Hepatoprotective effects of Dicliptera chinensis polysaccharides on dimethylnitrosamine-induced hepatic fibrosis rats and its underlying mechanism

Zhang, Kefeng; Gao, Ya; Zhong, Mingli; Xu, Ye; Li, Jun; Chen, Yifei; Duan, Xiaoqun; Zhu, Hua Long

doi:10.1016/j.jep.2015.12.053

Cited by 34 publications

(14 citation statements)

References 15 publications

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“…The liver TNF-α and IL-1β levels in the TOP-2 group mice at 400 mg/kg restored to normal level ( p > 0.05). These findings imply that TOP-2 have potential anti-inflammatory effects against alcoholic liver injury by down-regulating the expressions of liver TNF-α and IL-1β, which are in agreement with previous reports [36,37]. Pre-treatment with TOP-2 administration resulted in significant protective effects, which might be on account of stabilizing Kupffer cells and suppressing macrophage activation and prostaglandin production [38].…”

Section: Resultssupporting

confidence: 92%

Optimization of Ultrasonic-Microwave Assisted Extraction and Hepatoprotective Activities of Polysaccharides from Trametes orientalis

et al. 2019

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Ultrasonic-microwave assisted extraction (UMAE) of Trametes orientalis polysaccharides was optimized by response surface methodology. Hepatoprotective effects of a purified T. orientalis polysaccharide (TOP-2) were evaluated by alcohol-induced liver injury model mice. The optimal UMAE parameters were indicated as below: ratio of water to raw material 28 mL/g, microwave power 114 W, extraction time 11 min. The polysaccharides yield was 7.52 ± 0.12%, which was well consistent with the predicted value of 7.54%. Pre-treatment with TOP-2 effectively increased the liver index and spleen index in alcohol-treated mice. The elevated serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels of mice after alcohol exposure were inhibited by TOP-2 administration. The liver tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β) levels have decreased significantly as a result of alcohol exposure, while pre-treatment with TOP-2 could mitigate these consequences. Furthermore, pre-treatment with TOP-2 could efficiently boost the superoxidase dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities, and observably constrain the malondialdehyde (MDA) level. The findings suggest that TOP-2 might be useful for alleviating the alcohol-induced hepatotoxicity via its antioxidant and anti-inflammatory potential.

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Section: Resultssupporting

confidence: 92%

Optimization of Ultrasonic-Microwave Assisted Extraction and Hepatoprotective Activities of Polysaccharides from Trametes orientalis

et al. 2019

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“…A study showed that polysaccharides derived from plants protect against hepatic fibrosis and inhibit inflammation (23). A similar hepatoprotective effect was observed in rats treated with β-glucan-enriched Euglena gracilis Z.…”

Section: Discussionmentioning

confidence: 69%

“…In the present study, we did not use polysaccharides from rice or other plants as a negative control but selected the nontoxic concentration in a dose-dependent manner as illustrated by previous studies for determining the hepatoprotective effect of polysaccharide from plants (23,24). Ethanol non-fed mice or normal mice served as the negative control in this study.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, a recent study showed that TA-derived polysaccharides contain β-glucan which reduces hyperglycemia and controls diabetes (21,22). Many studies have shown that polysaccharides from different biological sources protect against hepatic fibrosis and injury due to their anti-inflammatory and antioxidant effects (23,24). However, no previous study has examined the hepatoprotective effect of Triticum aestivum sprout-derived polysaccharide (TASP) on ethanol-induced liver injury or the mechanisms involved.…”

Section: Triticum Aestivum Sprout-derived Polysaccharide Exerts Hepatmentioning

confidence: 99%

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Triticum aestivum sprout-derived polysaccharide exerts hepatoprotective effects against ethanol-induced liver damage by enhancing the antioxidant system in mice

Nepali

Lee

et al. 2017

International Journal of Molecular Medicine

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Triticum aestivum sprout-derived polysaccharide (TASP) has anti-diabetic properties, but no information is available in regards to its protective effect against ethanol-induced hepatic injury. This study aimed to investigate the mechanism behind the protective role of TASP against ethanol-induced liver injury in vivo. Male C57BL/6 mice were administered ethanol with or without TASP for 10 consecutive days by oral gavage. Silymarin was administered in the same manner as a positive control. TASP reduced ethanol-induced hepatic lipid accumulation and serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. TASP also prevented glutathione (GSH) depletion and increased the superoxide dismutase (SOD) in liver tissue. In addition, TASP significantly inhibited ethanol-induced cytochrome P450 2E1 (CYP2E1) activation, and upregulated the expressions of nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1), and downregulated NADPH oxidase genes in ethanol fed mice. Furthermore, the upregulation of Nrf2 was found to be regulated by a phosphatidylinositol 3-kinase (PI3K)/Akt pathway. TASP also attenuated hepatic injury by modulation of caspase-3 and apoptosis-associated mitochondrial proteins including B-cell lymphoma-2 (Bcl-2) and Bcl-2-associated X (Bax) in liver tissues of mice. The study demonstrated that TASP treatment protects against ethanol-induced hepatic injury via multiple pathways by inhibiting steatosis and improving antioxidant marker levels during hepatic injury. Such properties provide a basis for therapeutic agents against alcohol-induced liver injury.

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“…Afterwards Jezequel and coworkers conducted a pioneering study on various aspects of NDMA-induced hepatic fibrosis with special emphasis to pathophysiology and immunohistochemistry and demonstrated that it is a good and reproducible animal model, and appropriate for the study of the early events associated with the development of hepatic fibrosis 48–52 . Furthermore, the model has been employed recently to investigate various aspects of the molecular pathogenesis of hepatic fibrosis and to study therapeutic approaches including the arrest of activation of stellate cells 53–60 . Over the last 20 years, we have extensively studied various biochemical and pathophysiological aspects of the pathogenesis of NDMA-induced hepatic fibrosis in rats and mice involving glycoprotein metabolism 17 , collagen biosynthesis and metabolism 4–6 , LDH isoenzymes 61 , biochemical abnormalities 62 , oxidative stress and osteopontin 10,63–65 , hyaluronic acid and hyaluronidase 66,67 , mineral and trace element metabolism 68–70 , antioxidants 10,71,72 and gene therapy 13,73,74 , lysosomal fragility 75,76 , and the role of metalloproteinases 14,77,78 .…”

Section: N-nitrosodimethylamine-induced Hepatic Fibrosis and Liver CImentioning

confidence: 99%

Molecular mechanisms in the pathogenesis of N-nitrosodimethylamine induced hepatic fibrosis

2019

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Hepatic fibrosis is marked by excessive synthesis and deposition of connective tissue proteins, especially interstitial collagens in the extracellular matrix of the liver. It is a result of an abnormal wound healing in response to chronic liver injury from various causes such as ethanol, viruses, toxins, drugs, or cholestasis. The chronic stimuli involved in the initiation of fibrosis leads to oxidative stress and generation of reactive oxygen species that serve as mediators of molecular events involved in the pathogenesis of hepatic fibrosis. These processes lead to cellular injury and initiate inflammatory responses releasing a variety of cytokines and growth factors that trigger activation and transformation of resting hepatic stellate cells into myofibroblast like cells, which in turn start excessive synthesis of connective tissue proteins, especially collagens. Uncontrolled and extensive fibrosis results in distortion of lobular architecture of the liver leading to nodular formation and cirrhosis. The perpetual injury and regeneration process could also results in genomic aberrations and mutations that lead to the development of hepatocellular carcinoma. This review covers most aspects of the molecular mechanisms involved in the pathogenesis of hepatic fibrosis with special emphasize on N -Nitrosodimethylamine (NDMA; Dimethylnitorsmaine, DMN) as the inducing agent.

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Hepatoprotective effects of Dicliptera chinensis polysaccharides on dimethylnitrosamine-induced hepatic fibrosis rats and its underlying mechanism

Cited by 34 publications

References 15 publications

Optimization of Ultrasonic-Microwave Assisted Extraction and Hepatoprotective Activities of Polysaccharides from Trametes orientalis

Optimization of Ultrasonic-Microwave Assisted Extraction and Hepatoprotective Activities of Polysaccharides from Trametes orientalis

Triticum aestivum sprout-derived polysaccharide exerts hepatoprotective effects against ethanol-induced liver damage by enhancing the antioxidant system in mice

Molecular mechanisms in the pathogenesis of N-nitrosodimethylamine induced hepatic fibrosis

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