Search

Copyright of Journal of Food Safety & Quality is the property of Journal of Food Safety & Quality Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Food & Fermentation Industries is the property of Food & Fermentation Industries and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Acta Agriculturae Zhejiangensis is the property of Acta Agriculturae Zhejiangensis Editorial Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Food Safety & Quality is the property of Journal of Food Safety & Quality Editorial Department and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Acylation of anthocyanin with fatty acid has been extensively applied for the improvement of their lipophilicity and stability. However, their functionalities are not fully investigated. This work prepared cyanidin-3-O-glucoside–lauric acid ester (C3G–LA) and investigated its protective effect against oxidative stress in H2O2-induced human normal liver (LO2) cells. The results indicated that C3G–LA possessed notable antioxidant activity and better protective effect than its anthocyanin precursor cyanidin-3-O-glucoside (C3G). It protected the cells from H2O2-induced cell death and apoptosis by suppressing the overproduction of reactive oxygen species and malondialdehyde, restoring superoxide dismutase activity and ameliorating mitochondrial dysfunction and membrane damage. The increase in the expression levels of phosphorylated Akt, Nrf2, HO-1 and NQO1 further indicated that the antioxidant protective effect of C3G–LA involved the PI3K/Akt-mediated activation of the Nrf2–HO-1/NQO1 pathway. The findings indicated that, in addition to improve lipophilicity and stability, acylation of anthocyanin can enhance their anti-oxidative stress activity.

Copyright of Journal of Chinese Institute of Food Science & Technology / Zhongguo Shipin Xuebao is the property of Journal of Chinese Institute of Food Science & Technology Periodical Office and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The crude Hedysarum polysaccharides (HPS: HPS‐50 and HPS‐80) obtained from Radix Hedysari exhibited great pharmacological activities in our previous research. This study investigated the effects of HPS on lipopolysaccharide (LPS)/D‐galactosamine (D‐GalN)‐induced acute liver injury (ALI) in mice and LPS‐induced injury in LO2 cells, as well as the relationship between structural characteristics and hepatoprotective activities. The in vivo results showed that compared with HPS‐80, HPS‐50 showed stronger hepatoprotection, which improved histopathological changes to normal levels. HPS‐50 significantly decreased the levels of ALT, AST, MPO, and MDA, increased the activities of SOD, CAT, and GSH, and suppressed the LPS/D‐GalN‐triggered production of TNF‐α, IL‐1β, and IL‐6 (p <.05). The results in vitro showed that HPS‐50‐P (HPS‐50‐1, HPS‐50‐2, and HPS‐50‐3) purified from HPS‐50 played significant protective roles against LPS‐induced injury in LO2 cells by reducing cell apoptosis and relieving cell cycle arrest. HPS‐50‐2 restored the percentage of normal cells from 54.8% to 94.7%, and reduced the S phase cells from 59.40% to 47.05% (p <.01). By analyzing the structure of HPS‐50‐P, including monosaccharide composition, molecular weight, chain conformation, and surface morphology, we speculated that the best protective effect of HPS‐50‐2 might be attributed to its beta configuration, highest molecular weight, and high glucose and galactose contents. These findings indicate that HPS‐50 might be a promising source of functional foods for the protection and prevention of ALI. Practical applications: In this study, the protective effect of HPS on ALI was evaluated from multiple perspectives, and HPS‐50‐2 was screened as a potential active ingredient. This study has two practical applications. First, it provides a new way to improve ALI, and a new option for patients to prevent and treat ALI. Second, this work also complements the pharmacological activity of Radix Hedysari and provides a basis for the development of Radix Hedysari as a functional food. [ABSTRACT FROM AUTHOR]

Objective Unlike mammals, goose fatty liver shows a strong tolerance to fatty acids without obvious injury. Stearyl-coenzyme A desaturase 1 (SCD1) serves crucial role in desaturation of saturated fatty acids (SAFs), but its role in the SAFs tolerance of goose hepatocytes has not been reported. This study was conducted to explore the role of SCD1 in regulating palmitic acid (PA) tolerance of goose primary hepatocytes. Methods 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide was examined to reflect the effect of PA on hepatocytes viability, and quantitative polymerase chain reaction was used to detect the mRNA levels of several genes related to endoplasmic reticulum (ER) stress, inflammation, and apoptosis, and the role of SCD1 in PA tolerance of goose hepatocytes was explored using RNA interfere. Results Our results indicated that goose hepatocytes exhibited a higher tolerant capacity to PA than human hepatic cell line (LO2 cells). In goose primary hepatocytes, the mRNA levels of fatty acid desaturation-related genes (SCD1 and fatty acid desaturase 2) and fatty acid elongate enzyme-related gene (elongase of very long chain fatty acids 6) were significantly upregulated with 0.6 mM PA treatment. However, in LO2 cells, expression of ER stress-related genes (x box-binding protein, binding immunoglobulin protein, and activating transcription factor 6), inflammatory response-related genes (interleukin-6 [IL-6], interleukin-1β [IL-1β], and interferon-γ) and apoptosis-related genes (bcl-2-associated X protein, b-cell lymphoma 2, Caspase-3, and Caspase-9) was significantly enhanced with 0.6 mM PA treatment. Additionally, small interfering RNA (siRNA) mediated downregulation of SCD1 significantly reduced the PA tolerance of goose primary hepatocytes under the treatment of 0.6 mM PA; meanwhile, the mRNA levels of inflammatory-related genes (IL-6 and IL-1β) and several key genes involved in the phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT), forkhead box O1 (FoxO1), mammalian target of rapamycin and AMPK pathways (AKT1, AKT2, FoxO1, and sirtuin 1), as well as the protein expression of cytochrome C and the apoptosis rate were upregulated. Conclusion In conclusion, our data suggested that SCD1 was involved in enhancing the PA tolerance of goose primary hepatocytes by regulating inflammation- and apoptosis-related genes expression.

Objective To investigate the effect of irbesartan on steatosis in LO2 cells by regulating PPAR-γ-mediated AMPK/mTOR signaling pathway and autophagy. Methods The cell model was established by lipid mixture (LM). LO2 model cells were divided into model group, irbesartan group and irbesartan + PPAR-γ antagonist group. The normal cells were served as the normal group. After 24 hours of intervention, the triacylglycerol (TG) and total cholesterol (TC) levels in cells were measured using enzyme-linked immunosorbent assay (ELISA) kits, and cultured cells were stained with oil red O solution to assess the lipid content. The expression levels of PPAR-γ and AMPK/mTOR signaling pathway molecules in cells were detected by Western blot assay, and the changes of autophagy marker protein LC3B were observed by confocal microscopy and Western blot assay. The changes of autophagy marker protein LC3B were observed by laser confocal technique. Results The concentration of irbesartan in 10μmol/L and below had no obvious toxic effect on the growth of LO2 cells, but 20 μmol/L irbesartan had a significant inhibitory effect on cell viability. Compared with the normal group, the intracellular TG and TC levels as well as lipid deposition were significantly increased in model group, the expressions of PPAR-γ, P-AMPK and LC3B proteins were decreased, and the level of phosphorylated mTOR was increased (P＜0.05). Compared with the model group, the intracellular TG and TC levels as well as lipid deposition were significantly decreased in irbesartan group. Moreover, it was found that irbesartan strongly increased the expressions of PPAR-γ, p-AMPK and LC3B, and reduced the level of phosphorylated mTOR in LM-induced LO2 cells (P＜0.05). However, these effects were reversed by irbesartan and PPAR-γ inhibitor treatment. It was found that irbesartan strongly increased the expressions of PPAR-γ, p- AMPK and LC3B, and reduced the level of phosphorylated mTOR in LM-induced LO2 cells (P＜0.05). Conclusion Irbesartan alleviates lipid deposition and hepatic steatosis by activating PPAR-γ mediated AMPK/mTOR signaling pathway, thereby inducing hepatocyte autophagy. [ABSTRACT FROM AUTHOR]

Objective To investigate the protective effect of apigenin against H2O2-induced injury in human hepatocytes（L02）.Methods L02 cells were treated with H2O2 to establish a model of oxidative injury. CCK-8 assay was used to measure cell viability; DCFH-DA was used to measure the production of reactive oxygen species（ROS） in cells; test kits were used to measure the activities of lactate de-hydrogenase（LDH）, malondialdehyde（MDA）, and superoxide dismutase（SOD） in cell supernatant; Hoechst staining was performed toobserve cell apoptosis, and a test kit was used to observe the activity of caspase-3. A one-way analysis of variance was used for compari-son of continuous data between multiple groups, and the LSD-ttest was used for further comparison between two groups.Results Apige-nin at a concentration of ≥20 μmol/L significantly inhibited the proliferation of L02 cells（P< 0. 01）. Compared with the cells in the blankcontrol group, the cells treated with H2O2 at a concentration of ≥500 μmol/L had a significant reduction in cell viability（P< 0. 001）, andtherefore, 500 μmol/L was determined as the optimal concentration for modeling. There was a significant difference in cell viability betweenthe model group and the blank control group（P< 0. 01）, and compared with the model group, the 5 and 10 μmol/L apigenin groups had asignificant increase in cell viability（P< 0. 01）. The cells in the blank control group had good morphology, while those in the model groupwere contracted and round-shaped and had marked rupture and deformity, and compared with the model group, the 5 μmol/L apigenin group showed significant improvement with a reduction in ruptured and round-shaped cells. There was a significant difference in fluores-cence intensity between the blank control group, the model group, and the 5 μmol/L apigenin group（1. 00 ± 0. 26 vs 32. 94 ± 1. 29 vs13. 49 ± 1. 23,F= 1. 10,P< 0. 001）, and the model group had a significantly higher fluorescence intensity than the blank control group（P< 0. 001）. Compared with the model group, the 5 μmol/L apigenin group had a significant reduction in H2O2-induced ROS（P<0. 001）. Compared with the control group, the model group had significant increases in the levels of LDH and MDA and a significant reduc-tion in the level of SOD（F= 3. 21, 2. 03, and 3. 32, allP< 0. 05）, and compared with the model group, the 5 μmol/L apigenin group hadsignificant reductions in the levels of LDH and MDA and a significant increase in the level of SOD（allP< 0. 05）. There was a significantdifference in cell apoptosis rate between the blank control group, the model group, and the 5 μmol/L apigenin group(7. 54% ± 0. 52% vs39. 77% ± 3. 44% vs 14. 40% ± 0. 79%,F =9.439,P< 0. 01], and the model group had a significantly higher cell apoptosis rate than thecontrol group（P< 0. 01）; the cells treated with apigenin had a significantly lower apoptosis rate than those in the model group（P< 0. 01）.There was a significant difference in the activity of caspase-3 between the blank control group, the model group, and the 5 μmol/L apigeningroup（4. 38 ±0. 59 U/mg vs 16. 44 ±1. 13 U/mg vs 10. 60 ± 1. 04 U/mg,F =1.17,P< 0. 05）, and the model group had a significantlyhigher activity of caspase-3 than the blank control group（P< 0. 05）; compared with the cells in the model group, the cells treated withapigenin had a significant reduction in the activity of caspase-3（P< 0. 05）.Conclusion Apigenin may exert a protective effect againstH2O2-induced injury in L02 cells by eliminating ROS and reducing caspase-3 activity. [ABSTRACT FROM AUTHOR]

β -FeOOH nanorods were prepared via the urea hydrolysis process with the average length of 289.1 nm and average diameter of 61.2 nm, while magnetic α -Fe 2 O 3 /Fe 3 O 4 heterostructure nanorods were prepared via the urea calcination process with β -FeOOH nanorods as precursor, and the optimum conditions were the calcination temperature of 400 °C, the calcination time of 2 h, the β -FeOOH/urea mass ratio of 1:6. The average length, diameter, and the saturation magnetization of the heterostructure nanorods prepared under the optimum conditions were 328.8 nm, 63.4 nm and 42 emu·g -1 , respectively. The Prussian blue test demonstrated that the heterostructure nanorods could be taken up by HepG2 cells, and cytotoxicity tests proved that the heterostructure nanorods had no significant effect on the viabilities of LO2 and HepG2 cells within 72 h in the range of 100-1600 μ g·ml -1 . Therefore, magnetic α -Fe 2 O 3 /Fe 3 O 4 heterostructure nanorods had better biocompatibility with LO2 and HepG2 cells., (© 2023 IOP Publishing Ltd.)

Aberrant glycosylation has been commonly observed in various physiological and pathological disorders (including cancers), and quite a few glycoproteins have been approved by the US Food and Drug Administration (FDA) as markers for early diagnosis. Each glycoprotein may have multiple glycoforms, and cancer-related ones can be only some specific glycoforms which have much higher sensitivity and specificity; for example, AFP glycoform AFP-L3 with N-glycan of 01Y(61F)41Y41M(31M41Y41L41S61M41Y41L41S is of bigger diagnostic value for hepatocellular carcinoma than total AFP (i.e., combination of all glycoforms). Mass spectrometry-based glycomics is currently the state-of-the-art instrumental analytical pipeline for high-throughput characterization of various glycoforms, where not only monosaccharide composition but also comprehensive structural information (sequence and linkage) of N-glycans are now reported thanks to our recently developed N-glycan database search engine GlySeeker. With this new capability, here, we report our large-scale characterization of human liver N-glycome with primary structures; 214 unique N-glycans with unique primary structures were identified and visualized with spectrum-level false discovery rate ≤ 1% and number of best hits of 1. The LO2 N-glycans reported here serve as a basic reference for future liver N-glycome study, and further quantitative analysis will enable characterization of differentially expressed N-glycans and discovery of more effective markers for liver and other diseases. Data are available via ProteomeXchange with identifier PXD008158. [ABSTRACT FROM AUTHOR]

[Display omitted] • Acylation of cyanidin-3- O -glucoside (C3G) enhances its anti-oxidant activity. • C3G–laurate ester (C3G–LA) protected liver (LO2) cells from H 2 O 2 -induced injury. • C3G–LA protected cells by up-regulating PI3K/Akt-mediated Nrf2–HO-1/NQO1 pathway. Acylation of anthocyanin with fatty acid has been extensively applied for the improvement of their lipophilicity and stability. However, their functionalities are not fully investigated. This work prepared cyanidin-3- O -glucoside–lauric acid ester (C3G–LA) and investigated its protective effect against oxidative stress in H 2 O 2 -induced human normal liver (LO2) cells. The results indicated that C3G–LA possessed notable antioxidant activity and better protective effect than its anthocyanin precursor cyanidin-3- O -glucoside (C3G). It protected the cells from H 2 O 2 -induced cell death and apoptosis by suppressing the overproduction of reactive oxygen species and malondialdehyde, restoring superoxide dismutase activity and ameliorating mitochondrial dysfunction and membrane damage. The increase in the expression levels of phosphorylated Akt, Nrf2, HO-1 and NQO1 further indicated that the antioxidant protective effect of C3G–LA involved the PI3K/Akt-mediated activation of the Nrf2–HO-1/NQO1 pathway. The findings indicated that, in addition to improve lipophilicity and stability, acylation of anthocyanin can enhance their anti-oxidative stress activity. [ABSTRACT FROM AUTHOR]

Type 2 diabetes is a chronic disease and hyperglycemia is important in the pathogenesis of diabetic complications. Exposure of LO2 cells to high glucose resulted in cellular glucose consumption and uptake decreases, reactive oxygen species (ROS) and superoxide anion (O 2 − ) accumulation and mitochondrial dysfunction, which could be partly recovered by mulberry anthocyanin extract (MAE). And these protective effects were partly associated with regulation of nuclear factor erythroid 2-related factor 2 (Nrf2) and its downstream targets. As the insulin-signaling pathway is evolutionarily well conserved from Caenorhabditis elegans to mammals, C. elegans has been considered as a model system to study effects of glucose toxicity. Glucose shortened the lifespan of C. elegans , while MAE suppressed the damage, accompanied by malondialdehyde (MDA) and triglyceride accumulation reduction as well as total superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity recovery and PMK-1/p38 expression promotion. In contrast, MAE failed to recover shortened longevity, glucose and triglyceride accumulation in daf-2 (−) mutants fed a glucose-supplemented diet. Transcriptional profile revealed MAE intervention led to 92 genes alteration compared with the glucose-treatment. Interestingly, expressions of DAF-2/insulin receptor related genes were increased by glucose but impaired by MAE in nematodes. Our studies suggested that MAE might help to improve the antioxidant defense system, resulting in prevention of glucose-induced damage both in vitro and in vivo . [ABSTRACT FROM AUTHOR]

The purpose of this study was to compare messenger RNA (mRNA) expression of selenoprotein genes between hepatoma HepG2 and normal hepatocytes LO2 cell lines. Liver HepG2 and LO2 cells were cultured in 12-well plates under the same condition until cells grew to complete confluence, and then cells were harvested for total RNA and protein extraction. The qPCRs were performed to compare gene expression of 14 selenoprotein genes and 5 cancer signaling-related genes. Enzyme activities were also assayed. The results showed that human hepatoma HepG2 cells grew faster than normal hepatocytes LO2 cells. Among the genes investigated, 10 selenoprotein genes ( Gpx1, Gpx3, Gpx4, Selx, Sepp, Sepw1, Sepn1, Selt, Seli, Selh) and 3 cancer signaling-related genes ( Bcl-2A, caspase-3, and P38) were upregulated ( P < 0.05), while Selo and Bcl-2B were downregulated ( P < 0.05) in hepatoma HepG2 cells compared to LO2 cells. Significant correlations were found between selenoprotein genes and the cancer signaling-related genes Caspase3, P53, Bc1-2A, and Bc1-2B. Our results revealed that selenoprotein genes were aberrantly expressed in hepatoma HepG2 cells compared to normal liver LO2 cells, which indicated that those selenoprotein genes may play important roles in the occurrence and development of liver carcinogenesis. [ABSTRACT FROM AUTHOR]

The effect of structured triacylglycerols [1-oleoyl-2-palmitoyl-3-linoleoylglycerol (OPL), 3-dilinoleoyl-2-palmitoylglycerol (LPL), and 1,3-dioleoyl-2-palmitoylglycerol (OPO)] in human milk on the lipid metabolism was unclear. Hence, this study investigated the effects of different structured triacylglycerols and their mixtures (M) (OPL/LPL/OPO in M1, M2, and M3 were 1.5:0.5:1, 1.2:1.2:1, and 0.5:0.2:1, respectively) on lipid and expression levels of some critical proteins involved in lipid metabolism in LO2 cells. Results showed that there was more lipid accumulation in the LO2 cells exposed to 2,3-dioleoyl-1-palmitoylglycerol (POO) than OPL, LPL, and OPO ( p < 0.05), and more lipid accumulation was observed in the OPL group compared to LPL and OPO groups ( p < 0.05). Moreover, there was more lipid accumulation in the M3 group compared to M1 and M2 groups. The expression level of diacylglycerol acyltransferase was highest in the POO group compared to LPL, OPO, and OPL groups and was higher in the M3 group than M1 and M2 groups. The expression levels of acetyl-CoA carboxylase 1 and long-chain acyl-CoA synthetase 1 were highest in the OPL group compared to OPO and LPL groups. In comparison to OPO and LPL, OPL seemed to be more likely to increase the content of triacylglycerols and cholesterol in LO2 cells; therefore, whether this was beneficial to the growth and development of infants needs further verification.

Objective: Unlike mammals, goose fatty liver shows a strong tolerance to fatty acids without obvious injury. Stearyl-coenzyme A desaturase 1 (SCD1) serves crucial role in desaturation of saturated fatty acids (SAFs), but its role in the SAFs tolerance of goose hepatocytes has not been reported. This study was conducted to explore the role of SCD1 in regulating palmitic acid (PA) tolerance of goose primary hepatocytes., Methods: 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide was examined to reflect the effect of PA on hepatocytes viability, and quantitative polymerase chain reaction was used to detect the mRNA levels of several genes related to endoplasmic reticulum (ER) stress, inflammation, and apoptosis, and the role of SCD1 in PA tolerance of goose hepatocytes was explored using RNA interfere., Results: Our results indicated that goose hepatocytes exhibited a higher tolerant capacity to PA than human hepatic cell line (LO2 cells). In goose primary hepatocytes, the mRNA levels of fatty acid desaturation-related genes (SCD1 and fatty acid desaturase 2) and fatty acid elongate enzyme-related gene (elongase of very long chain fatty acids 6) were significantly upregulated with 0.6 mM PA treatment. However, in LO2 cells, expression of ER stressrelated genes (x box-binding protein, binding immunoglobulin protein, and activating transcription factor 6), inflammatory response-related genes (interleukin-6 [IL-6], interleukin- 1β [IL-1β], and interferon-γ) and apoptosis-related genes (bcl-2-associated X protein, b-cell lymphoma 2, Caspase-3, and Caspase-9) was significantly enhanced with 0.6 mM PA treatment. Additionally, small interfering RNA (siRNA) mediated downregulation of SCD1 significantly reduced the PA tolerance of goose primary hepatocytes under the treatment of 0.6 mM PA; meanwhile, the mRNA levels of inflammatory-related genes (IL-6 and IL-1β) and several key genes involved in the phosphoinositide 3-kinase (PI3K)/ protein kinase B (AKT), forkhead box O1 (FoxO1), mammalian target of rapamycin and AMPK pathways (AKT1, AKT2, FoxO1, and sirtuin 1), as well as the protein expression of cytochrome C and the apoptosis rate were upregulated., Conclusion: In conclusion, our data suggested that SCD1 was involved in enhancing the PA tolerance of goose primary hepatocytes by regulating inflammation- and apoptosisrelated genes expression.

This study investigated the effects of 9t18:1 (representing I-TFAs), 9t16:1, and 11t18:1 (representing R-TFAs) and their mixtures on the normal human hepatocyte LO2 cell function, the possible mechanism of lipid metabolism by lipidomics, and the relationship between phospholipase A2 (PLA2) and the arachidonic acid (AA) metabolic pathway. Here, we found that the damaging effect of 9t18:1 on the LO2 cell function was significantly greater than those of 11t18:1 and 9t16:1 ( p < 0.05), and the damaging effects of CHB and HSO were significantly greater than those of HHB and CM ( p < 0.05). The lipidomic results showed that TFAs and TFA mixtures caused a significant change in the lipid profiles of LO2 cells, in which the TAG, PL, and OL contents increased significantly. Moreover, 9t18:1 regulated only the protein expression of cPLA2 but did not participate in the AA metabolic pathway, while 11t18:1 and 9t16:1 participated in the COX-2 and CYP450 pathways, respectively.

The study was aimed to investigate the protective effect and pharmacodynamic difference of the ethanol extracts of Schisandrae Sphenantherae Fructus and Schisandrae Chinensis Fructus on the drug-induced liver injury induced by acetaminophen.The cell activations of LO2 cells treated by Schisandrae Sphenantherae Fructus and Schisandrae Chinensis Fructus ethanol extracts were tested by CCK-8 essay.The effects of ethanol extracts on cell survival rate,the activities of ALT and AST in culture medium were detected based on the injury model of LO2 cells induced by APAP.Further,in purpose to observe the protective effect of Schisandrae Sphenantherae Fructus and Schisandrae Chinensis Fructus ethanol extracts on a mouse model of liver injury induced by intraperitoneal injectionof acetaminophen was established.Mice were randomly divided into control group,model group,positive drug group and Schisandrae Sphenantherae Fructus and Schisandrae Chinensis Fructus ethanol extracts administration groups.The activities of ALT and AST in the serum and the levels of MDA,SOD,GSH and GSH-PX in the liver homogenate of the mice were detected by commercial kits.The HEstaining was used to observe the histopathological changes of liver tissue in each group and the TUNEL staining was used to observe the hepatocyte apoptosis.The results showed that the ethanol extracts at less than 1 g·L~(-1)did not affect the activity of LO2 cell.Compared with the model group,the cell survival rates of the Schisandrae Sphenantherae Fructus and Schisandrae Chinensis Fructus ethanol extract administration groups was significantly increased;the ALT and AST in the culture medium were distinct decreased(P<0.05 or P<0.01).The survival rate of Schisandrae Sphenantherae Fructus and Schisandrae Chinensis Fructus ethanol extract from different batches were similar,while that of the Schisandrea Sphenatherae Fructus ethanol extract from different batches were quite different(P<0.05or P<0.01).Further,animal experiments showed that Schisandrae Sphenantherae Fructus and Schisandrae Chinensis Fructus ethanol extract administration groups could markedly inhibit the increase of ALT and AST levels in serum(P<0.01),decrease MDA content significantly(P<0.01),and increase GSH,GSH-PX and SOD activity significantly(P<0.01).Among them,compared with other groups,Schisandrae Sphenantherae Fructus ethanol extract-2 group showed the best effect(P<0.05 or P<0.01)while Schisandrae Sphenantherae Fructus ethanol extract-1 showed a poor effect(P<0.05 or P<0.01).In conclusion,both Schisandrae Sphenantherae Fructus and Schisandrae Chinensis Fructus ethanol extracts have protective effect on APAP-induced drug-induced liver injury and there was a certain difference in the efficacy between Schisandrae Sphenantherae Fructus and Schisandrae Chinensis Fructus ethanol extracts from different habitats.