scholarly journals Effect of Uncaria rhynchophylla against Thioacetamide-Induced Acute Liver Injury in Rat

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Mi-Rae Shin ◽  
Min Ju Kim ◽  
Jin A Lee ◽  
Seong-Soo Roh
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Nuclear Factor Κb ◽  
Significant Rise ◽  
Tissue Inhibitors Of Metalloproteinases ◽  
Control Group ◽  
Histopathological Analysis ◽  
Uncaria Rhynchophylla ◽  
Related Proteins ◽  
Function Activity

Both oxidative stress (OS) and inflammation are two fundamental pathological processes of acute liver injury (ALI). The current work is to investigate the effect and possible mechanism of Uncaria rhynchophylla (UR) on thioacetamide- (TAA-) induced ALI in rats. UR (100 and 200 mg/kg) was orally administrated with TAA (200 mg/kg of bodyweight, intraperitoneal injection) for 3 consecutive days. ALI was confirmed using histological examination and the factors associated with OS and liver function activity measured in serum. Moreover, expressions of inflammation and collagen-related proteins were measured by the Western blot analysis. Myeloperoxidase (MPO), which mediates OS in the ALI control group, was manifested by a significant rise compared with the normal group. UR significantly reduced AST, ALT, and ammonia levels in serum. The nuclear factor-κB (NF-κB) activation induced by TAA led to increase both inflammatory mediators and cytokines. Whereas, UR administration remarkably suppressed such an overexpression. UR supplementation improved matrix metalloproteinases (MMPs) such as MMP-1, -2, and -8. In contrast, tissue inhibitors of metalloproteinases- (TIMP-) 1 level increased significantly by UR treatment. In addition, the histopathological analysis showed that the liver tissue lesions were improved obviously by UR treatment. UR may ameliorate the effects of TAA-induced ALI in rats by suppressing both OS through MPO activation and proinflammatory factors through NF-κB activation. In conclusion, UR exhibited a potent hepatoprotective effect on ALI through the suppression of OS.

scholarly journals Aloperine attenuates carbon tetrachloride-induced mouse hepatic injury via Nrf2/HO-1 pathway

2020 ◽  
Vol 19 (5) ◽  
pp. 983-988
Author(s):  
Rui Xiong ◽  
Shuzhong Shan ◽  
Xiaoming Wang ◽  
Xiaowen Zhang ◽  
Haixia Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Hepatic Injury ◽  
Acute Liver Injury ◽  
Control Group ◽  
Histopathological Analysis ◽  
Dependent Manner ◽  
Oxidative Stress Biomarkers ◽  
Cox 2

Purpose: To investigate whether aloperine pretreatment ameliorates acute liver injury in carbon tetrachloride (CCl4)-treated mice.Methods: Mice were injected with CCl4 and orally administered aloperine. Blood samples and liver tissues were used for histopathological and biochemical analyses, respectively. Protein expression levels were determined by western blotting.Results: Histopathological analysis indicate that aloperine pretreatment significantly alleviated CCl4- induced mouse hepatic injury. CCl4 treatment induced the upregulation of aspartate aminotransferase (AST), alkaline phosphatase (ALP), alanine amino transferase (ALT), and total bilirubin (p < 0.05). However, these alterations were significantly inhibited by aloperine treatment. Moreover, aloperine pretreatment markedly decreased (p < 0.05) the CCl4-induced expression of oxidative stress biomarkers, including malondrialdeline (MDA), glutathione (GSH), catalase (CAT), and  superoxide dismutase (SOD). Compared to the control group, the protein levels of Nrf2, HO-1, iNOS, and COX-2 were significantly increased in the CCl4 group, while Nrf2 and HO-1 were upregulated. Furthermore, iNOS and COX-2 were downregulated in mouse liver in CCl4 + aloperine group compared to CCl4 group in a concentration-dependent manner (p < 0.05).Conclusion: Aloperine pretreatment appears to markedly upregulate Nrf2 and HO-1 and downregulate iNOS and COX-2 to suppress hepatic injury in mice. Thus, aloperine is a promising treatment for acute liver injury. Keywords: Hepatic injury, Aloperine, Oxidative stress, Nrf2/HO-1 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.

scholarly journals Mechanism of KLF4 Protection against Acute Liver Injury via Inhibition of Apelin Signaling

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Weitao Ji ◽  
Hongyun Shi ◽  
Hailin Shen ◽  
Jing Kong ◽  
Jiayi Song ◽  
...  
Keyword(s):  
Liver Injury ◽  
Signaling Pathway ◽  
Acute Liver Injury ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Protein Levels ◽  
Klf4 Expression ◽  
Mrna And Protein Expression

Krüppel-like factor 4 (KLF4) is a key transcription factor that regulates genes involved in the proliferation or differentiation in different tissues. Apelin plays roles in cardiovascular functions, metabolic disease, and homeostatic disorder. However, the biological function of apelin in liver disease is still ongoing. In this study, we investigated the mechanism of KLF4-mediated protection against acute liver injury via the inhibition of the apelin signaling pathway. Mice were intraperitoneally injected with carbon tetrachloride (CCl4; 0.2 mL dissolved in 100 mL olive oil, 10 mL/kg) to establish an acute liver injury model. A KLF4 expression plasmid was injected through the tail vein 48 h before CCl4 treatment. In cultured LX-2 cells, pAd-KLF4 or siRNA KLF4 was overexpressed or knockdown, and the mRNA and protein levels of apelin were determined. The results showed that the apelin serum level in the CCl4-injected group was higher than that of control group, and the expression of apelin in the liver tissues was elevated while KLF4 expression was decreased in the CCl4-injected group compared to the KLF4-plasmid-injected group. HE staining revealed serious hepatocellular steatosis in the CCl4-injected mice, and KLF4 alleviated this steatosis in the mice injected with KLF4 plasmid. In vitro experiments showed that tumor necrosis factor-alpha (TNF-α) could downregulate the transcription and translation levels of apelin in LX-2 cells and also upregulate KLF4 mRNA and protein expression. RT-PCR and Western blotting showed that the overexpression of KLF4 markedly decreased basal apelin expression, but knockdown of KLF4 restored apelin expression in TNF-α-treated LX-2 cells. These in vivo and in vitro experiments suggest that KLF4 plays a key role in inhibiting hepatocellular steatosis in acute liver injury, and that its mechanism might be the inhibition of the apelin signaling pathway.

Inhibition of Endoplasmic Reticulum Stress Attenuated Ethanol-Induced Exosomal miR-122 and Acute Liver Injury in Mice

2019 ◽  
Vol 54 (5) ◽  
pp. 465-471 ◽  
Author(s):  
Sheng Wang ◽  
Jiajie Luan ◽  
Xiongwen Lv
Keyword(s):  
Endoplasmic Reticulum ◽  
Liver Injury ◽  
Endoplasmic Reticulum Stress ◽  
Er Stress ◽  
Acute Liver Injury ◽  
Hepatosomatic Index ◽  
Intragastric Administration ◽  
Alcoholic Liver Injury ◽  
Therapy Strategy ◽  
Related Proteins

ICR mice received ethanol (5 g/kg) by intragastric administration, showing an increase in hepatosomatic index and ALT. These effects were accompanied by increased expression of ER stress-related proteins and exosomal miR-122, PBA intervention can attenuate these changes induced by ethanol provides a potential therapy strategy for acute alcoholic liver injury.

scholarly journals Lactobacillus reuteri ZJ617 Culture Supernatant Attenuates Acute Liver Injury Induced in Mice by Lipopolysaccharide

2019 ◽  
Vol 149 (11) ◽  
pp. 2046-2055 ◽  
Author(s):  
Yanjun Cui ◽  
Sirui Qi ◽  
Wenming Zhang ◽  
Jiangdi Mao ◽  
Renlong Tang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Intraperitoneal Injection ◽  
Molecular Mechanisms ◽  
Culture Supernatant ◽  
Lactobacillus Reuteri ◽  
Acute Liver Injury ◽  
Saline Control ◽  
Control Group ◽  
Intestinal Integrity ◽  
Oral Inoculation

ABSTRACT Background Lactobacillus rhamnosus GG culture supernatant (LGGs) promotes intestinal integrity and ameliorates acute liver injury induced by alcohol in mice. Objectives The aim of this study was to investigate the protective effects and molecular mechanisms of Lactobacillus reuteri ZJ617 culture supernatant (ZJ617s) on acute liver injury induced by lipopolysaccharide (LPS) in mice. Methods Male C57BL/6 mice (20 ± 2 g, 8 wk old) were randomly divided into 4 groups (6 mice/group): oral inoculation with phosphate-buffered saline (control), intraperitoneal injection of LPS (10 mg/kg body weight) (LPS), oral inoculation with ZJ617s 2 wk before intraperitoneal injection of LPS (ZJ617s + LPS), or oral inoculation with LGGs 2 wk before intraperitoneal injection of LPS (LGGs + LPS). Systemic inflammation, intestinal integrity, biomarkers of hepatic function, autophagy, and apoptosis signals in the liver were determined. Results Twenty-four hours after LPS injection, the activities of serum alanine transaminase and aspartate transaminase were 32.2% and 30.3% lower in the ZJ617s + LPS group compared with the LPS group, respectively (P < 0.05). The ZJ617s + LPS group exhibited higher intestinal expression of claudin 3 (62.5%), occludin (60.1%), and zonula occludens 1 (60.5%) compared with the LPS group (P < 0.05). The concentrations of hepatic interleukin-6 and tumor necrosis factor-α were 21.4% and 27.3% lower in the ZJ617s + LPS group compared with the LPS group, respectively (P < 0.05). However, the concentration of interleukin-10 was 22.2% higher in the ZJ617s + LPS group. LPS increased the expression of Toll-like receptor 4 (TLR4; by 50.5%), phosphorylation p38 mitogen-activated protein kinase (p38MAPK; by 57.1%), extracellular signal-regulated kinase (by 77.8%), c-Jun N-terminal kinase (by 42.9%), and nuclear factor-κB (NF-κB; by 36.0%) compared with the control group. Supplementation with ZJ617s or LGGs ameliorated these effects (P < 0.05). Moreover, the hepatic expression of active caspase-3 and microtubule-associated protein 1 light chain 3 II was 23.8% and 28.6% lower in the ZJ617s + LPS group compared with the LPS group, respectively (P < 0.05). Conclusions ZJ617s exerts beneficial effects on the mouse liver through suppression of hepatic TLR4/MAPK/NF-κB activation, apoptosis, and autophagy. This trial was registered at Zhejiang University (http://www.lac.zju.edu.cn) as NO.ZJU20170529.

scholarly journals Puerarin mitigates acute liver injury in septic rats by regulating proinflammatory factors and oxidative stress levels

2021 ◽  
Vol 20 (11) ◽  
pp. 2305-2310
Author(s):  
Jinan Zheng ◽  
Qing Huang ◽  
Jingjing Fang
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Serum Levels ◽  
Expression Level ◽  
Sepsis Group ◽  
Control Group ◽  
Sprague Dawley ◽  
Tnf Α ◽  
Proinflammatory Factors

Purpose: To determine the protective effect of puerarin against acute liver injury in septic rats, and the mechanism involved.Methods: Eighty-seven Sprague-Dawley (SD) rats were assigned to control, sepsis and puerarin groups (each having 29 rats). Serum levels of NF-kB, TNF-α, IL-1 β, IL-6, ALT and AST were assayed. Liver lesions and levels of NO, SOD, iNOS and malondialdehyde (MDA) were measured using standard procedures.Results: Compared with the control group, the levels of NF-kB, TNF-α, IL-1β, IL-6, AST, ALT, NO, MDA and iNOS significantly increased in the sepsis group, while SOD level decreased significantly. In contrast, there were marked decreases in NF-kB, TNF-α, IL-1β, AST, ALT, NO, MDA and iNOS in puerarin group, relative to the sepsis group, while SOD expression level was significantly increased (p <0.05). The level of p-p38 in liver of septic rats was up-regulated, relative to control rats, while Nrf2 significantly decreased (p < 0.05). The expression level of p-p38 in the puerarin group was significantly decreased, relative to the sepsis group, while the expression level of Nrf2 significantly increased (p < 0.05).Conclusion: Puerarin mitigates acute liver injury in septic rats by inhibiting NF-kB and p38 signaling pathway, down-regulating proinflammatory factors, and suppressing oxidative stress. Thus, puerarin may be developed for use in the treatment liver injury.

scholarly journals TNF-alpha but not IL-1alpha are Correlated with PGE1-Dependent Protection Against Acute D-Galactosamine-Induced Liver Injury

2000 ◽  
Vol 14 (3) ◽  
pp. 175-180 ◽  
Author(s):  
J Muntané ◽  
JL Montero ◽  
JM Lozano ◽  
A Miranda-Vizuete ◽  
M de la Mata ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Experimental Studies ◽  
Acute Hepatic Failure ◽  
Inflammatory Cells ◽  
Control Group ◽  
Prostaglandin E ◽  
Necrosis Factor Alpha ◽  
Tnf Α

BACKGROUND: Prostaglandin E1(PGE1) treatment of humans and rodents during acute hepatic failure ameliorates different parameters of hepatic dysfunction.PURPOSE: To investigate whether prevention of acute liver injury induced by D-galactosamine (D-GalN) with preadministration of PGE1is correlated with a change in the concentration of two proinflammatory cytokines, as tumour necrosis factor-alpha (TNF-α) and interleukin (IL)-1α, and/or nitrite+nitrate (NOx), as nitric oxide-related end products in serum.RESULTS: D-GalN significantly increased alanine aminotransferase (ALT) and TNF- αconcentration in serum 5 and 10 mins, respectively, after treatment compared with the control group (P&#8804;0.05). D-GalN did not change the IL-1α concentration at any time during the study. Preadministration of PGE1to D-GalN-treated rats significantly reduced the ALT content and increased significantly the TNF-α concentration in serum 1, 2.5, 5 and 10 mins after D-GalN treatment compared with the D-GalN group (P&#8804;0.05). Nitric oxide was not involved in either the toxic effect due to D-GalN or the protection observed with PGE1against D-GalN toxicity.CONCLUSIONS: Acute liver injury induced by D-GalN is correlated with an increased TNF-α release. Preadministration of PGE1to D-GalN-treated rats exerted a priming effect on inflammatory cells to release enhanced levels of TNF-α but not IL-1α. These findings indicate that stimulation of TNF-α release may be involved in the acute D-GalN-induced liver injury and also in PGE1protection from hepatotoxicity in clinical and experimental studies.

scholarly journals Nanoencapsulation of Curcumin and Its Protective Effects against CCl4-Induced Hepatotoxicity in Mice

2019 ◽  
Vol 2019 ◽  
pp. 1-10 ◽  
Author(s):  
Jian Li ◽  
Ruixu Niu ◽  
Lixin Dong ◽  
Liming Gao ◽  
Jie Zhang ◽  
...  
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Curcuma Longa ◽  
Stress Factors ◽  
Hepatoprotective Effect ◽  
Control Group ◽  
Antioxidant Enzyme Activities ◽  
Protective Effects ◽  
Model Control ◽  
Model Control Group

Curcumin is a natural phenolic compound extracted from the herb Curcuma longa L. rhizome and has received much attention on account of its biological properties. However, its poor solubility and low bioavailability limit its use. The purpose of this study was to synthesize curcumin-loaded nanoliposomes (Cur-NLs) to improve their bioavailability and evaluate the hepatoprotective effect of Cur-NLs against tetrachloromethane- (CCl4-) induced acute liver injury in mice. We prepared Cur-NLs by thin film dispersion method, and the characterizations of Cur-NLs were measured by transmission microscope, laser particle size analyzer, infrared spectrometer, and X-ray diffraction. After 14 days pretreatment of Cur-NLs, free curcumin, silybin, or PBS, the models of acute liver injury were established by CCl4 intraperitoneal injection in mice. The organ index, biochemical liver function parameters, histopathology, and antioxidant enzyme activities of liver tissues were measured further to evaluate the protective effects of Cur-NLs on liver injury. Compared with the CCl4 model control group, pretreatment of Cur-NLs effectively reduced the serum levels of ALT, AST, and ALP and attenuated the hepatic necrosis induced by CCl4 intoxication. Furthermore, Cur-NL pretreatment remarkably exhibited decreased MDA level and increased SOD, GPx, and CAT activities compared to CCl4 model control group. Compared with the free curcumin group, the Cur-NLs also showed a better hepatoprotective effect. These observations imply that Cur-NLs act as a promising hepatoprotective agent in reducing liver oxidative stress produced by different stress factors.

scholarly journals Sodium butyrate protects against lipopolysaccharide-induced liver injury partially via the GPR43/ β-arrestin-2/NF-κB network

2020 ◽  
Author(s):  
Qian-Jiang Luo ◽  
Mei-Xing Sun ◽  
Yun-Wei Guo ◽  
Si-Wei Tan ◽  
Xiao-Ying Wu ◽  
...  
Keyword(s):  
Liver Injury ◽  
Sodium Butyrate ◽  
Acute Liver Injury ◽  
Nuclear Factor Κb ◽  
Raw264.7 Cells ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Inflammatory Factor ◽  
Rt Pcr ◽  
Tissue Morphology

Abstract Background Butyrate acts as a regulator in multiple inflammatory organ injuries. However, the role of butyrate in acute liver injury has not yet been fully explored. In the present study, we aimed to investigate the association between butyrate and lipopolysaccharide (LPS)-induced acute liver injury and the signaling pathways involved. Methods LPS-induced acute liver injury was induced by intraperitoneal injection of LPS (5 mg/kg) in G-protein-coupled receptor 43 (GPR43)-knockout (KO) and wild-type female C57BL/6 mice. Sodium butyrate (500 mg/kg) was administered intraperitoneally 30 min prior to LPS exposure. Liver injury was detected by serum markers, tissue morphology, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). Pro-inflammatory-factor levels were detected by enzyme-linked immunosorbent assay and real-time polymerase chain reaction (RT-PCR). Cell models were first treated with sodium butyrate (4 μmol/mL), followed by LPS (1 μg/mL) half an hour later in GPR43 small interfering RNA (siRNA)-transfected or control RAW264.7 cells. Cell-inflammation status was evaluated through detecting pro-inflammatory-factor expression by RT-PCR and also through checking toll-like receptor 4/nuclear factor-κB (TLR4/NF-κB)-element levels including TLR4, TRAF6, IKKβ, IкBα, phospho-IкBα, p65, and phospho-p65 by Western blot. The interaction between GPR43 and β-arrestin-2 was tested by co-immunoprecipitation. Results Sodium butyrate reversed the LPS-induced tissue-morphology changes and high levels of serum alanine aminotransferase, aspartate transaminase, myeloperoxidase, TUNEL, and pro-inflammatory cytokines such as tumor necrosis factor-α and interleukin-6. The ameliorating effect of sodium butyrate was weakened in GPR43-KO mice and GPR43 siRNA RAW264.7 cells, compared with those of GPR43-positive controls. Sodium butyrate downregulated some elements of the TLR4/NF-κB pathway, including phospho-IκBα and phospho-p65, in RAW264.7 cells. Increased interactions between GPR43 and β-arrestin-2, and between β-arrestin-2 and IкBα were observed. Conclusion Sodium butyrate significantly attenuated LPS-induced liver injury by reducing the inflammatory response partially via the GPR43/β-arrestin-2/NF-κB signaling pathway.

scholarly journals Metabonomic Profiling in Study Protective Effect of Sea Buckthorn Sterol on Acute Liver Injury Induced By Carbon Tetrachloride in Rats

2021 ◽  
Author(s):  
Changting Sheng ◽  
Yang Guo ◽  
Jing Ma ◽  
Eun-Kyung Hong， ◽  
Benyin Zhang ◽  
...  
Keyword(s):  
Endoplasmic Reticulum ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Aspartic Acid ◽  
Acute Liver Injury ◽  
Sea Buckthorn ◽  
Control Group ◽  
Expression Levels ◽  
Cox 2 ◽  
Liver Tissues

Abstract Objective: To study the effect and protection mechanism of sea buckthorn sterol on acute liver injury induced by carbon tetrachloride (CCl4) in rats. Methods: CCl4 was used to make a rat model of acute liver injury. The rats were divided into six groups including blank control group, model control group, bifendate treated positive control group, low-, medium-, and high-doses of sea buckthorn sterol treated groups. The enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), gamma-glutamyl transpeptidase (γ-GT), and catalase (CAT) were investigated. Total antioxidant capacity (T-AOC), total protein (TP), and the content of malondialdehyde (MDA), the level of cyclooxygenase-2 (COX-2) and prostaglandin E2 (PGE2) in liver tissues were determined. HE staining was used for the observation of inflammatory changes of liver tissues. The endoplasmic reticulum and mitochondria in liver tissues were observed by electron microscope. Wide range of targeted technologies were used for the detection of the full-spectrum metabolome, and metabolome differences among samples were investigated by means of the combination of UPLC-MS/MS detection platform, self-built database, and multivariate statistical analysis. Transcriptomics were studied using the RNA-SEQ method. Based on comparison results, gene expression levels were analyzed, and differentially expressed genes were identified according to their expression levels in different samples. Results: After the treatment of sea buckthorn sterol, the activities of SOD, GSH-Px, CAT, T-AOC, and TP in liver tissues were increased, while the activities of γ-GT, COX-2, and PGE2 were decreased, and the content of MDA was also reduced. Sea buckthorn sterol can reduce the inflammatory lesions in liver tissues, and the damage of the structure of endoplasmic reticulum and mitochondria of liver cells were significantly alleviated compared with the model group. The levels of L-malic acid, 7Z, 10Z, 13Z, 16Z, 19Z-docosapentaenoic acid, creatine, N-acetyl-l-alanine, N-acetyl-aspartic acid, trigonelline, 4-guanidine butyric acid, N-amidine L-aspartic acid, CE(16:1), CE(18:2), PE(16:1/16:0), DG(16:0/18:02/0:0), TG(14:0/18:0/20:4), TG(16:0/18:0/20:4), TG(16:0/16:1/22:5), N-glycine-l-leucine, and FFA(6:0) were significantly restored after the treatment of sea buckthorn sterol. Sea buckthorn sterol could participate in the citric acid cycle, arginine and proline metabolism, alanine, aspartate and glutamate metabolism, niacin and niacinamide metabolism, fat digestion and absorption, and glycerophospholipid metabolism. Besides, the expressions of Cyp1a1, Noct, and Tubb6 could be regulated by sea buckthorn sterol, and thus the metabolic damage by CCl4 was reduced. Conclusion: Sea buckthorn sterol could improve liver function in the animal model of CCl4-induced acute liver injury in rats. The mechanism of liver protection is likely related to the regulation of metabolic disorders, anti-lipid peroxidation, and inhibition of inflammatory response.

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