Fucoidan protects against dopaminergic neuron death in vivo and in vitro

Luo, Ding-Zhen; Zhang, Quanbin; Wang, Haomin; Cui, Yanqiu; Sun, Zuoli; Yang, Jian; Zheng, Yi; Jia, Jinping; Yu, Fang; Wang, Xuan; Wang, Xiaomin

doi:10.1016/j.ejphar.2009.06.015

Cited by 121 publications

(83 citation statements)

References 30 publications

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“…19 In addition, it has obvious protective effects against brain inflammation and renal ischemia-reperfusion injury. 17,18 Here we demonstrated that LMWF corrected the impaired endothelium-dependent vasorelaxation and eNOS function in diabetic rats. Importantly, these effects of LMWF are through the protections of eNOS phosphorylation at Ser1177 residue and its expression in vasoendothelium, highlighting its effectiveness on dysfunctional endothelium, and thus anti-hypertension in diabetic animals.…”

Section: Discussionmentioning

confidence: 97%

“…In previous studies, we have successfully prepared and characterized a low-molecular-weight fucoidan (LMWF, 7000 Da) from L aminaria japonica that shares similar biological activities with other fucoidans. [16][17][18] In particular, LMWF has an advantage over the others in that it exerts antithrombotic effect without impacting coagulation, 19 thus it has a lower hemorrhagic risk than other fucoidans. 14,15 Therefore, we hypothesized that LMWF may protect against the endothelial and vascular disorders caused by diabetes.…”

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confidence: 99%

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Low-molecular-weight fucoidan protects endothelial function and ameliorates basal hypertension in diabetic Goto-Kakizaki rats

Cui

Zheng

Zhang

et al. 2014

Laboratory Investigation

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Endothelial dysfunction, characterized by impairment of endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) bioavailability, has been implicated in diabetic cardiovascular pathogenesis. In this study, low-molecular-weight fucoidan (LMWF), which has multiple biological activities including anti-inflammatory and anti-oxidative properties, was investigated for its protective effect against endothelial dysfunction in Goto-Kakizaki type 2 diabetic rats. LMWF (50, 100, or 200 mg/kg/day) or probucol (100 mg/kg/day) were given to diabetic rats for 12 weeks. Basal blood pressure, acetylcholine-or flow-mediated relaxation of mesenteric and paw arteries, endothelium-dependent dilation of aorta, eNOS phosphorylation, and NO production were measured using laser Doppler flowmetry, force myograph, hematoxylin and eosin staining, western blot analysis, and an NO assay. We found that LMWF robustly ameliorated the basal hypertension and impairment of endothelium-dependent relaxation in the aorta, as well as mesenteric and paw arteries in diabetic rats. In addition, the reduction in eNOS phosphorylation at Ser1177, eNOS expression, and NO production because of diabetes were partially reversed by LMWF treatment. However, probucol, a lipid-modifying drug with antioxidant properties, displayed only mild effects. Moreover, LMWF induced, in a dose-dependent manner, endotheliumdependent vasodilation and eNOS phosphorylation at Ser1177 in normal aorta, and also promoted Ser1177 phosphorylation and NO synthesis in primary cultured vasoendothelial cells. Thus, these data demonstrate for the first time that fucoidan protects vasoendothelial function and reduces basal blood pressure in type 2 diabetes rats via, at least in part, preservation of eNOS function. Fucoidan is therefore a potential candidate drug for protection of endothelium in diabetic cardiovascular complications. KEYWORDS: diabetes; endothelium-dependent vasodilation; endothelial nitric oxide synthase; low-molecular-weight fucoidan; nitric oxide Diabetic patients are at high risk of endothelial dysfunction and vascular lesions, because of multiple harmful stimuli, such as hyperglycemia, hyperlipidemia, and oxidative stress. These patients are susceptible to atherosclerosis, hypertension, and peripheral vascular disease. 1,2 It is well established that endothelium-derived nitric oxide (NO) maintains vascular homeostasis and health through vasodilation and protection of vasculature from various damaging agents. [3][4][5] Loss of NO induces increased activity of proinflammatory transcription factors, such as nuclear factor kappa B, resulting in expression of leukocyte adhesion molecules and production of chemokines and cytokines, which further promote endothelial inflammation and atherosclerosis. 5,6 Therefore, the endothelial dysfunction caused by imbalance of NO bioavailability in early-stage diabetes has been implicated as a sign or a predictor of a future cardiovascular event. [6][7][8] Mechanistically, a disturbance in endothelial NO synthase (eNOS) activity, refe...

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Section: Discussionmentioning

confidence: 97%

mentioning

confidence: 99%

Low-molecular-weight fucoidan protects endothelial function and ameliorates basal hypertension in diabetic Goto-Kakizaki rats

Cui

Zheng

Zhang

et al. 2014

Laboratory Investigation

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“…31) Indeed, it has been reported that fucoidan showed significant antioxidative activity in immune cells, neurons, and the liver. 10,32) Kang et al (2008) have reported that fucoidan showed antioxidative properties by increasing such antioxidative enzymes as SOD and GPx against CCl 4 -induced acute liver injury. 19) In agreement, we observed that fucoidan increased SOD and GPx with concomitant reduction of MDA production in a liver homogenate and the plasma of rats with DMN-induced liver fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Suppression by Fucoidan of Liver Fibrogenesisviathe TGF-β/Smad Pathway in Protecting against Oxidative Stress

Hong

Jung

Lee

et al. 2011

Bioscience, Biotechnology, and Biochemistry

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“…Thus, it can be applicable to make an experimental form of PD [1,16]. Recently, fucoidan has been shown to inhibit the toxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) by exerting anti-oxidant activities [11]. However, no report has yet proposed the neuroprotective effect of fucoidan on 6-OHDA-mediated toxicity in dopaminergic SH-SY5Y neuroblastoma cells.…”

Section: Introductionmentioning

confidence: 99%

Fucoidan attenuates 6-hydroxydopamine-induced neurotoxicity by exerting anti-oxidative and anti-apoptotic actions in SH-SY5Y cells

Kim¹,

Namgoong²,

Jung³

et al. 2017

Korean Journal of Veterinary Research

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Parkinson's disease (PD) is an irreversible neurological disorder with related locomotor dysfunction and is characterized by the selective loss of nigral neurons. PD can be experimentally induced by 6-hydroxydopamine (6-OHDA). It has been reported that reactive oxygen species, which deplete endogenous glutathione (GSH) levels, may play important roles in the dopaminergic cell death characteristic of PD. Fucoidan, a sulfated algal polysaccharide, exhibits anti-inflammatory and anti-oxidant actions. In this study, we investigated whether fucoidan can protect against 6-OHDA-mediated cytotoxicity in SH-SY5Y cells. Cytotoxicity was evaluated by using MTT and LDH assays. Fucoidan alleviated cell damage evoked by 6-OHDA dose-dependently. Fucoidan reduced the number of apoptotic nuclei and the extent of annexin-V-associated apoptosis, as revealed by DAPI staining and flow cytometry. Elevation of lipid peroxidation and caspase-3/7 activities induced by 6-OHDA was attenuated by fucoidan, which also protected against cytotoxicity evoked by buthionine-sulfoximine-mediated GSH depletion. Reduction in the glutathione/glutathione disulfide ratio induced by 6-OHDA was reversed by fucoidan, which also inhibited 6-OHDA-induced disruption of mitochondrial membrane potential. The results indicate that fucoidan may have protective action against 6-OHDAmediated neurotoxicity by modulating oxidative injury and apoptosis through GSH depletion.

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Fucoidan protects against dopaminergic neuron death in vivo and in vitro

Cited by 121 publications

References 30 publications

Low-molecular-weight fucoidan protects endothelial function and ameliorates basal hypertension in diabetic Goto-Kakizaki rats

Low-molecular-weight fucoidan protects endothelial function and ameliorates basal hypertension in diabetic Goto-Kakizaki rats

Suppression by Fucoidan of Liver Fibrogenesisviathe TGF-β/Smad Pathway in Protecting against Oxidative Stress

Fucoidan attenuates 6-hydroxydopamine-induced neurotoxicity by exerting anti-oxidative and anti-apoptotic actions in SH-SY5Y cells

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