Neuroprotective effect of pentosan polysulphate on ischemia-related neuronal death of the hippocampus

Sakurai-Yamashita, Yasuko; Kinugawa, Hidekazu; Níwa, Masami

doi:10.1016/j.neulet.2006.09.041

Cited by 7 publications

(4 citation statements)

References 31 publications

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“…The presence of hyperphosphorylated tau protein and tau aggregates in patients with Niemann-Pick disease type C (Love et al 1995), and in mouse models of MPS IIIA (Bhaumik et al 1999), IIIB (Ohmi et al 2009), and IIIC (Martins et al 2015), has been previously shown, and it has even been suggested that the MPS III diseases should be considered "tauopathies," a diverse group of diseases associated with dementia, including Alzheimer's disease. The current finding that PPS attenuated the abnormal accumulation of P-tau s262 in MPS IIIA mice therefore suggests that PPS might have neuroprotective effects in other neurodegenerative diseases, in line with an earlier report that PPS exerted neuroprotective actions in a rodent model of ischemia (Sakurai-Yamashita et al 2006).…”

Section: Cortexsupporting

confidence: 92%

Pentosan Polysulfate Treatment of Mucopolysaccharidosis Type IIIA Mice

et al. 2018

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As seen in other MPS animal models, subQ PPS treatment reduced plasma cytokine levels and macrophage infiltration in systemic tissues. ICV administration did not elicit these systemic effects. SubQ PPS administration also significantly impacted brain neuropathology, inflammation, and behavior. The effect of early subQ treatment was more significant than dose. Surprisingly, ICV PPS treatment had intermediate effects on most of these brain markers, perhaps due to the limited dose and/or duration of treatment. Consistent with these neuropathological findings, we also observed significant improvements in the hyperactivity/anxiety and learning behaviors of the MPS IIIA mice treated with early subQ PPS.

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Section: Cortexsupporting

confidence: 92%

Pentosan Polysulfate Treatment of Mucopolysaccharidosis Type IIIA Mice

et al. 2018

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“…The ability of LBA to be permeable to BBB is beyond the scope of this study. However, there is evidence demonstrating that some polysaccharides are indeed able to pass through the BBB and protect the brain from various pathological factors [68,69]. Future study on animal models will assist in clarifying this concern.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective Effects of Polysaccharides from Wolfberry, the Fruits of Lycium barbarum, Against Homocysteine-induced Toxicity in Rat Cortical Neurons

Yang

et al. 2010

JAD

128

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Previous clinical and epidemiological studies have suggested that elevated plasma homocysteine (Hcy) levels increased the risk of Alzheime's disease (AD). Although the underlying mechanisms of its toxicity are elusive, it has been shown that Hcy damages neurons by inducing apoptosis, DNA fragmentation, and tau hyperphosphorylation. Wolfberry (Lycium barbarum) is a fruit that is known for its eye-protective and anti-aging properties in Asian countries. Previous studies from our laboratory have demonstrated that polysaccharides derived from wolfberry (LBA) have the ability to protect neurons from amyloid-beta (Abeta) peptide neurotoxicity. We hypothesize that the neuroprotective effects of wolfberry is not limited to Abeta and can also provide protection against other AD risk factors. In this study, we aim to elucidate the neuroprotective effects of wolfberry against Hcy-induced neuronal damage. Our data showed that LBA treatment significantly attenuated Hcy-induced neuronal cell death and apoptosis in primary cortical neurons as demonstrated by LDH and caspase-3 like activity assay. LBA also significantly reduced Hcy-induced tau phosphorylation at tau-1 (Ser198/199/202), pS396 (Ser396), and pS214 (Ser214) epitopes as well as cleavage of tau. At the same time, we also found that the phosphorylation level of p-GSK3beta (Ser9/Tyr 216) remained unchanged among different treatment groups at all detected time points. LBA treatment suppressed elevation of both p-ERK and p-JNK. In summary, our data demonstrated that LBA exerted neuroprotective effects on cortical neurons exposed to Hcy. Therefore, LBA has the potential to be a diseasemodifying agent for the prevention of AD.

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“…65) Moreover, it has been documented that some polysaccharides are indeed able to pass through the BBB and protect the brain from various pathological factors. [66][67][68] Since heparin has a polysaccharide backbone and has the potential to pass through the BBB to elicit its protective effects, there is a possibility that other neuroprotective polysaccharides also process similar properties. Currently it is unknown whether RVS can pass through the BBB.…”

Section: ) L-mentioning

confidence: 99%