & metabolism · 2018Review
- The Role of Glyoxalase-I (Glo-I), Advanced Glycation Endproducts (AGEs), and Their Receptor (RAGE) in Chronic Liver Disease and Hepatocellular Carcinoma (HCC).International journal of molecular sciences · 2017Review
- Effect of medicated serum ofSaudi pharmaceutical journal : SPJ : the official publication of the Saudi Pharmaceutical Society · 2017Article
- Huang Gan Formula Eliminates the Oxidative Stress Effects of Advanced Oxidation Protein Products on the Divergent Regulation of the Expression of AGEs Receptors via the JAK2/STAT3 Pathway.Evidence-based complementary and alternative medicine : eCAM · 2017Article
- Antifibrotic effect of total flavonoids of Astmgali Radix on dimethylnitrosamine-induced liver cirrhosis in rats.Chinese journal of integrative medicine · 2017Article
- Perilipin 5 restores the formation of lipid droplets in activated hepatic stellate cells and inhibits their activation.Laboratory investigation; a journal of technical methods and pathology · 2016Article
- Curcumin targets multiple pathways to halt hepatic stellate cell activation: updated mechanisms in vitro and in vivo.Digestive diseases and sciences · 2015Review
- Role of receptor for advanced glycation end products (RAGE) in liver disease.European journal of medical research · 2015Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Diabetes is featured by hyperglycemia, which facilitates the formation of advanced glycation end-products (AGEs). AGEs are a causal factor in development of diabetic complications. AGE receptor-1 (AGE-R1) is responsible for detoxification and clearance of AGEs. Type 2 diabetes mellitus is commonly accompanied by non-alcoholic steatohepatitis, which could cause hepatic fibrosis. Little attention has been paid to effects of AGEs on hepatic fibrogenesis. Curcumin, a phytochemical from turmeric, has been reported to inhibit the activation of hepatic stellate cells (HSCs), the major effectors during hepatic fibrogenesis, and to protect against hepatic fibrogenesis in vitro and in vivo. The current study was designed to evaluate the effects of AGEs on inducing HSC activation, to assess the role of curcumin in diminishing the AGE effects, and to explore the underlying mechanisms. Our results showed that AGEs stimulated HSC activation by inducing cell proliferation and expression of genes relevant to HSC activation, which were abrogated by curcumin. Curcumin induced gene expression of AGE-R1 in passaged HSCs, which might facilitate the attenuation of the stimulatory effects of AGEs on the activation of HSCs. Further experiments revealed that curcumin inhibited the activity of extracellular signal-regulated kinase (ERK), and induced gene expression and the activity of peroxisome proliferator-activated receptor-gamma (PPARγ), leading to the induction of the AGE-R1 gene expression. In summary, AGEs stimulated HSC activation. Curcumin eliminated the AGE effects at least partially by inducing the AGE-R1 gene expression. The process was mediated by inhibiting ERK activity, inducing gene expression of PPARγ and stimulating its transactivity.
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