Liquiritigenin Protects Rats from Carbon Tetrachloride Induced Hepatic Injury through PGC-1<i>α</i>Pathway

Zhang, Yiping; He, Yakun; Yu, Hongbo; Ma, Fuying; Wu, Jiaxi; Zhang, Xiaoyu

doi:10.1155/2015/649568

Cited by 12 publications

(8 citation statements)

References 30 publications

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“…In the present study, CCl 4 treatment reduced the level of PGC1α, as shown previously in models of liver injury[34,35]. Treatment with serelaxin, or the combination of serelaxin and rosiglitazone, restored PGC1α levels.…”

Section: Discussionsupporting

confidence: 91%

Serelaxin increases the antifibrotic action of rosiglitazone in a model of hepatic fibrosis

Bennett

Simpson

Hamel

2017

WJG

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AIMTo determine the effect of combined serelaxin and rosiglitazone treatment on established hepatic fibrosis.METHODSHepatic fibrosis was induced in mice by carbon tetrachloride administration for 6 wk, or vehicle alone (nonfibrotic mice). For the final 2 wk, mice were treated with rosiglitazone, serelaxin, or both rosiglitazone and serelaxin. Serum liver enzymes and relaxin levels were determined by standard methods. The degree of liver collagen content was determined by histology and immunohistochemistry. Expression of type I collagen was determined by quantitative PCR. Activation of hepatic stellate cells was assessed by alpha-smooth muscle actin (SMA) levels. Liver peroxisome proliferator activated receptor-gamma coactivator 1 alpha (PGC1α) was determined by Western blotting.RESULTSTreatment of mice with CCl4 resulted in hepatic fibrosis as evidenced by increased liver enzyme levels (ALT and AST), and increased liver collagen and SMA. Monotherapy with either serelaxin or rosiglitazone for 2 wk was generally without effect. In contrast, the combination of serelaxin and rosiglitazone resulted in significantly improved ALT levels (P < 0.05). Total liver collagen content as determined by Sirius red staining revealed that only combination treatment was effective in reducing total liver collagen (P < 0.05). These results were supported by immunohistochemistry for type I collagen, in which only combination treatment reduced fibrillar collagen levels (P < 0.05). The level of hepatic stellate cell activation was modestly, but significantly, reduced by serelaxin treatment alone, but combination treatment resulted in significantly lower SMA levels. Finally, while hepatic fibrosis reduced liver PGC1α levels, the combination of serelaxin and rosiglitazone resulted in restoration of PGC1α protein levels.CONCLUSIONThe combination of serelaxin and rosiglitazone treatment for 2 wk was effective in significantly reducing established hepatic fibrosis, providing a potential new treatment strategy.

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Section: Discussionsupporting

confidence: 91%

Serelaxin increases the antifibrotic action of rosiglitazone in a model of hepatic fibrosis

Bennett

Simpson

Hamel

2017

WJG

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“…A widely-accepted assumption is that the reactive oxygen species (ROS) are the main causes of CCl 4 -induced acute liver injury. Therefore, anti-oxidative therapy is an effective means of preventing and attenuating oxidative stress-related liver diseases ( 27 ). Antioxidant enzymes, such as SOD, perform important functions in defense mechanisms against the harmful effects of ROS and free radicals in biological systems.…”

Section: Discussionmentioning

confidence: 99%

Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma

Han

Wang

et al. 2017

Molecular Medicine Reports

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The present study aimed to investigate the hepatoprotective role of Licochalcone E (LCE) and its mechanism of action in a mouse model of carbon tetrachloride (CCl4)-induced liver toxicity. Hepatotoxicity was induced in Kunming mice via an intraperitoneal injection (IP) of CCl4, 10 ml/kg body weight, diluted with corn oil at a 1:500 ratio. LCE was administered once a day for 7 days (IP) as pretreatment at a dose of 5 mg/kg/day. The levels of C-reactive protein (CRP) and tumor necrosis factor (TNF)-α were analyzed to determine the inflammation status. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed using ELISA assays. Liver ultrastructure was observed via optical microscopy. The mRNA and protein expression levels of peroxisome proliferator-activated receptor (PPAR)γ, and nuclear factor (NF)-κB were assayed using quantitative polymerase chain reaction and western blot analysis, respectively. Pretreatment with LCE decreased levels of ALT, AST, CRP and TNF-α, and NF-κB expression in the experimental hepatotoxicity mice model induced by CCl4. In addition, LCE increased the expression of PPARγ and normalized the hepatic histoarchitecture. However, the effects of LCE were reversed by cotreatment with the PPARγ inhibitor GW9662. The present study suggests that LCE may be used for the treatment of hepatotoxicity, and primarily exhibits its protective role through a PPARγ/NF-κB-mediated pathway.

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“…The objective of such substances aims to improve quality of life, increase survival, slow disease progression, and, possibly, mitigate the damage caused by formation of ROS and free radicals (FRs)[8,9]. …”

Section: Introductionmentioning

confidence: 99%

Antioxidant and anti-inflammatory action of melatonin in an experimental model of secondary biliary cirrhosis induced by bile duct ligation

Colares¹,

Schemitt²,

Hartmann³

et al. 2016

WJG

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AIMTo evaluate the effects of melatonin (Mel) on oxidative stress in an experimental model of bile duct ligation (BDL).METHODSMale Wistar rats (n = 32, weight ± 300 g) were allocated across four groups: CO (sham BDL), BDL (BDL surgery), CO + Mel (sham BDL and Mel administration) and BDL + Mel (BDL surgery and Mel administration). Mel was administered intraperitoneally for 2 wk, starting on postoperative day 15, at a dose of 20 mg/kg.RESULTSMel was effective at the different standards, reestablishing normal liver enzyme levels, reducing the hepatosomatic and splenosomatic indices, restoring lipoperoxidation and antioxidant enzyme concentrations, reducing fibrosis and inflammation, and thereby reducing liver tissue injury in the treated animals.CONCLUSIONThe results of this study suggest a protective effect of Mel when administered to rats with secondary biliary cirrhosis induced by BDL.

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Liquiritigenin Protects Rats from Carbon Tetrachloride Induced Hepatic Injury through PGC-1αPathway

Cited by 12 publications

References 30 publications

Serelaxin increases the antifibrotic action of rosiglitazone in a model of hepatic fibrosis

Serelaxin increases the antifibrotic action of rosiglitazone in a model of hepatic fibrosis

Licochalcone E protects against carbon tetrachloride-induced liver toxicity by activating peroxisome proliferator-activated receptor gamma

Antioxidant and anti-inflammatory action of melatonin in an experimental model of secondary biliary cirrhosis induced by bile duct ligation

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