Prostaglandin E1 for preventing the progression of diabetic kidney disease

Wang, Han; Deng, Jue Lin; Yue, Jirong; Li, Jun; Hou, Yan

doi:10.1002/14651858.cd006872.pub2

Cited by 13 publications

(8 citation statements)

References 21 publications

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“…However, after alprostadil treatment, we show that urinary protein and creatinine clearance rate were significantly reduced along with attenuation of other pathological renal features, which is consistent with previous reports that alprostadil has a protective effect on the kidneys [12,13,14]. …”

Section: Discussionsupporting

confidence: 92%

“…Clinical studies have shown that alprostadil can decrease proteinuria and protect renal function. Alprostadil was also reported to play a role in improving and protecting the kidneys through inhibition of the immune response, reducing kidney inflammation and reducing kidney cell apoptosis [12,13,14]. However, the exact mechanisms remain unclear and is the focus of our current study.…”

Section: Discussionmentioning

confidence: 97%

“…Clinical studies also show that alprostadil can reduce urinary protein and protect renal function through unclear mechanisms [12,13,14]. In this study, we sought to establish a DN model by STZ induction, as a means to observe the early morphological changes that occur in DN, while simultaneously monitoring the expression levels of key angiogenesis-related factors such as, Ang-2/Tie-2 and the inflammatory cytokine, IL-18.…”

Section: Introductionmentioning

confidence: 99%

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Therapeutic Effect of Alprostadil in Diabetic Nephropathy: Possible Roles of Angiopoietin-2 and IL-18

Chen

Zhang

et al. 2014

Cell Physiol Biochem

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Background/Aims: To investigate the role of angiopoietin-2 (Ang-2) and IL-18 in the pathogenesis of diabetic nephropathy (DN) and the molecular mechanisms through which alprostadil protects renal function. Methods: DN was induced by streptozotocin and intraperitoneal injection of alprostadil was given to diabetic mice. After 2, 4 and 8 weeks of alprostadil treatment, the mRNA and protein expression of kidney Ang-2 and IL-18 were detected by reverse transcription PCR, Western blot and immunohistochemistry analyses. Mouse glomerular endothelial cells (GEnCs) were cultured in high glucose and treated with alprostadil. After transfection with an Ang-2-pcDNA and Ang-2-siRNA, both Ang-2 and IL-18 expression were measured by Western blot analyses. Results: Alprostadil treatment caused a significant decrease in the renal damage parameters. Both Ang-2 and IL-18 were significantly increased in DN mice and in GEnCs cultured in high glucose; however, their expression was greatly reduced by alprostadil treatment. Ang-2 could also increase IL-18 expression in cultured endothelial cells under high glucose, and this response was partially blocked by Ang-2 siRNA. Conclusions: Ang-2 and IL-18 may be associated with the development and progression of DN in mice. Alprostadil treatment can protect renal function by reducing proteinuria. These effects are mediated, at least in part, through down-regulation of Ang-2 and IL-18 expression.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

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Therapeutic Effect of Alprostadil in Diabetic Nephropathy: Possible Roles of Angiopoietin-2 and IL-18

Chen

Zhang

et al. 2014

Cell Physiol Biochem

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“…PGI2 is produced from prostaglandin H2 (PGH2) by prostacyclin synthase [ 31 ]. In addition, prostaglandin E1 has a protective effect on diabetic kidney disease by decreasing UAE [ 32 ], whereas prostaglandin E2 decrease myocardium contractility and cause cardiorenal syndrome [ 33 ]. AA is associated with PGH2, through separation from phospholipids in the cell membrane and receiving COX.…”

Section: Discussionmentioning

confidence: 99%

Low circulating arachidonic acid is associated with macroalbuminuria in diabetic patients: a cross-sectional examination of the KAMOGAWA-DM cohort study

et al. 2021

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Background Diabetic nephropathy, a major complication of diabetes, is the primary risk factor for dialysis, cardiovascular diseases, and mortality. Dietary fatty acids (FAs) have been revealed to be related with cardiovascular diseases in the general populations. The aim of this study was to investigate the association of circulating FAs with diabetic nephropathy. Methods In this cross-sectional study, 190 Japanese patients with type 2 diabetes were included. Circulating FAs were measured by gas chromatography-mass spectrometry. Spearman rank correlation coefficients were used to investigate the association between the logarithm of FAs and the logarithm of urinary albumin excretion (UAE). We have performed logistic regression analysis to determine the effect of FAs on the presence of macroalbuminuria, defined as UAE value ≥300 mg/g creatinine. Results Mean age, body mass index, and duration of diabetes were 62.7 ± 12.1 years, 25.0 ± 4.5 kg/m2, and 9.8 ± 8.7 years, respectively. In total, 26 patients were diagnosed with macroalbuminuria. The logarithm of circulating arachidonic acid (AA) was negatively associated with the logarithm of UAE (r = − 0.221, p = 0.002). Additionally, circulating AA in patients with macroalbuminuria was lower than that in patients without macroalbuminuria (112.3 ± 75.3 mg/day vs. 164.8 ± 66.0 mg/day, p < 0.001). The logarithm of circulating AA was associated with the presence of macroalbuminuria after adjusting for covariates (odds ratio of Δ1 incremental: 0.32, 95% confidence interval: 0.10–0.99, p = 0.042). Conclusions Circulating AA was negatively associated with UAE and the presence of macroalbuminuria.

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“…However, the precise mechanism of action remains to be established. It has been suggested that PPAR α agonists may inhibit prostaglandin production, a key regulator of renal blood flow and diabetic renal pathology, may also be responsible [ 76 ].…”

Section: The Renoprotective Actions Of Ppar α mentioning

confidence: 99%

The Renoprotective Actions of Peroxisome Proliferator-Activated Receptors Agonists in Diabetes

2012

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Pharmaceutical agonists of peroxisome proliferator-activated receptors (PPARs) are widely used in the management of type 2 diabetes, chiefly as lipid-lowering agents and oral hypoglycaemic agents. Although most of the focus has been placed on their cardiovascular effects, both positive and negative, these agents also have significant renoprotective actions in the diabetic kidney. Over and above action on metabolic control and effects on blood pressure, PPAR agonists also appear to have independent effects on a number of critical pathways that are implicated in the development and progression of diabetic kidney disease, including oxidative stress, inflammation, hypertrophy, and podocyte function. This review will examine these direct and indirect actions of PPAR agonists in the diabetic kidney and explore recent findings of clinical trials of PPAR agonists in patients with diabetes.

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Prostaglandin E1 for preventing the progression of diabetic kidney disease

Cited by 13 publications

References 21 publications

Therapeutic Effect of Alprostadil in Diabetic Nephropathy: Possible Roles of Angiopoietin-2 and IL-18

Therapeutic Effect of Alprostadil in Diabetic Nephropathy: Possible Roles of Angiopoietin-2 and IL-18

Low circulating arachidonic acid is associated with macroalbuminuria in diabetic patients: a cross-sectional examination of the KAMOGAWA-DM cohort study

The Renoprotective Actions of Peroxisome Proliferator-Activated Receptors Agonists in Diabetes

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