Geniposide Suppresses Hepatic Glucose Production &lt;i&gt;via&lt;/i&gt; AMPK in HepG2 Cells

Guo, Lixia; Zheng, Xiangkuo; Liu, Jianhui; Yin, Zhongyi

doi:10.1248/bpb.b15-00591

Cited by 27 publications

(11 citation statements)

References 33 publications

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“…It also reverses glucose-induced impairment of insulin release, induces phosphorylation of AMPK, and inhibits hepatic glucose production. It appears that AMPK plays a key role in geniposideregulated GSIS in pancreatic β cells and glucose production in HepG2 cells [60]. These results are consistent with outcomes of other studies [61,62].…”

Section: Iridoids In Fatty Liver Diseasesupporting

confidence: 91%

The Effects of Natural Iridoids and Anthocyanins on Selected Parameters of Liver and Cardiovascular System Functions

Danielewski

Matuszewska

Nowak

et al. 2020

Oxidative Medicine and Cellular Longevity

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The old adage says, “you are what you eat.” And although it is a banality repeated by many with a grain of salt, it also has quite a bit of truth in it, as the products we eat have a considerable impact on our health. Unfortunately, humanity is eating worse from one year to another, both in terms of product quality and eating habits. At the same time, it is brought up frequently that plant products should form the basis of our diet. This issue was also reflected in the new version of the food pyramid. Iridoids and anthocyanins are groups of plant compounds with proven beneficial effects on health. Both groups affect the cardiovascular system and the liver functions. Although many mechanisms of action and the therapeutic effects of these compounds have already been learned, intensive animal and clinical research is still underway to explore their new curative mechanisms and effects or to broaden our knowledge of those previously described. In this article, we review the effects of natural iridoids and anthocyanins on selected parameters of liver and cardiovascular system functions.

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Section: Iridoids In Fatty Liver Diseasesupporting

confidence: 91%

The Effects of Natural Iridoids and Anthocyanins on Selected Parameters of Liver and Cardiovascular System Functions

Danielewski

Matuszewska

Nowak

et al. 2020

Oxidative Medicine and Cellular Longevity

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“…Caco-2 cells were transfected with small interfering RNA (siRNA) or c-DNA as previously described [15] . Caco-2 cells were placed into 6-well plates for 24 h. Cells were transfected with specific siRNA (Genepharma, Shanghai, China) or c-DNA targeting AMPK with Lipofectamine 2000 (Invitrogen).…”

Section: Cell Transfectionmentioning

confidence: 99%

Geniposide ameliorates TNBS-induced experimental colitis in rats via reducing inflammatory cytokine release and restoring impaired intestinal barrier function

et al. 2017

Acta Pharmacol Sin

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Geniposide is an iridoid glycosides purified from the fruit of Gardenia jasminoides Ellis, which is known to have antiinflammatory, antioxidative and anti-tumor activities. The present study aimed to investigate the effects of geniposide on experimental rat colitis and to reveal the related mechanisms. Experimental rat colitis was induced by rectal administration of a TNBS solution. The rats were treated with geniposide (25, 50 mg·kg, ig) or with sulfasalazine (SASP, 100 mg·kg, ig) as positive control for 14 consecutive days. A Caco-2 cell monolayer exposed to lipopolysaccharides (LPS) was used as an epithelial barrier dysfunction model. Transepithelial electrical resistance (TER) was measured to evaluate intestinal barrier function. In rats with TNBS-induced colitis, administration of geniposide or SASP significantly increased the TNBS-decreased body weight and ameliorated TNBS-induced experimental colitis and related symptoms. Geniposide or SASP suppressed inflammatory cytokine (TNF-α, IL-1β, and IL-6) release and neutrophil infiltration (myeloperoxidase activity) in the colon. In Caco-2 cells, geniposide (25-100 μg/mL) ameliorated LPS-induced endothelial barrier dysfunction via dose-dependently increasing transepithelial electrical resistance (TER). The results from both in vivo and in vitro studies revealed that geniposide down-regulated NF-κB, COX-2, iNOS and MLCK protein expression, up-regulated the expression of tight junction proteins (occludin and ZO-1), and facilitated AMPK phosphorylation. Both AMPK siRNA transfection and AMPK overexpression abrogated the geniposide-reduced MLCK protein expression, suggesting that geniposide ameliorated barrier dysfunction via AMPKmediated inhibition of the MLCK pathway. In conclusion, geniposide ameliorated TNBS-induced experimental rat colitis by both reducing inflammation and modulating the disrupted epithelial barrier function via activating the AMPK signaling pathway.

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“…The experimental procedure of RNA interference on AMPK was carried out as described before (Guo et al, ). Generally, before transient transfection, INS‐1 cells were placed into six‐well plates, and continued to incubate overnight.…”

Section: Methodsmentioning

confidence: 99%

Geniposide protects pancreatic β cells from high glucose‐mediated injury by activation of AMP‐activated protein kinase

Liu

Hao

Yin

et al. 2017

Cell Biology International

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Our previous works indicated that geniposide could regulate glucose-stimulated insulin secretion (GSIS), and improved chronic high glucose-induced dysfunctions in pancreatic β cells, but the molecular mechanisms remain largely unknown. In the present study, we investigated the role of 5'-AMP-activated protein kinase (AMPK) in high glucose induced cell injury and explored the associated molecular mechanisms in rat INS-1 pancreatic β cells. Data suggested that geniposide obviously prevented the cell damage induced by high (25 mM) glucose in INS-1 cells, which increased the protein levels of cell apoptosis-associated enzymes, including heme oxygenase-1 (HO-1), and Bcl-2, but apparently attenuated the protein level of Bax, an apoptotic protein. In addition, Compound C, an AMPK inhibitor, remarkably inhibited the effects of geniposide on the protein levels of HO-1, Bcl-2, and Bax, but AICAR, an AMPK activator, potentiated the role of geniposide on the protein levels of HO-1, Bcl-2, and Bax. More importantly, geniposide directly prevented the cleavage of caspase-3 induced by high glucose, and this effect was also evidently prohibited by the pre-incubation of compound C in high glucose-treated INS-1 cells. Furthermore, using the method of RNA interfere, we further proved that treatment with AMPK siRNA attenuated the effects of geniposide on the apoptosis-associated proteins and cell viability. All these data suggest that AMPK plays a crucial role on geniposide antagonizing high glucose-induced pancreatic β cells injury.

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Geniposide Suppresses Hepatic Glucose Production <i>via</i> AMPK in HepG2 Cells

Cited by 27 publications

References 33 publications

The Effects of Natural Iridoids and Anthocyanins on Selected Parameters of Liver and Cardiovascular System Functions

The Effects of Natural Iridoids and Anthocyanins on Selected Parameters of Liver and Cardiovascular System Functions

Geniposide ameliorates TNBS-induced experimental colitis in rats via reducing inflammatory cytokine release and restoring impaired intestinal barrier function

Geniposide protects pancreatic β cells from high glucose‐mediated injury by activation of AMP‐activated protein kinase

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