Imbalance of glomerular VEGF-NO axis in diabetic rats: prevention by chronic therapy with propyl gallate

Tian, Shuge; Gan, Yanjie; Li, Junfeng; Wang, Liping; Shen, Jianming; Liu, Tao; Ye, Tingting; Liu, Huihui; Liu, Dianjun; Deng, Yanyan; Wang, Wei

doi:10.5301/jn.2011.6458

Cited by 5 publications

(6 citation statements)

References 13 publications

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“…The uncoupling of the VEGF-NO • axis in the glomeruli resulting from eNOS inactivation has been reported in glomerular endothelial dysfunction (182) . Tian et al (145) confirmed the improvement of glomerular pathological changes in diabetic rats through oxidative stress reduction and VEGF-NO • axis recovery and prevention of glomerular endothelial dysfunction by propyl gallate.…”

Section: Polyphenols In the Amelioration Of Endothelial Dysfunctionmentioning

confidence: 91%

“…Gallic acid, a trihydroxy benzoic acid, restored eNOS activity in glomerular endothelial cells of diabetic rats through oxidative stress reduction in diabetic nephropathy ( 144 , 145 ) . Daidzein, a phyto-oestrogen, reversed changes in vascular reactivity through NO ∙ and PG-related pathways, and attenuated oxidative stress in aortic tissue of diabetic rats ( 146 ) .…”

Section: Polyphenols In the Amelioration Of Endothelial Dysfunctionmentioning

confidence: 99%

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Reversibility of endothelial dysfunction in diabetes: role of polyphenols

et al. 2016

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The endothelium, a thin single sheet of endothelial cells, is a metabolically active layer that coats the inner surface of blood vessels and acts as an interface between the circulating blood and the vessel wall. The endothelium through the secretion of vasodilators and vasoconstrictors serves as a critical mediator of vascular homeostasis. During the development of the vascular system, it regulates cellular adhesion and vessel wall inflammation in addition to maintaining vasculogenesis and angiogenesis. A shift in the functions of the endothelium towards vasoconstriction, proinflammatory and prothrombic states characterise improper functioning of these cells, leading to endothelial dysfunction (ED), implicated in the pathogenesis of many diseases including diabetes. Major mechanisms of ED include the down-regulation of endothelial nitric oxide synthase levels, differential expression of vascular endothelial growth factor, endoplasmic reticulum stress, inflammatory pathways and oxidative stress. ED tends to be the initial event in macrovascular complications such as coronary artery disease, peripheral arterial disease, stroke and microvascular complications such as nephropathy, neuropathy and retinopathy. Numerous strategies have been developed to protect endothelial cells against various stimuli, of which the role of polyphenolic compounds in modulating the differentially regulated pathways and thus maintaining vascular homeostasis has been proven to be beneficial. This review addresses the factors stimulating ED in diabetes and the molecular mechanisms of natural polyphenol antioxidants in maintaining vascular homeostasis.

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Section: Polyphenols In the Amelioration Of Endothelial Dysfunctionmentioning

confidence: 91%

Section: Polyphenols In the Amelioration Of Endothelial Dysfunctionmentioning

confidence: 99%

Reversibility of endothelial dysfunction in diabetes: role of polyphenols

et al. 2016

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“…Diabetic nephropathy is one of the leading causes of end-stage renal failure (1). The inactivation of endothelial nitric oxide synthase (eNOS) has been considered to be a recently discovered mechanism of diabetic nephropathy (2,3), which severely impairs glomerular endothelial cell nitric oxide (NO) production and causes glomerular endothelial cell dysfunction, which are impairments that contribute to the development of diabetic nephropathy (2,4). However, the specific mechanism that causes eNOS inactivation remains elusive.…”

Section: Introductionmentioning

confidence: 99%

“…Human glucagon-like peptide-1 (GLP-1) analogues, such as liraglutide, have been demonstrated to elicit protective effects in diabetic vascular complications (4), thus suggesting that liraglutide exhibits an endothelial cell function. Other investigations have also demonstrated that the protective effect Liraglutide ameliorates renal injury in streptozotocin-induced diabetic rats by activating endothelial nitric oxide synthase activity via the downregulation of the nuclear factor-κB pathway of liraglutide on vascular systems involves the reduction of chronic inflammation (7,8).…”

Section: Introductionmentioning

confidence: 99%

Liraglutide ameliorates renal injury in streptozotocin-induced diabetic rats by activating endothelial nitric oxide synthase activity via the downregulation of the nuclear factor-κB pathway

Zhou

Bai

Lin

et al. 2014

Molecular Medicine Reports

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Accumulating evidence has implicated that liraglutide, one of the human glucagon‑like peptide‑1 (GLP‑1) analogues, elicits protective effects on diabetic nephropathy; however, the mechanism has yet to be fully elucidated. The present study aimed to assess the effect and underlying mechanisms of liraglutide in diabetic nephropathy. Wistar rats with streptozotocin‑induced diabetes mellitus were subcutaneously injected with liraglutide or phosphate buffer for 12 weeks at a dose of 0.3 mg/kg/12 h. The biochemical parameters were determined, renal histological examination was performed by hematoxylin and eosin and periodic acid Schiff base staining, and the mRNA levels of nuclear factor κB (NF‑κB) and endothelial nitric oxide synthase (eNOS) were assessed by quantitative polymerase chain reaction. Furthermore, the protein expression of NF‑κB and eNOS as well as eNOS phosphorylation were examined by western blot analysis and the levels of inflammatory cytokines downstream of NF‑κB were evaluated by fluorescence-assisted cell sorting and finally, the eNOS activity and nitric oxide (NO) production were evaluated by ELISA. Liraglutide decreased the levels of total cholesterol, urine, 24-h urinary albumin, blood urea nitrogen, serum creatinine and histological damage. Liraglutide also reduced the expression of NF‑κB at mRNA and protein levels; the expression of tumor necrosis factor‑α, interferon‑γ, interleukin‑6 and monocyte chemoattractant protein‑1 were also reduced. By contrast, eNOS phosphorylation, eNOS activity and NO production appeared to have increased. Liraglutide may have a direct beneficial effect on diabetic nephropathy by improving eNOS activity by inhibiting the NF‑κB pathway without eliciting a glucose lowering effect.

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“…Considering the high expression of VEGF is a common phenomenon in diabetic nephropathy [5], the factors related to NO deficiency are the most concerned for endothelial cell proliferation. Our recent studies have shown that oxidative stress may implicated to glomerular NO deficiency through inhibiting eNOS activity, and an antioxidant agent—propyl gallate—can restore eNOS activity [10]. However, whether propyl gallate can inhibit the proliferation of endothelial cells and arrest the progression of diabetic nephropathy is yet to be explored.…”

Section: Introductionmentioning

confidence: 99%

Propyl Gallate Plays a Nephroprotective Role in Early Stage of Diabetic Nephropathy Associated with Suppression of Glomerular Endothelial Cell Proliferation and Angiogenesis

Tian

Tang²,

Liu³

et al. 2012

Experimental Diabetes Research

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There is growing evidence suggesting that glomerular endothelial cell proliferation and angiogenesis may be responsible for the pathophysiological events in the early stage of diabetic nephropathy. This study was designed to investigate the factors related to glomerular endothelial cell proliferation and glomerular angiogenesis and assess the effect of propyl gallate on preventing these disorders in diabetic rats. We found that glomerular hypertrophy, glomerular mesangial matrix expansion, and albuminuria were significantly increased in DN rats. CD31+ endothelial cells significantly increased in glomerulus of diabetic rats. Double immunofluorescence staining showed some structurally defective vasculus tubes in glomerulus. Real-time PCR and western blot demonstrated the glomerular eNOS expression remained at the same level, while remarkable decreased NO productions and suppressed eNOS activities were observed in diabetic rats. Treatment with propyl gallate improved glomerular pathological changes, reduced endothelial cell proliferation, decreased albuminuria, and restored eNOS activity, but did not alter eNOS expression. These data suggest that endothelial cell proliferation and immature angiogenesis may be the contributors to progression of DN. Propyl gallate is a potential novel therapeutic agent on prevention of diabetic nephropathy.

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Imbalance of glomerular VEGF-NO axis in diabetic rats: prevention by chronic therapy with propyl gallate

Cited by 5 publications

References 13 publications

Reversibility of endothelial dysfunction in diabetes: role of polyphenols

Reversibility of endothelial dysfunction in diabetes: role of polyphenols

Liraglutide ameliorates renal injury in streptozotocin-induced diabetic rats by activating endothelial nitric oxide synthase activity via the downregulation of the nuclear factor-κB pathway

Propyl Gallate Plays a Nephroprotective Role in Early Stage of Diabetic Nephropathy Associated with Suppression of Glomerular Endothelial Cell Proliferation and Angiogenesis

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