Protective effects of neohesperidin dihydrochalcone against carbon tetrachloride-induced oxidative damage in vivo and in vitro

Hu, Lihua; Li, Lingrui; Xu, Dan; Xia, Xiaomin; Pi, Ruxian; Xu, Duo; Wang, Wenchao; Du, Hongyin; Song, Erqun; Song, Yang

doi:10.1016/j.cbi.2014.02.003

Cited by 39 publications

(42 citation statements)

References 46 publications

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“…Elevated ROS are an important indicator of oxidative stress and their generation contributed to the accumulation of lipid oxidation products, leading to cell necrosis and liver injury (14). Inflammation is another important pathological mechanism propagating TAA-induced liver injury (15).…”

Section: Discussionmentioning

confidence: 99%

Inhibition of RKIP aggravates thioacetamide‑induced acute liver failure in mice

et al. 2018

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Accumulating evidence has indicated that Raf kinase inhibitor protein (RKIP) is involved in several intracellular signaling pathways; its abnormal expression is associated with tumor progression and metastasis in several human neoplasms. However, the role of RKIP in acute liver injury has remained elusive. In the present study, acute liver failure was induced by thioacetamide in mice, and locostatin was used to interfere with RKIP expression. It was found that RKIP expression was significantly inhibited by locostatin. Down-regulation of RKIP expression resulted in severe liver injury and extensive release of alanine aminotransferase and aspartate aminotransferase. In addition, reduced RKIP expression significantly enhanced the levels of reactive oxygen species and the content of pro-inflammatory factors such as tumor necrosis factor-α as well as interleukin-6 and −1β, and decreased the levels of nuclear factor E2-related factor-2 and heme oxygenase-1. Furthermore, down-regulation of RKIP promoted the activation of the nuclear factor-κB and extracellular signal-regulated kinase signaling pathways. In conclusion, the present study indicates an inverse correlation between RKIP level and the degree of hepatic injury, that is, a decrease in RKIP expression may exacerbate acute liver failure.

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Section: Discussionmentioning

confidence: 99%

Inhibition of RKIP aggravates thioacetamide‑induced acute liver failure in mice

et al. 2018

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“…CCl 4 is a highly hepatotoxic chemical that is widely used in experimental models to induce hepatocellular injury, which mimics human hepatotoxicity and to screen hepatoprotective drugs (Al‐Sayed & Abdel‐Daim, ; Hu et al, ). The highly reactive trichloromethyl radicals (CCl 3 .…”

Section: Discussionmentioning

confidence: 99%

“…Liver injury is caused by excessive exposure to drugs and toxins, which overwhelm the detoxification power of the liver leading to enzyme leakage, lipid peroxidation, and oxidative stress (Al‐Sayed et al, ). Inflammation is also crucial pathological mechanism in producing hepatic injury (Hu et al, ). Chronic liver injury may develop into several liver diseases, including fibrosis, cirrhosis, and even fatal hepatocellular carcinoma (Al‐Sayed et al, ).…”

Section: Introductionmentioning

confidence: 99%

Hepatoprotective activity of praecoxin A isolated from Melaleuca ericifolia against carbon tetrachloride‐induced hepatotoxicity in mice. Impact on oxidative stress, inflammation, and apoptosis

Al‐Sayed

Abdel‐Daim

Khattab

2018

Phytotherapy Research

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The hepatoprotective activity of praecoxin A, an ellagitannin from Melaleuca ericifolia, was determined against CCl 4 -induced toxicity in mice. Praecoxin A was administered (25, 50, and 100 mg/kg) for 5 days followed by CCl 4 . Praecoxin A markedly ameliorated the CCl 4 -induced increase in AST (by 19, 52, and 56%), ALP (22, 45, and 48%), ALT (11, 47, and 54%), total bilirubin (14, 27, and 28%), and MDA (26, 44, and 51%) at the tested doses, respectively, as compared with CCl 4 group. It was evident that praecoxin A significantly (p < 0.001) increased the antioxidant parameters GSH (45, 99, and 137%) and SOD (61, 129, and 159%). Histological findings revealed a marked amelioration of hepatocyte degeneration, necrosis, inflammatory cell infiltration, and hemorrhage in the groups treated with praecoxin A. COX-2 and caspase-3 hepatic expressions were significantly downregulated (p < 0.001) in praecoxin A-treated groups (up to 57, 83, and 93% for COX-2 and by 30, 82, and 99% for caspase-3). These findings suggest that praecoxin A exerts a beneficial effect against oxidative stress by reducing lipid peroxidation, enhancing the antioxidant defense status, and protecting against the histopathological changes induced by CCl 4 . This study highlights a promising natural hepatoprotective candidate derived from M. ericifolia that might be an alternative to silymarin.

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“…All these changes are expected consequences of treatment with CCl 4 which induces elevation of reactive oxygen species ROS and MDA that lead to destruction and disruption of lipids of the membranous system, cellular proteins, intracellular organelles and causes DNA damage inducing several pathological changes 34,37 . CCl 4 is transformed in the liver to trichloromethyl free radical that disrupts Ca 2 homeostasis and induces lipid peroxidation that leads to hepatocellular injury 38 .…”

Section: Discussionmentioning

confidence: 99%