The Effectiveness of Glycosaminoglycans in Peripheral Vascular Disease Therapy: A Clinical and Experimental Trial

Corsi, Carlos Alexandre Curylofo; Bocci, L; Cipriani, Carla; Gazzini, Alessandra; Marrapodi, E

doi:10.1177/030006058501300106

Cited by 17 publications

(17 citation statements)

References 11 publications

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“…Glycosaminoglycans (GAGs) ameliorate injury to and maintain the contractile function of, ischaemic myocardium . Sulodexide (SDX) is a GAG purified from porcine mucosa that comprises 80% low‐molecular weight heparin and 20% dermatan sulphate and exerts anti‐inflammatory and lipid‐lowering effects . Sulodexide is used for the treatment of chronic venous and arterial diseases .…”

Section: Introductionmentioning

confidence: 99%

Sulodexide attenuates endoplasmic reticulum stress induced by myocardial ischaemia/reperfusion by activating the PI3K/Akt pathway

Shen

Chen

Zhang

et al. 2019

J Cellular Molecular Medi

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Acute myocardial ischaemia/reperfusion (MI/R) injury causes severe arrhythmias with a high rate of lethality. Extensive research focus on endoplasmic reticulum (ER) stress and its dysfunction which leads to cardiac injury in MI/R Our study evaluated the effects of sulodexide (SDX) on MI/R by establishing MI/R mice models and in vitro oxidative stress models in H9C2 cells. We found that SDX decreases cardiac injury during ischaemia reperfusion and decreased myocardial apoptosis and infarct area, which was paralleled by increased superoxide dismutase and reduced malondialdehyde in mice plasm, increased Bcl‐2 expression, decreased BAX expression in a mouse model of MI/R. In vitro, SDX exerted a protective effect by the suppression of the ER stress which induced by tert‐butyl hydroperoxide (TBHP) treatment. Both of the in vivo and in vitro effects were involved in the phosphatidylinositol 3‐kinase (PI3K)/Akt signalling pathway. Inhibition of PI3K/Akt pathway by specific inhibitor, LY294002, partially reduced the protective effect of SDX. In short, our results suggested that the cardioprotective role of SDX was related to the suppression of ER stress in mice MI/R models and TBHP‐induced H9C2 cell injury which was through the PI3K/Akt signalling pathway.

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Section: Introductionmentioning

confidence: 99%

Sulodexide attenuates endoplasmic reticulum stress induced by myocardial ischaemia/reperfusion by activating the PI3K/Akt pathway

Shen

Chen

Zhang

et al. 2019

J Cellular Molecular Medi

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“…Sulodexide is a mixture of glycosaminoglycans with a documented antiinflammatory, profibrynolytic and lipid lowering activity [5][6][7]. It is used in the treatment of chronic venous disease [5] and in arterial diseases [8].…”

Section: Introductionmentioning

confidence: 99%

Sulodexide Reduces the Proinflammatory Effect of Serum from Patients with Peripheral Artery Disease in Human Arterial Endothelial Cells

Sosińska

Baum²,

Maćkowiak³

et al. 2016

Cell Physiol Biochem

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Background/Aims: Dysfunction of the arterial endothelial cells promotes the progression of atherosclerosis. We studied how exposure of human arterial endothelial cells to atherosclerotic serum from patients with peripheral artery disease changes the secretory activity of these cells, and whether that reaction is modified by sulodexide. Methods: Endothelial cells in in vitro culture were exposed to standard culture medium ± 100pg/mL Interleukin-1(IL-1) or to medium supplemented with 20% atherosclerotic serum. Afterwards, the expression of genes responsible for the synthesis of Interleukin-6 (IL-6), Vascular Cell Adhesion Protein-1 (VCAM-1) and Von Willebrand Factor (VWF) was evaluated, together with the secretion of these compounds. Additionally, the effect of sulodexide on these processes was studied. Results: Atherosclerotic serum stimulated the expression of IL6, VCAM-1 and VWF genes in endothelial cells, which was followed by increased secretion of these compounds by 179%, 121% and 116%, respectively. Sulodexide (0.5 LRU/mL) reduced atherosclerotic serum-induced increased expression of genes for IL-6 (-32%), VCAM-1 (-20%) and VWF (-42%), and lowered secretion of these molecules: IL-6 (-27%), VCAM-1(-27%), VWF (-25%). Sulodexide also reduced, in a dose- dependent manner, secretion of IL6 from unstimulated and stimulated with IL-1 endothelial cells. Conclusions: Atherosclerotic serum induces proinflammatory and prothrombotic phenotype in arterial endothelium, which is partially reduced by sulodexide, via inhibition of genes expression, and in consequence lower secretory activity.

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“…Due to such properties it is widely used in various cases of ischemia caused by atherosclerosis and/or thrombosis [4,5] . It was also documented that beneficial vascular action of sulodexide does not depend only on its effect on hemostasis [6] .…”

Section: Introductionmentioning

confidence: 99%

Anti-Inflammatory Effect of Sulodexide during Acute Peritonitis in Rats

Karoń¹,

Połubińska

Antoniewicz

et al. 2007

Blood Purif

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Background/Aims: Peritonitis is one of the complications of peritoneal dialysis. We demonstrate the systemic and intraperitoneal anti-inflammatory action of sulodexide given systemically. Methods: Dialysis was performed in male Wistar rats with acute peritonitis induced by addition of endotoxin to the fluid. Sulodexide (10 mg/kg b.w.) was used acutely as supplement to the dialysis fluid or chronically, during 7 days preceding the study by intramuscular (IM) injection. Results: In rats given IM sulodexide the dialysate cell count was lower by 45% (p < 0.001) versus untreated rats with peritonitis. Dialysate elastase activity in IM sulodexide-treated rats was lower by 22% (p < 0.05) compared to peritonitis. In rats treated with IM sulodexide the increase of plasma tumor necrosis factor-α was reduced by 53% (p < 0.002). Pretreatment with IM sulodexide reduced transperitoneal loss of total protein and albumin during peritonitis by 26% (p < 0.002) and by 16% (p < 0.05), respectively. Conclusion: Sulodexide given systemically reduces the intraperitoneal and vascular inflammatory response during acute peritonitis in rats.

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The Effectiveness of Glycosaminoglycans in Peripheral Vascular Disease Therapy: A Clinical and Experimental Trial

Cited by 17 publications

References 11 publications

Sulodexide attenuates endoplasmic reticulum stress induced by myocardial ischaemia/reperfusion by activating the PI3K/Akt pathway

Sulodexide attenuates endoplasmic reticulum stress induced by myocardial ischaemia/reperfusion by activating the PI3K/Akt pathway

Sulodexide Reduces the Proinflammatory Effect of Serum from Patients with Peripheral Artery Disease in Human Arterial Endothelial Cells

Anti-Inflammatory Effect of Sulodexide during Acute Peritonitis in Rats

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