Hepatoprotective activity of flavonoids from Cichorium glandulosum seeds in vitro and in vivo carbon tetrachloride-induced hepatotoxicity

Tong, Jing; Yao, Xiaofeng; Zeng, Hong; Zhou, Gao; Chen, Yuxin; B, Ma; Wang, Youwei

doi:10.1016/j.jep.2015.08.045

Cited by 46 publications

(22 citation statements)

References 40 publications

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“…The ALT, AST, and LDH activity levels in the cell supernatants were determined using commercial kits according to the instructions [ 26 ]. Absorbances were measured using a microplate reader, and the activities of AST, ALT, and LDH were expressed as units per liter (U L −1 ).…”

Section: Methodsmentioning

confidence: 99%

Ethyl Acetate Fraction of Hemerocallis citrina Baroni Decreases Tert‐butyl Hydroperoxide‐Induced Oxidative Stress Damage in BRL‐3A Cells

Wang

Hou

et al. 2018

Oxidative Medicine and Cellular Longevity

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The main purposes of this study were to screen the antioxidant activities of various fractions of Hemerocallis citrina Baroni and test their hepatoprotective effects in vitro. Antioxidant assays (2,2-diphenyl-1-picrylhydrazyl (DPPH), 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) (ABTS), and reducing power experiments) and tert-butyl hydroperoxide- (t-BHP-) induced BRL-3A oxidative damage experiments were performed in vitro. The H. citrina ethyl acetate fraction (HCEA) was determined to have strong antioxidant activity because of its high flavonoid and polyphenol content. Ultraperformance liquid chromatography- (UPLC-) photodiode array (PDA)/mass spectrometry (MS) analysis showed that the main components of the HCEA were flavonoids and caffeic acid derivatives. A total of 17 compounds were identified. HCEA also effectively protected the liver against t-BHP-induced oxidative stress injury and significantly reduced reactive oxygen (ROS) accumulation. Moreover, HCEA significantly reduced levels of alanine aminotransferase (ALT), aspartate transaminase (AST), and lactate dehydrogenase (LDH). Further studies have shown that HCEA inhibits t-BHP-induced apoptosis by increasing B-cell lymphoma-2 (BCL-2) activity and decreasing caspase-3 and caspase-9 activity. Moreover, HCEA enhanced the activity of antioxidant enzymes superoxide dismutase (SOD) and catalase (CAT), as well as the total antioxidant capacity (T-AOC), and increased the antioxidant level of glutathione (GSH) in BRL-3A cells. HCEA increased the antioxidant capacity of cells by increasing the gene expression of AMP-activated protein kinase (AMPK), extracellular signal-regulated kinase (ERK), P38, nuclear factor, erythroid 2 like 2 (Nrf2), SOD, glutamate-cysteine ligase catalytic subunit (GCLC), glutamate-cysteine ligase modifier subunit (GCLM), and heme oxygenase 1 (HO-1), which are associated with antioxidant pathways to protect against oxidative stress. In conclusion, HCEA protected BRL-3A cells against t-BHP-induced oxidative stress damage via antioxidant and antiapoptosis pathways. Therefore, H. citrina Baroni may serve as a potential hepatoprotective drug.

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Section: Methodsmentioning

confidence: 99%

Ethyl Acetate Fraction of Hemerocallis citrina Baroni Decreases Tert‐butyl Hydroperoxide‐Induced Oxidative Stress Damage in BRL‐3A Cells

Wang

Hou

et al. 2018

Oxidative Medicine and Cellular Longevity

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“…no. 1037806; Gibco; Thermo Fisher Scientific, Inc.) under a humidified atmosphere of 5% CO 2 at 37°C for 24 h. Following this, the cells were used for the experiments and divided into the following groups: Groups 1 and 2 (normal control): Culture media were removed and cells were treated with 100 µl of serum-free medium for 2 h. A further 100 µl of serum-free medium was then added for the following 24 h; groups 3 and 4 (CCl 4 treatment): Culture media were removed, and the cells were treated with 100 µl of serum-free medium for 2 h. A further 100 µl of serum-free medium containing CCl 4 at the selected concentration (1% v/v) ( 17 ) was added for the following 24 h. CCl 4 cytotoxicity was determined using a CCK-8 assay kit. The cells were treated with CCK-8 reagent (10 µl/well) and incubated for a further 3–4 h. The optical density (OD) was recorded at 450 nm in a microplate reader (Thermo Fisher Scientific, Inc.).…”

Section: Methodsmentioning

confidence: 99%

Downregulation of Glt25d1 aggravates carbon tetrachloride‑induced acute hepatic injury through activation of the TGF‑β1/Smad2 signaling pathway

et al. 2018

Mol Med Report

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Collagen β (1-O) galactosyltransferase 1 (GLT25D1) has been reported to transfer galactose to hydroxylysine residues via β (1-O) linkages in collagen. The present study investigated the function of the collagen galactosyltransferase activity of GLT25D1 against carbon tetrachloride (CCl4)-induced acute liver injury in vitro. Glt25d1+/− mice and wild-type (WT) mice were injected intraperitoneally with the same dose of CCl4. The grade of hepatic injury and the extent of hepatocyte necrosis in the acute phase were assessed 48 h following CCl4 injection. Hepatocyte necrosis was evaluated by histological examination and by serum alanine aminotransferase and aspartate aminotransferase levels, which were higher in the Glt25d1+/− mice compared with those in the WT mice. Reverse transcription-quantitative polymerase chain reaction was performed, and the results demonstrated that the mRNA expression levels of inflammatory cytokines, including tumor necrosis factor-α and interleukin-6 were significantly increased in the Glt25d1+/− mice. Furthermore, western blot analyses were performed, and the results demonstrated that the protein levels of cleaved caspase-3 and −9 were also markedly increased in the Glt25d1+/− liver, indicating that hepatocyte apoptosis was induced. Additionally, the expression levels of transforming growth factor (TGF)-β1 and phosphorylated small mothers against decapentaplegic (Smad)2 were markedly upregulated, indicating activation of the TGF-β1/Smad2 signaling pathway during CCl4-induced acute liver injury in Glt25d1+/− mice. CCl4 administration also resulted in severe damage to Glt25d1+/− primary hepatocytes in vitro. Taken together, the downregulation of Glt25d1 deteriorated CCl4-induced liver injury in mice, which may involve triggering inflammatory responses, apoptosis and TGF-β1/Smad2 signaling pathway activation.

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“…[34] Briefly, HepG2 cells (3 × 10 6 cells/well) were maintained in different groups in 96 well culture plates. Solutions of CCl 4 (1% v/v), silymarin, and extracts were prepared in serum free DMEM containing DMSO (0.1% v/v).…”

Section: In Vitro Hepatoprotective Effect On Hepg2 Cell Line Against mentioning

confidence: 99%

Untitled

Modi¹

2017

IJGP

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Introduction: This work was done to determine phytochemical content, antioxidant activity, and hepatoprotective effects of Zizyphus xylopyrus leaves extracts against carbon tetrachloride-induced hepatotoxicity in in vitro and in vivo models. Materials and Methods: The total flavonoids content (TFC), total phenolic content (TPC), and total tannin content (TTC) were determined using quercetin and tannic acid equivalents, as standard while antioxidant activities of extracts were determined using the standard in vitro methods. All the extracts subjected to in-vitro HepG2 cell line study as well as to evaluate in vivo hepatoprotective effects against carbon tetrachloride (CCl 4 ) intoxicated rats. Results: Among all extracts, ethyl acetate extract (EAE) possess potent antioxidant activity, viz., ferric reducing ability of plasma (abs = 0.379 ± 0.07), 2,2-diphenyl-1-picrylhydrazyl (inhibitory concentration 50% [IC 50 ]: 103.50 ± 2.05 µg/mL), OH• (89.33 ± 1.79 µg/mL), NO • (IC 50 129.34 ± 1.29 µg/mL), O 2ˉ (IC 50 62.03 ± 2.78 µg/mL), and inhibition of lipid peroxidation (110.05 ± 2.96 µg/mL). Treatment with EAE significantly increased the cell viability (IC 50 80.93 ± 1.02 µg/mL) by preventing CCl 4 induced cell damage in in-vitro HepG2 cell line. In case of both prophylactic and curative study, EAE extract significantly (P < 0.001) decreased CCl 4 -induced increased serum liver enzymes activities in CCl 4 -intoxicated rats, comparable to silymarin. Hepatoprotective potential further supported by pentobarbitone induced sleeping time and improved hepatic tissue histopathology. Study results suggest that antioxidant activity and hepatoprotective effect of EAE might be due to presence of polyphehols, viz., TFC (43.76 ± 0.78 Quercetin equivalent [QE] mg/g extract), TPC (194.16 ± 0.74 gallic acid equivalent [GAE] mg/g extract), and TTC (20.45 ± 2.31 GAE mg/g extract). Reversed-phase highperformance liquid chromatography analysis results showed highest quercetin content (32.8 ± 0.24 mg/g) in EAE. Conclusion: This study advocated that due to the presence of flavonoids, Z. xylopyrus leaves exhibited marked antioxidant and hepatoprotective activities.

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Hepatoprotective activity of flavonoids from Cichorium glandulosum seeds in vitro and in vivo carbon tetrachloride-induced hepatotoxicity

Cited by 46 publications

References 40 publications

Ethyl Acetate Fraction of Hemerocallis citrina Baroni Decreases Tert‐butyl Hydroperoxide‐Induced Oxidative Stress Damage in BRL‐3A Cells

Ethyl Acetate Fraction of Hemerocallis citrina Baroni Decreases Tert‐butyl Hydroperoxide‐Induced Oxidative Stress Damage in BRL‐3A Cells

Downregulation of Glt25d1 aggravates carbon tetrachloride‑induced acute hepatic injury through activation of the TGF‑β1/Smad2 signaling pathway

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