Protective effect of forsythiaside A on lipopolysaccharide/d-galactosamine-induced liver injury

Pan, Chen‐Wei; Zhou, Guangyao; Chen, Wei-lai; Zhuge, Lu; Jin, LJ; Zheng, Yi; Lin, Wei; Pan, Zhenzhen

doi:10.1016/j.intimp.2015.03.009

Cited by 69 publications

(43 citation statements)

References 34 publications

(18 reference statements)

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“…Hepatitis is a common worldwide disease with high mortality in patients (Sun & Karin ). Administration of lipopolysaccharide (LPS), also called endotoxin of Gram‐negative bacteria, has been used for simulating sepsis‐induced hepatitis in several animal models, such as mouse, rat and pig (Pallares et al ; Leng et al ; Pan et al ). The liver is selectively enriched with macrophages, natural killer cells and natural killer T cells, which are key components of the innate immune system and play a significant role in maintaining homeostasis and health.…”

Section: Introductionmentioning

confidence: 99%

Forsythia suspensa extract attenuates lipopolysaccharide‐induced inflammatory liver injury in rats via promoting antioxidant defense mechanisms

Zhao

Piao

Pan

et al. 2016

Animal Science Journal

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Reactive oxygen species (ROS) have been shown to have a role in inflammation. We investigated whether Forsythia suspensa extract (FSE) could exert its antioxidant potential against lipopolysaccharide (LPS)-induced inflammatory liver injury in rats. Rats were orally fed FSE once daily for 7 consecutive days prior to LPS (Escherichia coli, serotype O55:B5) injection. LPS treatment caused liver dysfunction as evidenced by massive histopathological changes and increased serum alanine aminotransferase and aspartate aminotransferase activities which were ameliorated by FSE pretreatment. FSE attenuated LPS-induced depletion of cytosolic nuclear factor-erythroid 2-related factor 2 (Nrf2) and suppression of Nrf2 nuclear translocation in liver, and the generation of ROS and malondialdehyde in serum and liver. FSE increased the Nrf2-mediated induction of heme oxygenase-1 in liver, as well as superoxide dismutase and glutathione peroxidase activities in serum and liver. Importantly, FSE attenuated LPS-induced nuclear factor-кB (NF-кB) nuclear translocation in liver, and subsequently decreased tumor necrosis factor-α, interleukin (IL)-1β and IL-6 levels in serum and liver, which were associated with FSE-induced activation of Nrf2 in liver. These results indicate that the protective mechanisms of FSE may be involved in the attenuation of oxidative stress and the inhibition of the NF-кB-mediated inflammatory response by modulating the Nrf2-mediated antioxidant response against LPS-induced inflammatory liver injury.

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Section: Introductionmentioning

confidence: 99%

Forsythia suspensa extract attenuates lipopolysaccharide‐induced inflammatory liver injury in rats via promoting antioxidant defense mechanisms

Zhao

Piao

Pan

et al. 2016

Animal Science Journal

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“…In this study, the hepatic level of malondialdehyde (MDA) was analyzed by the thiobarbituric acid (TBA) method [22]. Con A treatment markedly increased the hepatic MDA level compared with the control group, whereas the pre-administration of nicotiflorin (25, 50, and 100 mg/kg bw) significantly decreased the MDA levels ( p < 0.05, Figure 4).…”

Section: Resultsmentioning

confidence: 99%

Hepatoprotective Effects of Nicotiflorin from Nymphaea candida against Concanavalin A-Induced and D-Galactosamine-Induced Liver Injury in Mice

Zhao

Zhang

Shang

et al. 2017

IJMS

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Nymphaea candida was used to treat hepatitis in Ugyhur medicine, and nicotiflorin (kaempferol 3-O-β-rutinoside) is the main characteristic component in this plant. In this study, The the hepatoprotective activities of nicotiflorin from N. candida were investigated by Concanavalin A (Con A, 20 mg/kg bw)-and D-Galactosamine (D-GalN, 800 mg/kg bw)-induced acute liver injury in mice. Pretreatment with nicotiflorin (25, 50, 100 mg/kg bw/day, p.o.) for ten days significantly reduced the impact of Con A toxicity (20 mg/kg bw) on the serum markers of liver injury, aspartate aminotransferase (AST), and alanine aminotransferase (ALT). The hepatic anti-oxidant parameters (malondialdehyde, MDA; superoxide dismutase, SOD; glutathione, GSH; and nitric oxide, NO) in mice with nicotiflorin treatment were significantly antagonized for the pro-oxidant effects of Con A. Moreover, pretreatment with nicotiflorin (100 mg/kg bw) significantly decreased Con A-induced elevation in the serum levels of pro-inflammatory cytokines interleukin-1β (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and interferon-γ (IFN-γ) (p < 0.05). A protective effect was reconfirmed against D-GalN-induced chemical liver injury, elevated serum enzymatic and cytokines levels were significantly decreased by nicotiflorin, and liver homogenate antioxidant indicators were significantly restored toward normal levels. Both histopathological studies also supported the protective effects of nicotiflorin. Therefore, the presented results suggest that nicotiflorin is the potent hepatoprotective agent that could protect the liver against acute immunological and chemical injury; this ability might be attributed to its antioxidant and immunoregulation potential.

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“…Loss of UDP will seriously affect the energy metabolism of liver cell and the synthesis of DNA, RNA and protein. Some following studies also found that D-Gal had the relationship with the integrity of liver cell membrane, the exhaustion of glutathione and tumor necrosis factor [21] . Many new researches point out that LPS and D-Gal in combination can cause very serious liver injury [22,23] .…”

Section: D-galactosamine (D-gal)mentioning

confidence: 89%

Research progress on hepatic encephalopathy: animal models and disease mechanisms

Xiao

2015

Abdomen

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Hepatic encephalopathy (HE) is a hepatic disease with neuronal confusion, altered level of consciousness, and coma as a result of severe liver damage/failure. HE is with complicated pathological mechanisms and high mortality, which seriously affects patients' daily life. Roughly, it can be divided into three types, A, B and C. Type A is acute HE and Types B and C are chronic. At present, the pathogenesis of HE is still unclear. In addition, there is no specific clinical treatment. Therefore, establishing appropriate HE animal model is vital for the mechanistic study of the disease and the development of clinical therapy. This review makes a summary on the recent progress of HE animal model establishment and current study of its underlying molecular mechanisms.

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Protective effect of forsythiaside A on lipopolysaccharide/d-galactosamine-induced liver injury

Cited by 69 publications

References 34 publications

Forsythia suspensa extract attenuates lipopolysaccharide‐induced inflammatory liver injury in rats via promoting antioxidant defense mechanisms

Forsythia suspensa extract attenuates lipopolysaccharide‐induced inflammatory liver injury in rats via promoting antioxidant defense mechanisms

Hepatoprotective Effects of Nicotiflorin from Nymphaea candida against Concanavalin A-Induced and D-Galactosamine-Induced Liver Injury in Mice

Research progress on hepatic encephalopathy: animal models and disease mechanisms

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