Dieckol Attenuates Microglia-mediated Neuronal Cell Death via ERK, Akt and NADPH Oxidase-mediated Pathways

Chong

Korean J Physiol Pharmacol

et al. 2016

Abnormal localization of tumor suppressor proteins is a common feature of renal cancer. Nuclear export of these tumor suppressor proteins is mediated by chromosome region maintenance-1 (CRM1). Here, we investigated the antitumor eff ects of a novel reversible inhibitor of CRM1 on renal cancer cells. We found that S109 inhibits the CRM1-mediated nuclear export of RanBP1 and reduces protein levels of CRM1. Furthermore, the inhibitory eff ect of S109 on CRM1 is reversible. Our data demonstrated that S109 signifi cantly inhibits proliferation and colony formation of renal cancer cells. Cell cycle assay showed that S109 induced G1-phase arrest, followed by the reduction of Cyclin D1 and increased expression of p53 and p21. We also found that S109 induces nuclear accumulation of tumor suppressor proteins, Foxo1 and p27. Most importantly, mutation of CRM1 at Cys528 position abolished the eff ects of S109. Taken together, our results indicate that CRM1 is a therapeutic target in renal cancer and the novel reversible CRM1 inhibitor S109 can act as a promising candidate for renal cancer therapy.

Section: Methodsmentioning

confidence: 99%

CRM1 inhibitor S109 suppresses cell proliferation and induces cell cycle arrest in renal cancer cells

Chong

Korean J Physiol Pharmacol

et al. 2016

“…Dieckol isolated from EC suppressed the phosphorylation of ERK in LPS-stimulated BV-2 microglia (1 lg/mL), attenuated Akt phosphorylation, and increased the expression of gp91 phox , a catalytic component of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase complex responsible for microglial ROS generation. Furthermore, dieckol offered neuroprotection, as confirmed in an enhanced green fluorescent protein-transfected B35 neuroblastoma cell line (Cui et al 2015). Dieckol isolated from EC showed potent activity on rotenone-induced oxidative stress in SH-SY5Y cells, a human dopaminergic neuronal cell line.…”

Section: Neuroprotective Activitymentioning

confidence: 78%

Recent advances in pharmacological research on Ecklonia species: a review

2017

The genus Ecklonia (Lessoniaceae, Phaeophyceae), commonly called kelp (brown algae), is abundant on the coasts of Japan and Korea. During the past few decades, Ecklonia species have received tremendous attention for their wide range of therapeutic properties and multiple health benefits, such as great nutritional value and being rich in vitamins, minerals, dietary fiber, proteins, and polysaccharides. Several novel functional ingredients with diversified biological activities have been isolated and possess antimicrobial, antiviral, hepatoprotective, cardioprotective, anti-inflammatory, neuroprotective, anticarcinogenic, immunomodulatory, hypolipidemic, anti-diabetic, and antioxidant therapeutic properties. The present review discusses the phytochemical, pharmacological, therapeutic, nutritional, and health benefits of different species of genus Ecklonia, as well as their use in the prevention of disease and maintenance of good health.

Turk Arch Otorhinolaryngol

“…ECP provides a neuroprotective effect by activating the antioxidant systems and contributing to homeostasis (22,23). Dieckol, an ECP component, has been suggested to provide neuroprotective effect by providing microglial suppression (24).…”

Section: Discussionmentioning

confidence: 99%

Untitled

2017

Objective: Cisplatin is a widely used agent for the treatment of adult and childhood malignancies. Side effects such as nephrotoxicity, neurotoxicity, and ototoxicity lead to dose limitations. Ecklonia cava polyphenol extract (ECP) is a molecule obtained from algae that live in seawater in the Far East. ECP has recently been shown to have protective effects against oxidative stress. The aim of this study was to evaluate the possible protective effects of ECP on cisplatin ototoxicity. Methods:In this study, we investigated the protective effects of ECP against cisplatin-induced cell death in mouse-derived House Ear Institute Organ of Corti (HEI-OC1) cochlear cells. Cisplatin (100 µM) and 1, 10, and 25 µM doses of ECP were administered to the cells, and the protective effects of ECP at 24 and 72 hours were investigated. Cell viability was evaluated by the WST-1 (water soluble tetrazolium salt).Results: Cisplatin (100 µM) reduced cell viability in both the 24 th and 72 nd hour evaluation. Although the 25 µM dose of ECP showed otoprotective effects in the 24 th hour, in the 72 nd hour this effect disappeared. Other doses of ECP showed no otoprotective effects in the 24 th and 72 nd hours. Conclusion:Although ECP showed some protective effects in the 24 th hour against cisplatin ototoxicity, these effects disappeared by the 72 nd hour. Further studies using recurrent and higher doses of ECP are required.