Isoliquiritigenin attenuates oxidative hepatic damage induced by carbon tetrachloride with or without buthionine sulfoximine

Zhao, Zhenglin; Park, Sang Mi; Guan, Lina; Wu, Yihui; Lee, Jong Rok; Kim, Sang Chan; Kim, Young Woo; Zhao, Rongjie

doi:10.1016/j.cbi.2014.10.030

Cited by 27 publications

(11 citation statements)

References 36 publications

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“…It is found ubiquitously in foods and beverages, and tobacco. ISL has been reported to exhibit a wide range of distinct biological properties and pharmacological activities, including anti-inflammatory, anti-oxidation, antiplatelet aggregation, cardioprotective effects against ischemia-reperfusion, and estrogenic properties (11)(12)(13). ISL has also been reported to suppress the proliferation and to induce the apoptosis of…”

Section: Introductionmentioning

confidence: 99%

Isoliquiritigenin inhibits proliferation and metastasis of MKN28 gastric cancer cells by suppressing the PI3K/AKT/mTOR signaling pathway

Zhang

Wang

Sun³

et al. 2018

Mol Med Report

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Isoliquiritigenin (ISL) is a ﬂavonoid extracted from licorice root, which is known to serve important antitumor roles in numerous types of cancers; however, its effect on gastric cancer remains to be elucidated. The present study aimed to explore the roles and underlying mechanisms of ISL in MKN28 gastric cancer cells. MKN28 cell proliferation was measured using the Cell Counting Kit‑8 (CCK8) assay. A Transwell assay was used to determine the effects of ISL on the migration and invasion of MKN28 cells. Apoptosis was assessed by flow cytometry, and the expression levels of apoptosis‑, autophagy‑ and signaling pathway‑related proteins were detected by western blot analysis. The results of the CCK8 assay demonstrated that ISL significantly inhibited the proliferation of MKN28 cells (P<0.05). Transwell assays demonstrated that the migration and invasion of MKN28 cells were significantly inhibited following treatment with ISL (P<0.05). Flow cytometric analysis indicated that ISL induced apoptosis of MKN28 cells. In addition, western blot analysis revealed that the ratio of microtubule‑associated proteins 1A/1B light chain 3B (LC3)II/LC3I was upregulated, as was Beclin 1 expression; however, p62 was downregulated following ISL pretreatment, thus suggesting that ISL triggered autophagy in MKN28 cells. In addition, the phosphorylation levels of protein kinase B (AKT) and mammalian target of rapamycin (mTOR) were significantly reduced following ISL treatment. These results indicated that ISL may influence apoptosis and autophagy in MKN28 cells by suppressing the phosphoinositide 3‑kinase/AKT/mTOR signaling pathway. In conclusion, the findings of the present study suggested that ISL may inhibit MKN28 cell proliferation, migration and invasion by inducing apoptosis and autophagy, implying potential as a therapeutic agent for gastric cancer.

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Section: Introductionmentioning

confidence: 99%

Isoliquiritigenin inhibits proliferation and metastasis of MKN28 gastric cancer cells by suppressing the PI3K/AKT/mTOR signaling pathway

Zhang

Wang

Sun³

et al. 2018

Mol Med Report

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“…To induce liver injury, CCl 4 (0.5 mL/kg/day) dissolved in corn oil was intraperitoneally (i.p.) injected into the mice ( n = 5/group) for 2 days as described by Zhao et al with minor modification [19]. In addition, BFE dissolved in water was administered orally (p.o.)…”

Section: Methodsmentioning

confidence: 99%

Activation of AMPK byBuddleja officinalisMaxim. Flower Extract Contributes to Protecting Hepatocytes from Oxidative Stress

Jung

Lee

Park

et al. 2017

Evidence-Based Complementary and Alternative Medicine

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The Buddleja officinalis Maxim. flower is used in traditional Chinese and Korean medicine to treat inflammation, vascular diseases, headache, and stroke, as well as enhance liver function. This research investigated the effects of B. officinalis Maxim. flower extract (BFE) on hepatotoxicity. The cytoprotective effects and mechanism of BFE against severe mitochondrial dysfunction and H2O2 production in hepatotoxicity induced by coadministration of arachidonic acid (AA) and iron were observed in the HepG2 cell line. In addition, we performed blood biochemical, histopathological, and histomorphometric analyses of mice with carbon tetrachloride- (CCl4-) induced acute liver damage. BFE inhibited the AA + iron-mediated hepatotoxicity of HepG2 cells. Moreover, it inhibited mitochondrial dysfunction, H2O2 production, and glutathione depletion mediated by AA + iron in the same cells. Meanwhile, the cytoprotective effects of BFE against oxidative stress were associated with the activation of AMP-activated protein kinase (AMPK). In particular, based on the histopathological observations, BFE (30 and 100 mg/kg) showed clear hepatoprotective effects against CCl4-induced acute hepatic damage. Furthermore, it inhibited 4-hydroxynonenal and nitrotyrosine immunoreactivity in hepatocytes. These results provide evidence that BFE has beneficial hepatoprotective effects against hepatic damage via the activation of AMPK pathway. Accordingly, BFE may have therapeutic potential for diverse liver disorders.

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“…The stored NaccSh tissue samples were sonicated (10%, w / v ) in ice-cold 0.1 M phosphate buffer (pH 7.4), centrifuged at 700× g for 10 min at 4 °C, and the supernatants were collected to measure parameters of oxidative stress. Malondialdehyde (MDA) levels, which are an index of lipid peroxidation, were determined using a thiobarbituric acid method and an MDA kit (Jiancheng Bioengineering Institute, Nanjing, China) [ 14 ]. The activities of accumbal antioxidant enzymes, including superoxide dismutase (SOD) and catalase (CAT), were assayed spectrophotometrically using the respective kits from Jiancheng Bioengineering Institute.…”

Section: Methodsmentioning

confidence: 99%

“…G. radix contains flavonoids and different types of pentacyclic triterpene saponin, a group which includes liquiritigenin, liquiritin, isoliquiritigenin, glycyrrhizin, and glycyrrhizic acid [ 13 ]. Historically, G. radix has received pharmacological interest due to its anti-oxidant, anti-inflammatory, antitumor, and antitussive actions [ 14 , 15 ]. However, over the past decade, several studies have revealed G. radix has neuropharmacological properties such as neuroprotective, antidepressant, and anxiolytic effects [ 16 – 18 ].…”

Section: Introductionmentioning

confidence: 99%

Blockade of nicotine sensitization by methanol extracts of Glycyrrhizae radix mediated via antagonism of accumbal oxidative stress

Zhao

Kim

Liu

et al. 2017

BMC Complement Altern Med

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BackgroundWe previously reported that a methanol extract of Glycyrrhizae radix (MEGR) blocked methamphetamine-induced locomotor sensitization and conditioned place preference in rats. In the present study, the effects of MEGR on repeated nicotine-induced locomotor sensitization and enhanced extracellular dopamine (DA) release in the nucleus accumbens (Nacc) were evaluated.MethodsMale Sprague–Dawley rats received repeated administrations of nicotine (0.4 mg/kg, subcutaneous) or saline twice a day for 7 d and were challenged with nicotine 4 d after the last daily dosing. During the 4-d withdrawal period, the rats were treated once a day with MEGR (60 or 180 mg/kg/d). Extracellular DA levels were measured by in vivo microdialysis, the malondialdehyde levels and the activities of superoxide dismutase and catalase in the Nacc were biochemically evaluated, and the expression of antioxidant proteins was confirmed by Western blot assays. All data were assessed with analysis of variance tests followed by post-hoc comparison tests and p values <0.05 were considered statistically significant.ResultsThe expression of repeated nicotine-induced locomotor sensitization was dose-dependently attenuated by MEGR, and 180 mg/kg/d MEGR significantly inhibited augmented accumbal DA release induced by a direct local challenge of nicotine. Moreover, 180 mg/kg/d MEGR reversed increases in malondialdehyde production, decreases in superoxide dismutase and catalase activities, and the reduced expression of nuclear factor erythroid 2–related factor 2 and heme oxygenase 1 in the nicotine-sensitized Nacc.ConclusionsThese results suggest that MEGR inhibited nicotine-induced locomotion and dopaminergic sensitization via antioxidant action.

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Isoliquiritigenin attenuates oxidative hepatic damage induced by carbon tetrachloride with or without buthionine sulfoximine

Cited by 27 publications

References 36 publications

Isoliquiritigenin inhibits proliferation and metastasis of MKN28 gastric cancer cells by suppressing the PI3K/AKT/mTOR signaling pathway

Isoliquiritigenin inhibits proliferation and metastasis of MKN28 gastric cancer cells by suppressing the PI3K/AKT/mTOR signaling pathway

Activation of AMPK byBuddleja officinalisMaxim. Flower Extract Contributes to Protecting Hepatocytes from Oxidative Stress

Blockade of nicotine sensitization by methanol extracts of Glycyrrhizae radix mediated via antagonism of accumbal oxidative stress

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