Ginkgolide A ameliorates non-alcoholic fatty liver diseases on high fat diet mice

Jeong, Hoyoung; Kim, Kang-Hoon; Lee, In Seung; Park, Ji Young; Kim, Yumi; Kim, Ki Suk; Jang, Hyeung-Jin

doi:10.1016/j.biopha.2017.01.114

Cited by 41 publications

(24 citation statements)

References 49 publications

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“…Ginkgolides are primarily terpenoids and have been associated with more pharmacological effect, including ginkgolides A, B, C, L, M, P, and Q [14,18]. Previous studies have found that ginkgolide A may improve NAFLD in high-fat diet (HFD)-induced obese mice [19]. Our earlier experiments also indicated that ginkgolide C can modulate adipogenesis by activating the AMPK signaling pathway in 3T3-L1 adipocytes [20].…”

Section: Introductionmentioning

confidence: 84%

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WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

Wang¹,

Liou²,

Wu³

et al. 2018

Oncotarget

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Ginkgolide B is isolated from Ginkgo biloba leaves. It has multiple biological functions, including alleviating lung injury and ischemic stroke in mice and protecting pancreatic beta cells and improving endothelial dysfunction in diabetic mice. Here we sought to determine whether ginkgolide B ameliorates nonalcoholic fatty liver disease (NALFD) in high-fat diet (HFD)-induced obese mice. We also evaluated whether or not ginkgolide B reduces lipid accumulation of hepatocytes in vitro. C57BL/6 mice were fed with HFD and treated with ginkgolide B by intraperitoneal injection twice a week for last 10 weeks of the 14-week HFD feeding period. In addition, HepG2 cells were treated with oleic acid to establish a fatty liver cell model and exposed to various concentrations of ginkgolide B. Ginkgolide B significantly decreased hepatic lipid accumulation and alleviated steatosis in HFD-induced obese mice. It also reduced body weight and epididymal adipose tissue weight. Serum assay results showed that ginkgolide B inhibited leptin, alanine aminotransferase, and aspartate aminotransferase levels and increased HDL levels compared to obese mice. It also decreased fatty acid synthase expression and increased Sirt-1 and phosphorylation of AMP-activated protein kinase α in liver tissue. Furthermore, ginkgolide B significantly inhibited lipid accumulation and expression of adipogenesis-related proteins and increased adipolysis-associated protein expression in hepatocytes in vitro. These results suggest that ginkgolide B is an effective natural compound for alleviating hepatic lipid accumulation and reducing body weight in obese mice. It also ameliorated NALFD in HFD-induced obese mice. www.impactjournals.com/oncotarget/

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Section: Introductionmentioning

confidence: 84%

“…An important indicator of NAFLD is excess lipid accumulation in hepatocytes [19]. NAFLD is defined as lipid content greater than 5% in liver tissue or liver slices containing more than 10% fat vacuoles [33].…”

Section: Discussionmentioning

confidence: 99%

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

Wang¹,

Liou²,

Wu³

et al. 2018

Oncotarget

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“…Moreover, the lipid droplets were observed in results of H&E (Figure 1) and Oil red stainings (Figure 2A) as well, while the quantification of stained areas showed the significant increase (p<0.05) between Control and HFD groups ( Figure 2B). Several previous studies also indicated the similar phenotypes under a HFD induced mouse model [16,17]. In addition, it was proclaimed that chronic inflammatory responses in livers or adipose tissues might be the driving force for NAFLD pathological progressing [15].…”

Section: Discussionmentioning

confidence: 76%

Preventive Effects of Ophiocordyceps sinensis Mycelium on High-Fat Diet Induced Lipid Dysregulation and Hepatic Inflammation of Mice

Chou¹,

Lin²,

Wu³

et al. 2017

JFNR

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Dyslipidemia is regarded as one of risk factors related to cardiovascular disease and hepatosteatosis widely. Due to westernized diet habits and lifestyle changes, there is a high prevalence of those lipid-dysregulated diseases, i.e. fatty liver, hyperlipidemia, diabetes etc. However, the liver holds the lipid homeostasis so hepatoprotective nutraceuticals against high-fat diet (HFD) induced dyslipidemia may be potential for a public demand. This study demonstrated that OSM containing 10% polysaccharides and 0.25% adenosine can decrease (p<0.05) serum and liver triglyceride (TG) contents, and meanwhile, increased (p<0.05) fecal cholesterol (TC) levels in HFD fed mice. Moreover, Ophiocordyceps sinensis mycelium (OSM) also decreased (p<0.05) serum low-density lipoprotein cholesterol (LDLC) levels and the atherosclerosis index (LDLC/high-density lipoprotein cholesterol (HDLC)) in HFD fed mice. Regarding the liver damage, OSM supplementation attenuated serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) values, and liver tumor necrosis factor-α (TNF-α) levels in HFD fed mice. Taken together, OSM showed an ameliorative effect of the hepatosteatosis development and lipid-dysregulated-related diseases in a HFD habit.

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“…Data from a study by Malhi et al [96] show that saturated fatty acids also induce JNK-dependent hepatocyte apoptosis by activating pro-apoptotic Bid-Bach proteins from the internal signalling pathway. Antioxidant gingolide A increased the levels of antiapoptotic Bcl-2, while it decreased Bax, phosphorylated JNK and cleaved caspase-3 and -9 levels in the livers of animals with high fat diet [97]. The manifestation of a synergistic effect on the activation of the JNK signalling pathway from depletion of mitochondrial reduced glutathione and elevated peroxides, such as MDA, was found in the steatal liver in experimental animals and patients [74].…”

Section: Hne and Liver Injury In Nafldmentioning

confidence: 89%

4-Hydroxynonenal (HNE) and hepatic injury related to chronic oxidative stress

Bekyarova

Tzaneva

Bratoeva

et al. 2019

Biotechnology & Biotechnological Equipment

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4-Hydroxynonenal (HNE), a major end-product of free-radical activated peroxidation of polyunsaturated fatty acids, has attracted great scientific interest. HNE is more stable than free radicals and can diffuse within the cell or leave it and react with targets far from the initial site. These reactive aldehyde species are considerably reactive, producing multiple intra-and inter-molecular covalent adducts with biomolecules such as proteins, DNA and phospholipids. HNE is the most intensively studied aldehyde in relation to its physiological and protective function as a signalling molecule that stimulates gene expression and cell survival, as well as for its pathophysiological role as a toxic messenger that can propagate and amplify oxidative injury and promote mitochondrial dysfunction and cell death. Non-alcoholic fatty liver disease (NAFLD) is the most prevalent form of chronic liver disease in the world associated with oxidative stress, mitochondrial dysfunction and hepatocellular apoptosis. In this review we focus our attention on the molecular mechanism of the signalling and regulatory action of HNE. The role of HNE as a potent mediator for progression of liver injury in NAFLD is also discussed.

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Ginkgolide A ameliorates non-alcoholic fatty liver diseases on high fat diet mice

Cited by 41 publications

References 49 publications

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

WITHDRAWN: Ginkgolide B reduces hepatic lipid accumulation and ameliorates nonalcoholic fatty liver disease in high-fat dietâ€“induced obese mice

Preventive Effects of <i>Ophiocordyceps </i><i>s</i><i>inensis </i>Mycelium on High-Fat Diet Induced Lipid Dysregulation and Hepatic Inflammation of Mice

4-Hydroxynonenal (HNE) and hepatic injury related to chronic oxidative stress

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