Chebulic acid prevents hepatic fibrosis induced by advanced glycation end-products in LX-2 cell by modulating Nrf2 translocation via ERK pathway

Koo, Yun Chang; Pyo, Min Cheol; Nam, Mi Hyun; Hong, Chung Oui; Yang, Sung Yong; Lee, Kwang Won

doi:10.1016/j.tiv.2016.03.013

Cited by 24 publications

(19 citation statements)

References 39 publications

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“…In addition, AGEs are produced at a high frequency in a hyperglycemic state and are considered to be associated with the pathogenesis of NASH 35 . Among AGEs, GA-AGEs influence hepatocytes and hepatic stellate cells (HSCs) intra- and extracellularly 19 – 22 , 36 , 37 . We hypothesized that GA-AGEs are one of the “multiple parallel hits”.…”

Section: Discussionmentioning

confidence: 99%

“…Regarding extracellular GA-AGEs, apoptotic cell death is induced via the receptor for AGE (RAGE) interaction, for example, in β cells of the pancreas 49 . Extracellular AGEs are involved not only in apoptosis, but also in the activation of HSCs, which participate in hepatic fibrosis 36 , 37 , 50 , 51 . Therefore, we speculate that the accumulation of GA-AGEs causes hepatic necrosis in the early phase of NASH, the leakage of GA-AGEs from necrotic cells induces apoptosis via RAGE in caspase-3 intact cells, and HSCs are activated in the progressive stages of NASH.…”

Section: Discussionmentioning

confidence: 99%

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Impact of intracellular glyceraldehyde-derived advanced glycation end-products on human hepatocyte cell death

Sakasai-Sakai

Takata

Takino

et al. 2017

Sci Rep

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Hepatocyte cell death is a key feature of nonalcoholic steatohepatitis (NASH); however, the pathogenesis of NASH currently remains unclear. We aimed to investigate the effects of intracellular glyceraldehyde (GA)-derived advanced glycation end-products (GA-AGEs) on human hepatocyte cell death. The accumulation of intracellular GA-AGEs has been associated with the induction of DNA damage and hepatocyte necrotic cell death. Among intracellular GA-AGEs, caspase-3 has been identified as a GA-AGE-modified protein with abrogated protein function. Furthermore, the activation of caspase-3 and induction of hepatocyte apoptosis by camptothecin, a DNA-damaging agent, was suppressed by a treatment with GA. These results suggest the inhibitory effects of GA-AGE-modified caspase-3 on the induction of DNA-damage-induced apoptosis, which is associated with hepatocyte necrosis. Therefore, the suppression of necrosis, the inflammatory form of cell death, by the accumulation of GA-AGEs and GA-AGE-modified caspase-3 may represent a novel therapeutic target for the pathogenesis of NASH.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Impact of intracellular glyceraldehyde-derived advanced glycation end-products on human hepatocyte cell death

Sakasai-Sakai

Takata

Takino

et al. 2017

Sci Rep

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“…Hyperglycemia has been reported to be associated with multiple factors that can result in oxidative stress, one of which is involved in AGEs [26]. It has been clarified that AGEs-induced ROS inhibits the translocation of Nrf2 into nucleus, which causes upregulation of antioxidant protein production [27]. In the development of diabetic nephropathy (DN), AGEs induces expressions of fibronectin and TGF-β1, which is attenuated by sirt1 through activating the Nrf2/ARE pathway [28].…”

Section: Discussionmentioning

confidence: 99%

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

et al. 2016

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Hyperglycemia, as well as diabetes mellitus, has been shown to trigger cardiac cell apoptosis. We have previously demonstrated that myricitrin prevents endothelial cell apoptosis. However, whether myricitrin can attenuate H9c2 cell apoptosis remains unknown. In this study, we established an experiment model in H9c2 cells exposed to high glucose. We tested the hypothesis that myricitrin may inhibit high glucose (HG)-induced cardiac cell apoptosis as determined by TUNEL staining. Furthermore, myricitrin promoted antioxidative enzyme production, suppressed high glucose-induced reactive oxygen species (ROS) production and decreased mitochondrial membrane potential (MMP) in H9c2 cells. This agent significantly inhibited apoptotic protein expression, activated Akt and facilitated the transcription of NF-E2-related factor 2 (Nrf2)-mediated protein (heme oxygenase-1 (HO-1) and quinone oxidoreductase 1 (NQO-1) expression as determined by Western blotting. Significantly, an Akt inhibitor (LY294002) or HO-1 inhibitor (ZnPP) not only inhibited myricitrin-induced HO-1/NQO-1 upregulation but also alleviated its anti-apoptotic effects. In summary, these observations demonstrate that myricitrin activates Nrf2-mediated anti-oxidant signaling and attenuates H9c2 cell apoptosis induced by high glucose via activation of Akt signaling.

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“…[16][17][18] In our recent study, total expression of Nrf2 protein was significantly induced by glyceraldehyde-bovine serum albumin (BSA) conjugate. 19) This is to our knowledge the first study of the involvement of Nrf2 in induction of antioxidant and phase II defense gene expression by Glc-WPC in HepG2 cells of human origin. Thus, the purpose of this study is to investigate whether the Nrf2 target proteins HO-1, NQO1 and GCL are induced by Glc-WPC treatment via the expression of Nrf2, and the link between MAPK signaling pathways and Nrf2-dependent regulation in HepG2 cells.…”

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confidence: 81%

Protective Effects of Maillard Reaction Products of Whey Protein Concentrate against Oxidative Stress through an Nrf2-Dependent Pathway in HepG2 Cells

Pyo

Yang

Chun

et al. 2016

Biological & Pharmaceutical Bulletin

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Whey protein concentrate (WPC), which contains α-lactalbumin and β-lactoglobulin, is utilized widely in the food industry. The Maillard reaction is a complex reaction that produces Maillard reaction products (MRPs), which are associated with the formation of antioxidant compounds. In this study, the hepatoprotection activity of MRPs of WPC against oxidative stress through the nuclear factor-E2-related factor 2 (Nrf2)-dependent antioxidant pathway in HepG2 cells was examined. Glucose-whey protein concentrate conjugate

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Chebulic acid prevents hepatic fibrosis induced by advanced glycation end-products in LX-2 cell by modulating Nrf2 translocation via ERK pathway

Cited by 24 publications

References 39 publications

Impact of intracellular glyceraldehyde-derived advanced glycation end-products on human hepatocyte cell death

Impact of intracellular glyceraldehyde-derived advanced glycation end-products on human hepatocyte cell death

Myricitrin Attenuates High Glucose-Induced Apoptosis through Activating Akt-Nrf2 Signaling in H9c2 Cardiomyocytes

Protective Effects of Maillard Reaction Products of Whey Protein Concentrate against Oxidative Stress through an Nrf2-Dependent Pathway in HepG2 Cells

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