2016
DOI: 10.1016/j.clnu.2016.03.002
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Chlorogenic acid protects against liver fibrosis in vivo and in vitro through inhibition of oxidative stress

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Cited by 157 publications
(122 citation statements)
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“…Also, our study showed that treatment with the ROS inhibitor recovered the activation of TGF‐β/Smad signaling in cultured L02 cells, indicating that ROS production in response to AOPP treatment may provide a sustaining regulator and thereby stimulated TGF‐β/Smad signaling and trigger hepatocyte EMT. Besides the intracellular TGF‐β/Smad pathway, previous studies have confirmed that mitogen‐activated protein kinase (MAPK) and nuclear factor kappa B (NF‐κB)‐mediated signaling are also required for oxidative stress‐dependent liver fibrosis (Acquaviva et al, ; Cai et al, ; Shi et al, ). For these reasons, we plan to perform future studies on the roles of MAPK and NF‐κB signaling pathways in AOPP‐mediated hepatocyte EMT.…”
Section: Discussionmentioning
confidence: 99%
“…Also, our study showed that treatment with the ROS inhibitor recovered the activation of TGF‐β/Smad signaling in cultured L02 cells, indicating that ROS production in response to AOPP treatment may provide a sustaining regulator and thereby stimulated TGF‐β/Smad signaling and trigger hepatocyte EMT. Besides the intracellular TGF‐β/Smad pathway, previous studies have confirmed that mitogen‐activated protein kinase (MAPK) and nuclear factor kappa B (NF‐κB)‐mediated signaling are also required for oxidative stress‐dependent liver fibrosis (Acquaviva et al, ; Cai et al, ; Shi et al, ). For these reasons, we plan to perform future studies on the roles of MAPK and NF‐κB signaling pathways in AOPP‐mediated hepatocyte EMT.…”
Section: Discussionmentioning
confidence: 99%
“…This makes the native Huagalina potato a health-promoting agent as CGA acid and caffeic acid have been reported as inhibitors of carcinogenesis (Huang et al, 1998, Sancho and Pastore, 2012, Serafim et al, 2015, reducing obesity (Cho et al, 2010) hypotensive activity, providing cardiovascular protection (Susuki et al, 2002;Jiang et al, 2016). Shi et al (2016) showed that a new mechanism of CGA acid mediated in the protection of liver fibrosis (a stage before cirrhosis), inhibits oxidative stress and increases antioxidant defense and could become a promising new treatment for liver disease. Mikami and Yamazawa (2015) studied the protective effects of CGA acid on neuronal cell death induced by glutamate because the release of glutamate during cerebral ischemia triggers the death of neurons, suggesting that this polyphenol protects neurons from glutamate neurotoxicity by controlling calcium ion entry through glutamate receptors.…”
Section: Resultsmentioning
confidence: 99%
“…In addition, CGA could inhibit lipopolysaccharide (LPS)-induced microglial activation and improve the survival of dopaminergic neurons (21). CGA could also reduce carbon tetrachloride-induced liver fibrosis in rats through inhibition of the Toll-like receptor 4 signaling pathway (22,23) and through the suppression of oxidative stress in liver and hepatic stellate cells (24).…”
mentioning
confidence: 99%