Ishige okmurae are commonly used in treatments of obesity, diabetes, anti-oxidation and newly known as anti-cancer effect of various cancer cells. Recently, several studies suggested that reactive oxygen species (ROS) play a role on cell death signal... Ishige okmurae are commonly used in treatments of obesity, diabetes, anti-oxidation and newly known as anti-cancer effect of various cancer cells. Recently, several studies suggested that reactive oxygen species (ROS) play a role on cell death signaling. However, mechanism of ROS by I.O is presently unclear. This study aimed to explore the molecular mechanism of apoptosis by I.O in human prostate cancer PC3 and DU145 cells. Cell viability was measured by WST-1 assay. and apoptosis-related protein expression was appeared by western blotting. In addition, the levels of apoptosis was a significant difference in ROS. The results showed that I.O dramatically reduced cell viability in a dose dependent. We confirmed that I.O induced apoptosis through reduction of caspase3,9 and cleavage of poly ADP-ribose polymerase (PARP) in PC3 and DU145 cells. In addition, I.O stimulated ROS production in a dose dependent and pretreatment with N-acetylcysteine (NAC), a ROS scavenger, notably restored apoptosis and I.O-induced ROS. Thus, we concluded that I.O induces apoptosis through generation of ROS in human prostate cancer PC3 and DU145 cells and provides a promising approach to improve the efficacy of cancer therapy. Oxidative stress mediated the pathogenesis of Alzheimer’s disease (AD). I.O has been returned to exert anti-oxidant activities as well as neuroprotective effects in vitro. But it is unknown whether the Akt signaling mediated the neuroprotective effect of I.O in HT22 cells. a fluorescence microplate reader was used to evaluate reactive oxygen species (ROS) generation. The expressions of heme oxygenase-1 (HO-1), nuclear factor-E2-related factor 2 (Nrf2), Bcl-2, Bax and p-Akt were appreciated to accurate the basing mechanism. Our results showed that I.O noticeably reduced glutamate-induced cell viability loss and decreased the expression of caspase-3 activity suppressed the intracellular accumulation of ROS in glutamate-induced HT22 cells. I.O also increased Bax and decreased Bcl-2. Moreover, I.O also induced the HO-1 expression in a dose-dependent , increased the antioxidant-responsive nuclear Nrf2 expression. Furthermore, I.O restored the p-Akt as well as HO-1 expression reduced by glutamate. Our results provide the first witness that I.O can protect glutamate-induced cytotoxicity in HT22 via attenuating caspase activation and modulating the Akt signaling, indicating I.O may be useful for the treatment of neurodegenerative disorders such as AD. Neuro-inflammatory induced by amyloid-beta peptide are important causes in the pathogenesis of Alzheimer’s disease (AD). closed of Aβ peptide has emerged as a possible therapeutic approach to control the onset of AD. This study suggested the neuro-protective effects and molecular mechanisms of I.O against Aβ peptide 25−35-induced toxicity in PC12 cells. I.O inhibited the expression of iNOS and COX-2 in Aβ peptide 25−35 induced PC12 cells. I.O reduced ERK, p-38 phosphorylation. The results present new information into the pharmacological modes of I.O their potential therapeutic application to AD. ，韩语论文题目，韩语论文范文 |
