(<i>S</i>)-[6]-Gingerol inhibits TGF-β-stimulated biglycan synthesis but not glycosaminoglycan hyperelongation in human vascular smooth muscle cells

Kamato, Danielle; Babaahmadi‐Rezaei, Hossein; Getachew, Robel; Thach, Lyna; Guidone, Daniel; Osman, Narin; Roufogalis, Basil D.; Duke, Colin C.; Tran, Van Hoan; Zheng, Wenhua; Little, Peter J.

doi:10.1111/jphp.12060

Cited by 34 publications

(22 citation statements)

References 46 publications

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“…Thrombin signalling pathways leads to proteoglycan synthesis, GAG elongation [10] and an increase in the mRNA expression of GAG synthesizing genes [11]. TGF-β mediated proteoglycan synthesis [20,32] and GAG gene expression [19,21] are regulated by the phosphorylation of transcription factor Smad2 in the linker region. Multiple signalling pathways are involved in Smad2 linker region phosphorylation [3,8].…”

Section: Discussionmentioning

confidence: 99%

Individual Smad2 linker region phosphorylation sites determine the expression of proteoglycan and glycosaminoglycan synthesizing genes

Kamato

Burch

Zhou

et al. 2019

Cellular Signalling

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Section: Discussionmentioning

confidence: 99%

Individual Smad2 linker region phosphorylation sites determine the expression of proteoglycan and glycosaminoglycan synthesizing genes

Kamato

Burch

Zhou

et al. 2019

Cellular Signalling

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“…The shift toward the uPA-enriched profibrinolytic state favors renal collagen degradation. Given its pathophysiological role, studies into TGF-β1 have found that [6]-gingerol inhibits its stimulation of myofibroblast differentiation and collagen production in nasal polyp-derived fibroblasts [53] and of proteoglycan core protein synthesis in human vascular smooth muscle cells [54]. In the present study, fructose-induced upregulation of MCP-1, CCR-2, IL-6, TGF-β1 and PAI-1 gene expression in kidney was suppressed by ginger supplement (50 mg/kg).…”

Section: Discussionmentioning

confidence: 99%

Ginger extract diminishes chronic fructose consumption-induced kidney injury through suppression of renal overexpression of proinflammatory cytokines in rats

Yang

Liu

Jiang³

et al. 2014

BMC Complement Altern Med

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BackgroundThe metabolic syndrome is associated with an increased risk of development and progression of chronic kidney disease. Renal inflammation is well known to play an important role in the initiation and progression of tubulointerstitial injury of the kidneys. Ginger, one of the most commonly used spices and medicinal plants, has been demonstrated to improve diet-induced metabolic abnormalities. However, the efficacy of ginger on the metabolic syndrome-associated kidney injury remains unknown. This study aimed to investigate the impact of ginger on fructose consumption-induced adverse effects in the kidneys.MethodsThe fructose control rats were treated with 10% fructose in drinking water over 5 weeks. The fructose consumption in ginger-treated rats was adjusted to match that of fructose control group. The ethanolic extract of ginger was co-administered (once daily by oral gavage). The indexes of lipid and glucose homeostasis were determined enzymatically, by ELISA and/or histologically. Gene expression was analyzed by Real-Time PCR.ResultsIn addition to improve hyperinsulinemia and hypertriglyceridemia, supplement with ginger extract (50 mg/kg) attenuated liquid fructose-induced kidney injury as characterized by focal cast formation, slough and dilation of tubular epithelial cells in the cortex of the kidneys in rats. Furthermore, ginger also diminished excessive renal interstitial collagen deposit. By Real-Time PCR, renal gene expression profiles revealed that ginger suppressed fructose-stimulated monocyte chemoattractant protein-1 and its receptor chemokine (C-C motif) receptor-2. In accord, overexpression of two important macrophage accumulation markers CD68 and F4/80 was downregulated. Moreover, overexpressed tumor necrosis factor-alpha, interleukin-6, transforming growth factor-beta1 and plasminogen activator inhibitor (PAI)-1 were downregulated. Ginger treatment also restored the downregulated ratio of urokinase-type plasminogen activator to PAI-1.ConclusionsThe present results suggest that ginger supplement diminishes fructose-induced kidney injury through suppression of renal overexpression of macrophage-associated proinflammatory cytokines in rats. Our findings provide evidence supporting the protective effect of ginger on the metabolic syndrome-associated kidney injury.

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“…The S-enantiomer of 6-GN was found to exhibit a potent anti-atherosclerotic activity, by inhibiting the incorporation of [35S]-Met/Cys into proteoglycans and total proteins in human vascular smooth muscle cells. It also inhibited TGF-b-stimulated proteoglycan core protein synthesis and biglycan mRNA expression (Kamato et al, 2013).…”

Section: Cardiovascular Activitymentioning

confidence: 99%

Gingerols and shogaols: Important nutraceutical principles from ginger

et al. 2015

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(S)-[6]-Gingerol inhibits TGF-β-stimulated biglycan synthesis but not glycosaminoglycan hyperelongation in human vascular smooth muscle cells

Cited by 34 publications

References 46 publications

Individual Smad2 linker region phosphorylation sites determine the expression of proteoglycan and glycosaminoglycan synthesizing genes

Individual Smad2 linker region phosphorylation sites determine the expression of proteoglycan and glycosaminoglycan synthesizing genes

Ginger extract diminishes chronic fructose consumption-induced kidney injury through suppression of renal overexpression of proinflammatory cytokines in rats

Gingerols and shogaols: Important nutraceutical principles from ginger

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