scholarly journals Antioxidant and Hepatoprotective Effect of Swertiamarin on Carbon Tetrachloride-Induced Hepatotoxicity via the Nrf2/HO-1 Pathway

2017 ◽  
Vol 41 (6) ◽  
pp. 2242-2254 ◽  
Author(s):  
Tao Wu ◽  
Jingjing Li ◽  
Yong Li ◽  
Hongping Song
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Detoxification Enzymes ◽  
Efflux Transporters ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Bioactive Component ◽  
Antioxidase Activity ◽  
Oxide Synthase ◽  
Experimental Liver

Background/Aims: Swertiamarin (STM), the main bioactive component in Swertia mussotii Franch (Gentianaceae), has been shown to exert hepatoprotective effects on experimental liver injury. However, the effects and exact mechanisms of STM on carbon tetrachloride (CCl4) causing hepatotoxicity are still unknown. This study investigated the potential protective effects and mechanisms of STM on CCl4-induced liver injury in rats. Methods: Adult male Sprague-Dawley (SD) rats were exposed to CCl4 with or without STM co-administration for consecutive eight weeks. Results: STM significantly ameliorated CCl4-induced increase in serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) levels and histopathological changes in the liver. Hepatic oxidative stress was repressed by STM, as evidenced by the decrease in malondialdehyde (MDA), with concomitant increase in antioxidase activity (e.g. superoxide dismutase (SOD); glutathione peroxidase (GPx)), glutathione (GSH) level. STM also obviously attenuated inflammatory response in CCl4-lesioned livers as evidenced by the decrease in inflammatory cytokines/ chemokines (e.g. inducible nitric oxide synthase (iNOS), interleukin-1β (IL-1β)). Additionally, STM significantly induced the expression of CYPs, efflux transporters and PDZK1 as compared with the CCl4 group. Moreover, co-administration of STM with CCl4 remarkably up-regulated the expression of Nrf2, HO-1 and NQO1 compared with the CCl4 group. Conclusions: The present study demonstrates that STM exerts a protective effect against CCl4-induced liver injury and inflammation with its antioxidant effects and induction of hepatic detoxification enzymes and efflux transporters expression, at least in part, via the Nrf2/HO-1 pathway in rats.

Effects and Mechanisms of Acremoniumterricola milleretal mycelium on Liver Fibrosis Induced by Carbon Tetrachloride in Rats

2011 ◽  
Vol 39 (03) ◽  
pp. 537-550 ◽  
Author(s):  
Xiao-Peng Tian ◽  
Yan-Yan Yin ◽  
Xia Li
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Fibrosis ◽  
Liver Injury ◽  
Chinese Herb ◽  
Immunoblot Analysis ◽  
Hepatoprotective Activity ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Procollagen Type ◽  
Tgf Β1

Acremoniumterricola milleretal mycelium (AMM) is one of the most precious traditional Chinese medicines. It has numerous protective effects on organs, and has been used in Chinese herb prescription to treat refractory diseases. Our preliminary studies demonstrated that AMM had hepatoprotective activity in acute liver injury. We further investigated the effects of AMM on liver fibrosis in rats induced by carbon tetrachloride ( CCl 4) and explore its possible mechanisms. The animal model was established by injection with 50% CCl 4 subcutaneously in male Sprague-Dawley rats twice a week for eight weeks. Meanwhile, AMM (175, 350 and 700 mg/kg) was administered intragastrically per day until sacrifice. We found that treatment with AMM (175, 350 and 700 mg/kg) decreased CCl 4-induced elevation of serum transaminase activities, hyaluronic acid, laminin and procollagen type III levels, and contents of hydroxyproline in liver tissues. It also restored the decreased SOD and GSH-Px activities and inhibited the formation of lipid peroxidative products during CCl 4 treatment. Moreover, AMM (350 and 700 mg/kg) decreased the elevation of TGF-β1 by 19.6% and 34.3%, respectively. In the pathological study, liver injury and the formation of liver fibrosis in rates treated by AMM were improved significantly. Immunoblot analysis showed that AMM (175, 350 and 700 mg/kg) inhibited Smad 2/3 phosphorylation, and elevated inhibitor Smad 7 expression. These results suggested that AMM could protect liver damage and inhibit the progression of hepatic fibrosis induced by CCl 4, and its mechanisms might be associated with its ability to scavenge free radicals, decrease the level of TGF-β1 and block TGF-β/Smad signaling pathway.

scholarly journals Lemon Balm and Dandelion Leaf Extracts Synergistically Protect against Carbon Tetrachloride-Induced Acute Liver Injury in Mice

2021 ◽  
Vol 11 (1) ◽  
pp. 390
Author(s):  
Beom-Rak Choi ◽  
Il-Je Cho ◽  
Su-Jin Jung ◽  
Jae-Kwang Kim ◽  
Dae-Geon Lee ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Antioxidant Activities ◽  
Body Weight Gain ◽  
Histopathological Analysis ◽  
Related Factor ◽  
Mrna Levels ◽  
Protective Effects ◽  
Lemon Balm

Lemon balm and dandelion are commonly used medicinal herbs exhibiting numerous pharmacological activities that are beneficial for human health. In this study, we explored the protective effects of a 2:1 (w/w) mixture of lemon balm and dandelion extracts (MLD) on carbon tetrachloride (CCl4)-induced acute liver injury in mice. CCl4 (0.5 mL/kg; i.p.) injection inhibited body weight gain and increased relative liver weight. Pre-administration of MLD (50–200 mg/kg) for 7 days prevented these CCl4-mediated changes. In addition, histopathological analysis revealed that MLD synergistically alleviated CCl4-mediated hepatocyte degeneration and infiltration of inflammatory cells. MLD decreased serum aspartate aminotransferase and alanine transferase activities and reduced the number of liver cells that stained positive for cleaved caspase-3 and cleaved poly(ADP-ribose) polymerase, suggesting that MLD protects against CCl4-induced hepatic damage via the inhibition of apoptosis. Moreover, MLD attenuated CCl4-mediated lipid peroxidation and protein nitrosylation by restoring impaired hepatic nuclear factor erythroid 2-related factor 2 mRNA levels and its dependent antioxidant activities. Furthermore, MLD synergistically decreased mRNA and protein levels of tumor necrosis factor-α, interleukin-1β, and interleukin-6 in the liver. Together, these results suggest that MLD has potential for preventing acute liver injury by inhibiting apoptosis, oxidative stress, and inflammation.

Protective effects of theasinensin A against carbon tetrachloride-induced liver injury in mice

2017 ◽  
Vol 8 (9) ◽  
pp. 3276-3287 ◽  
Author(s):  
Wei-Lun Hung ◽  
Guliang Yang ◽  
Yu-Chuan Wang ◽  
Yi-Shiou Chiou ◽  
Yen-Chen Tung ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Protective Effects

TSA markedly reduced the CCl4-induced liver injury in mice.

Protective effects of BML-111, a lipoxin A4receptor agonist, on carbon tetrachloride-induced liver injury in mice

2007 ◽  
Vol 37 (11) ◽  
pp. 948-956 ◽  
Author(s):  
Li Zhang ◽  
Jingyuan Wan ◽  
Hongzhong Li ◽  
Ping Wu ◽  
Shengwei Jin ◽  
...  
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Protective Effects

Ginsenoside Rb1, A Major Saponin from Panax ginseng, Exerts Protective Effects Against Acetaminophen-Induced Hepatotoxicity in Mice

2019 ◽  
Vol 47 (08) ◽  
pp. 1815-1831 ◽  
Author(s):  
Shen Ren ◽  
Jing Leng ◽  
Xing-Yue Xu ◽  
Shuang Jiang ◽  
Ying-Ping Wang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Panax Ginseng ◽  
Inflammatory Responses ◽  
Interleukin 1 ◽  
Protective Effects ◽  
Ginsenoside Rb1 ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Oxide Synthase

Acute liver injury (ALI) induced by acetaminophen (APAP) is the main cause of drug-induced liver injury. Previous reports indicated liver failure could be alleviated by saponins (ginsenosides) from Panax ginseng against APAP-induced inflammatory responses in vivo. However, validation towards ginsenoside Rb1 as a major and marker saponin may protect liver from APAP-induced ALI and its mechanisms are poorly elucidated. In this study, the protective effects and the latent mechanisms of Rb1 action against APAP-induced hepatotoxicity were investigated. Rb1 was administered orally with 10[Formula: see text]mg/kg and 20[Formula: see text]mg/kg daily for 1 week before a single injection of APAP (250[Formula: see text]mg/kg, i.p.) 1[Formula: see text]h after the last treatment of Rb1. Serum alanine/aspartate aminotransferases (ALT/AST), liver glutathione (GSH) depletion, as well as the inflammatory cytokines, such as tumor necrosis factor-[Formula: see text] (TNF-[Formula: see text]), interleukin-1[Formula: see text] (IL-1[Formula: see text]), inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2), were analyzed to indicate the underlying protective effects of Rb1 against APAP-induced hepatotoxicity with significant inflammatory responses. Histological examination further proved Rb1’s protective effects. Importantly, Rb1 mitigated the changes in the phosphorylation of MAPK and PI3K/Akt, as well as its downstream factor NF-[Formula: see text]B. In conclusion, experimental data clearly demonstrated that Rb1 exhibited a remarkable liver protective effect against APAP-induced ALI, partly through regulating MAPK and PI3K/Akt signaling pathways-mediated inflammatory responses.

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