Effect of 6-gingerol on AMPK- NF-κB axis in high fat diet fed rats

Hashem, Reem M.; Rashed, Laila A.; Hassanin, Kamel M. A.; Hetta, Mona H.; Ahmed, A. M.

doi:10.1016/j.biopha.2017.01.035

Cited by 34 publications

(22 citation statements)

References 57 publications

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“…In a high-fat high-carbohydrate diet-fed rat model, ginger extract increased AMPKα phosphorylation and total AMPKα in skeletal muscle [ 30 ]. Hashem et al have reported that 6-gingerol treatment in rats fed high-fat diet improves inflammatory state and metabolic disorders via targeting the AMPK-NF-κB pathway [ 31 ]. In the present study, AMPK activity was enhanced by the HPG supplementation in WAT of HF diet fed rats.…”

Section: Discussionmentioning

confidence: 99%

Ginger Extract Ameliorates Obesity and Inflammation via Regulating MicroRNA-21/132 Expression and AMPK Activation in White Adipose Tissue

et al. 2018

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Ginger is a plant whose rhizome is used as a spice or folk medicine. We aimed to investigate the effect of ginger root extract on obesity and inflammation in rats fed a high-fat diet. Sprague-Dawley rats were divided into three groups and fed either a 45% high-fat diet (HF), HF + hot-water extract of ginger (WEG; 8 g/kg diet), or HF + high-hydrostatic pressure extract of ginger (HPG; 8 g/kg diet) for 10 weeks. The HPG group had lower body weight and white adipose tissue (WAT) mass compared to the HF group. Serum and hepatic lipid levels of HPG group were lower, while fecal lipid excretion of the HPG group was higher than that of the HF group. In the WAT of the WEG and HPG groups, mRNA levels of adipogenic genes were lower than those of the HF group. Moreover, HPG group had lower mRNA levels of pro-inflammatory cytokines than did the HF group. MicroRNA (miR)-21 expression was down-regulated by both WEG and HPG. Additionally, miR-132 expression was down-regulated by HPG. The adenosine monophosphate-activated protein kinase (AMPK) activity of HPG group was greater than that of the HF group. HPG may have beneficial effects on obesity and inflammation, partially mediated by regulation of miR-21/132 expression and AMPK activation in WAT.

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Section: Discussionmentioning

confidence: 99%

Ginger Extract Ameliorates Obesity and Inflammation via Regulating MicroRNA-21/132 Expression and AMPK Activation in White Adipose Tissue

et al. 2018

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“…Several studies have shown that 6‐gingerol may regulate plasma adiponectin level related to the beneficial effects in insulin sensitivity and hyperlipidemia . Moreover, 6‐gingerol reduces blood glucose levels in diabetic animal models and promotes glucose uptake in L6 myotubes, which involve AMPKα activation . However, the effects and mechanisms through which 6‐gingerol modulates adiponection/AdipoRs have not been clarified.…”

Section: Introductionmentioning

confidence: 99%

6‐Gingerol Improves Ectopic Lipid Accumulation, Mitochondrial Dysfunction, and Insulin Resistance in Skeletal Muscle of Ageing Rats: Dual Stimulation of the AMPK/PGC‐1α Signaling Pathway via Plasma Adiponectin and Muscular AdipoR1

Liu

Yao

Wang

et al. 2019

Molecular Nutrition Food Res

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Scope This study investigates the dual actions of 6‐gingerol in stimulating both plasma adiponectin and muscular adiponectin receptor signaling in naturally ageing rats. Methods and results Twenty‐two‐month‐old male SD rats were treated with 6‐gingerol (0.2 mg kg–1, once daily) for 7 weeks. 6‐Gingerol can attenuate age‐associated high plasma triglyceride, glucose, and insulin concentrations under fasting conditions as well as suppress the increase in the HOMA‐IR index and inhibit the decrease of muscular p‐Akt/Akt protein in ageing rats, which indicates an improvement of systemic and muscular insulin sensitivity. Accompanying these changes, treatment with 6‐gingerol attenuates excessive triglyceride accumulation, enhances mitochondrial function, and promotes a transition from a fast‐ to slow‐fiber type and muscle oxidative metabolism in the red gastrocnemius of ageing rats. More importantly, 6‐gingerol not only increases the plasma and adipose tissue adiponectin concentrations, but also elevates muscular AdipoR1 expression and activates downstream AMPK phosphorylation as well as upregulates PGC‐1α in vivo and in vitro. Conclusion 6‐Gingerol may improve ectopic lipid accumulation, mitochondrial dysfunction, and insulin resistance in skeletal muscle of ageing rats. These effects rely, at least in part, on the elevated plasma adiponectin concentration and muscle AdipoR1 level to dually activate the AMPK/PGC‐1α signaling pathway.

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“…Dfe treatment improved mitochondrial dysfunction through Kv2.1/CaMKKβ/AMPK/PGC-1α pathway : Given the pivotal role of AMPK/PGC-1α signaling in mitochondrial energy homeostasis ( Calcutt et al., 2017 ; Herzig et al., 2018 ; Hashem et al., 2017 ), we detected the potential of Dfe treatment in regulating AMPK/PGC-1α signaling in DRG tissue of DPN mice by western blot. The results demonstrated that the levels of phosphorylated AMPK and PGC-1α were decreased from DPN mice (STZ, db/db ) compared with those from control mice (Control, db /m) but increased from the Dfe-treated DPN mice (STZ + Dfe, db/db + Dfe) compared with the vehicle-treated DPN mice (STZ, db/db ) ( Figures 5 I–5L) (for p-AMPK, F (2, 6) = 91.83 in STZ mice, 56.34 in db/db mice; for PGC1-α, F (2, 6) = 79.92 in STZ mice, 20.91 in db/db mice; for AMPK, F (2, 6) = 3.235 in STZ mice, 1.179 in db/db mice; for p-ACC, F (2, 6) = 3.615 in STZ mice, 4.675 in db/db mice).…”

Section: Resultsmentioning

confidence: 99%

Antispasmodic Drug Drofenine as an Inhibitor of Kv2.1 Channel Ameliorates Peripheral Neuropathy in Diabetic Mice

Hao

et al. 2020

iScience

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Summary Diabetic peripheral neuropathy (DPN) is a common diabetic complication and has yet no efficient medication. Here, we report that antispasmodic drug drofenine (Dfe) blocks Kv2.1 and ameliorates DPN-like pathology in diabetic mice. The underlying mechanisms are investigated against the DPN mice with in vivo Kv2.1 knockdown through adeno associated virus AAV9-Kv2.1-RNAi. Streptozotocin (STZ) induced type 1 or db/db type 2 diabetic mice with DPN exhibited a high level of Kv2.1 protein in dorsal root ganglion (DRG) tissue and a suppressed neurite outgrowth in DRG neuron. Dfe promoted neurite outgrowth by inhibiting Kv2.1 channel and/or Kv2.1 mRNA and protein expression level. Moreover, it suppressed inflammation by repressing IκBα/NF-κB signaling, inhibited apoptosis by regulating Kv2.1-mediated Bcl-2 family proteins and Caspase-3 and ameliorated mitochondrial dysfunction through Kv2.1/CaMKKβ/AMPK/PGC1α pathway. Our work supports that Kv2.1 inhibition is a promisingly therapeutic strategy for DPN and highlights the potential of Dfe in treating this disease.

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Effect of 6-gingerol on AMPK- NF-κB axis in high fat diet fed rats

Cited by 34 publications

References 57 publications

Ginger Extract Ameliorates Obesity and Inflammation via Regulating MicroRNA-21/132 Expression and AMPK Activation in White Adipose Tissue

Ginger Extract Ameliorates Obesity and Inflammation via Regulating MicroRNA-21/132 Expression and AMPK Activation in White Adipose Tissue

6‐Gingerol Improves Ectopic Lipid Accumulation, Mitochondrial Dysfunction, and Insulin Resistance in Skeletal Muscle of Ageing Rats: Dual Stimulation of the AMPK/PGC‐1α Signaling Pathway via Plasma Adiponectin and Muscular AdipoR1

Antispasmodic Drug Drofenine as an Inhibitor of Kv2.1 Channel Ameliorates Peripheral Neuropathy in Diabetic Mice

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