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Cha, Seon-Heui,Hwang, Yongha,Heo, Soo-Jin,Jun, Hee-Sook Hindawi 2018 Oxidative medicine and cellular longevity Vol.2018 No.-
<P>Diabetic nephropathy is the leading cause of end-stage renal disease in patients with diabetes mellitus. Oxidative stress has been shown to play an important role in pathogeneses of renal damage in diabetic patients. Here, we investigated the protective effect of diphlorethohydroxycarmalol (DPHC), which is a polyphenol isolated from an edible seaweed, <I>Ishige okamurae</I>, on methylglyoxal-induced oxidative stress in HEK cells, a human embryonic kidney cell line. DPHC treatment inhibited methylglyoxal- (MGO-) induced cytotoxicity and ROS production. DPHC activated the Nrf2 transcription factor and increased the mRNA expression of antioxidant and detoxification enzymes, consequently reducing MGO-induced advanced glycation end product formation. In addition, DPHC increased glyoxalase-1 mRNA expression and attenuated MGO-induced advanced glycation end product formation in HEK cells. These results suggest that DPHC possesses a protective activity against MGO-induced cytotoxicity in human kidney cells by preventing oxidative stress and advanced glycation end product formation. Therefore, it could be used as a potential therapeutic agent for the prevention of diabetic nephropathy.</P>
Cha, Seon-Heui,Kim, Hyun-Soo,Hwang, Yongha,Jeon, You-Jin,Jun, Hee-Sook Hindawi 2018 Oxidative medicine and cellular longevity Vol.2018 No.-
<P>Beta-cell loss is a major cause of the pathogenesis of diabetes. Elevated levels of free fatty acids may contribute to the loss of <I>β</I>-cells. Using a transgenic zebrafish, we screened ~50 seaweed crude extracts to identify materials that protect <I>β</I>-cells from free fatty acid damage. We found that an extract of the red seaweed <I>Polysiphonia japonica</I> (PJE) had a <I>β</I>-cell protective effect. We examined the protective effect of PJE on palmitate-induced damage in <I>β</I>-cells. PJE was found to preserve cell viability and glucose-induced insulin secretion in a pancreatic <I>β</I>-cell line, Ins-1, treated with palmitate. Additionally, PJE prevented palmitate-induced insulin secretion dysfunction in zebrafish embryos and mouse primary islets and improved insulin secretion in <I>β</I>-cells against palmitate treatment. These findings suggest that PJE protects pancreatic <I>β</I>-cells from palmitate-induced damage. PJE may be a potential therapeutic functional food for diabetes.</P>
Cha, Seon-Heui,Jun, Hee-Sook The Korean Society of Fisheries and Aquatic Scienc 2022 Fisheries and Aquatic Sciences Vol.25 No.10
Over production of methylglyoxal (MGO) a highly reactive dicarbonyl compound, has been associated in progressive diabetes with vascular complication. Therefore, we investigated whether hot water extract of Loliolus beka meat (LBM-HWE) presents a preserve effect against MGO-induced cellular damage in human umbilical vein endothelial cells (HUVECs). The LBM-HWE extract showed to inhibit MGO-induced cytotoxicity. Additionally, the LBM-HWE reduced mRNA expression of pro-inflammatory cytokines, and reduced MGO-induced advanced glycation end product (AGEs) formation. Furthermore, LBM-HWE induced glyoxalase-1 mRNA expression and reduced MGO-induced carbonyl protein formation in HUVECs. The results implicate that LBM-HWE has protective ability against MGO-induced HUVECs toxicity by preventing AGEs formation. In conclusion, LBM-HWE could be used as a potential treatment material for the prevention of vascular complications of diabetes.
Palmitate induces nitric oxide production and inflammatory cytokine expression in zebrafish
Cha, Seon-Heui,Hwang, Yongha,Kim, Kil-Nam,Jun, Hee-Sook Elsevier 2018 FISH AND SHELLFISH IMMUNOLOGY Vol.79 No.-
<P><B>Abstract</B></P> <P>Inflammation markers in zebrafish embryos reflect a toxic response that is common to other animal models and humans. Free fatty acids (FFAs) are known to cause damage in various tissues by inducing inflammation. In this study, we investigated whether a FFA (palmitate) induces inflammation in zebrafish embryos. Nitrous oxide (NO) production and cyclooxygenase-2 (COX-2) mRNA expression were increased in palmitate-treated zebrafish embryos in a dose-dependent manner. mRNA expression of pro-inflammatory cytokines, interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF- α), were also increased. Additionally, the mRNA expression of p65 nuclear factor-kB and I-kB-α were significantly increased after palmitate-treatment. Increased reactive oxygen species (ROS) expression was observed in palmitate-treated zebrafish embryos as well as pericardial edema. Additionally, mRNA expression of pro-inflammatory cytokines were increased in zebrafish liver and pancreas fed with palmitate-contained diet. Taken together, these results indicated that palmitate increases pro-inflammatory mediators in zebrafish embryos, suggesting that zebrafish could be an alternative animal model for inflammatory disease including diabetes.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Palmitate is a fatty acid, one of the major causing factor of diabetes. </LI> <LI> Palmitate induces inflammation, but it is not known in zebrafish. </LI> <LI> Zebrafish is useful as an alternative <I>in vivo</I> model for disease research. </LI> <LI> Palmitate induced inflammation in zebrafish. </LI> <LI> Zebrafish would be possible diabetic model to study palmitate-induced. </LI> </UL> </P>