Inhibition of liver X receptor-α-dependent hepatic steatosis by isoliquiritigenin, a licorice antioxidant flavonoid, as mediated by JNK1 inhibition

Kim, Young Mi; Kim, Tae Hyun; Yang, Yoon Mee; Ryu, Da Hye; Hwang, Se Jin; Lee, Jong Rok; Kim, Sang Chan; Kim, Sang Geon

doi:10.1016/j.freeradbiomed.2010.09.001

Cited by 43 publications

(37 citation statements)

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“…Previously, we reported that several Nrf2 activators such as isoliquiritigenin, liquiritigenin, ajoene, and sauchinone inhibit LXRa-mediated lipogenesis (17,(23)(24)(25). Treatment with each of these agents decreased HFD-induced body and liver weight gains, fasting blood glucose content, and plasma free fatty acid levels, strengthening the role of Nrf2 in the treatment of hepatic steatosis.…”

Section: Nrf2's Activation Of Fxr For Anti-steatosismentioning

confidence: 87%

Nrf2 Inhibits LXRα-Dependent Hepatic Lipogenesis by Competing with FXR for Acetylase Binding

Kay

Kim

Hwang

et al. 2011

Antioxidants & Redox Signaling

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Section: Nrf2's Activation Of Fxr For Anti-steatosismentioning

confidence: 87%

Nrf2 Inhibits LXRα-Dependent Hepatic Lipogenesis by Competing with FXR for Acetylase Binding

Kay

Kim

Hwang

et al. 2011

Antioxidants & Redox Signaling

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“…Cyclooxygenase-2, a pro-inflammatory enzyme, can be up-regulated by redox-sensitive transcription factors at inflammation sites [16], and upregulation of its expression plays an important role on hepatocyte damage under increased oxidative stress conditions [18,39]. In different liver damage models, beneficial effects of inhibition of COX-2 enzyme by antioxidant therapies were observed [18,40].…”

Section: Discussionmentioning

confidence: 99%

“…In different liver damage models, beneficial effects of inhibition of COX-2 enzyme by antioxidant therapies were observed [18,40]. This is the first study that evaluates the effects of AP treatment on COX-2 level in this liver damage model.…”

Section: Discussionmentioning

confidence: 99%

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Allopurinol Ameliorates Thioacetamide-Induced Acute Liver Failure by Regulating Cellular Redox-Sensitive Transcription Factors in Rats

et al. 2012

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Oxidative stress plays important role in the development of acute liver failure. In this study, we investigated effects of allopurinol (AP) upon thioacetamide (TAA)-induced liver injury and the potential mechanisms leading to amelioration in inflammation with AP treatment. Acute liver failure was induced by intraperitoneal administration of TAA (300 mg/kg/day for 2 days). Thirty-five rats were divided into five groups as control (group 1), TAA (group 2), TAA + 25AP (group 3), TAA + 50 AP (group 4), and TAA + 100AP (group 5). The number of animals in each group was seven. At the end of the study, histopathological, biochemical, and western blot analysis were done. TAA treatment significantly increased serum levels of aminotransferases, liver malondialdehyde (MDA), nuclear factor-kappa B (NF-қB ), activator protein-1 (AP-1), tumor necrosis factor-alpha (TNF-α), cyclooxygenase-2 (COX-2) and interleukin-6 (IL-6) levels, and the necro-inflammation scores. Nevertheless, nuclear factor E2-related factor-2 and heme oxygenase-1 (HO-1) expressions in the liver were decreased by TAA. AP treatment significantly lowered the serum levels of aminotransferases (P < 0.01) and liver MDA, NF-κB, AP-1, TNF-α, COX-2, and IL-6 expressions (P < 0.05). Moreover, AP restored the liver Nrf2 and HO-1 expressions and improved the necro-inflammation scores significantly. AP improves oxidative stress-induced liver damage by regulating cellular redox-sensitive transcriptor factors and expression of pro-inflammatory and antioxidant defense mechanisms. AP probably exerts these beneficiary features by its free radical scavenging ability in a dose-dependent manner.

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“…Previous research has demonstrated that ISL has a variety of pharmacological activities, such as antioxidant, vasorelaxant, anti-inflammatory, estrogenic, and antiplatelet aggregation effects [7][8][9]. In addition, some studies have proven that ISL also possesses antitumor activity against different cancers, including hepatoma [10], uterine leiomyoma [11], prostate cancer [6,12,13], melanoma [14], gastric cancer [15], and breast cancer [16], but the effects of ISL on osteosarcoma cells are still unclear.…”

Section: Introductionmentioning

confidence: 99%

Isoliquiritigenin Suppresses Osteosarcoma U2OS Cell Proliferation and Invasion by Regulating the PI3K/Akt Signalling Pathway

Chen¹,

Liu

Yang³

et al. 2018

Chemotherapy

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Aims: Isoliquiritigenin (ISL) is a flavonoid, that has been shown to have antioxidant, vasorelaxant, anti-inﬂammatory, and antitumor activities. This study aimed to explore the antitumor effect of ISL on human osteosarcoma U2OS cells and investigate the mechanism of this effect. Methods: The effect of ISL on osteosarcoma U2OS cell proliferation, invasion, migration, and apoptosis were determined by a CCK8 assay, a transwell invasion assay, a transwell migration assay, and fluorescence-activated cell sorting, respectively. In addition, the protein expression levels of Bcl2, Bax, active Caspase-3, Akt, mTOR, p70, and Cyclin D1 were detected by western blotting. Results: ISL suppressed cell proliferation, inhibited invasion and migration, and promoted apoptosis in U2OS cells. After treatment with ISL, the protein expression levels of Bax and active Caspase-3 increased, while the level of Bcl-2 declined significantly. Furthermore, the phosphorylation levels of Akt and mTOR declined significantly compared with that of the control. Conclusion: ISL could retard proliferation and promote apoptosis of U2OS cells possibly by suppressing the PI3K/Akt signalling pathway, indicating that it might be a potential therapeutic agent for osteosarcoma treatment.

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Inhibition of liver X receptor-α-dependent hepatic steatosis by isoliquiritigenin, a licorice antioxidant flavonoid, as mediated by JNK1 inhibition

Cited by 43 publications

References 50 publications

Nrf2 Inhibits LXRα-Dependent Hepatic Lipogenesis by Competing with FXR for Acetylase Binding

Nrf2 Inhibits LXRα-Dependent Hepatic Lipogenesis by Competing with FXR for Acetylase Binding

Allopurinol Ameliorates Thioacetamide-Induced Acute Liver Failure by Regulating Cellular Redox-Sensitive Transcription Factors in Rats

Isoliquiritigenin Suppresses Osteosarcoma U2OS Cell Proliferation and Invasion by Regulating the PI3K/Akt Signalling Pathway

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