Protection against Oxidative Stress-Induced Apoptosis by Fermented Sea Tangle (Laminaria japonica Aresch) in Osteoblastic MC3T3-E1 Cells through Activation of Nrf2 Signaling Pathway

被引:8
作者
Kim, So Young [1 ,2 ]
Cha, Hee-Jae [3 ]
Hwangbo, Hyun [1 ,4 ]
Park, Cheol [5 ]
Lee, Hyesook [1 ,2 ]
Song, Kyoung Seob [6 ]
Shim, Jung-Hyun [7 ]
Noh, Jeong Sook [8 ]
Kim, Heui-Soo [9 ]
Lee, Bae-Jin [10 ]
Kim, Suhkmann [11 ]
Kim, Gi-Young [12 ]
Jeon, You-Jin [12 ]
Choi, Yung Hyun [1 ,2 ]
机构
[1] Dong Eui Univ, Antiaging Res Ctr, Busan 47340, South Korea
[2] Dong Eui Univ, Dept Biochem, Coll Korean Med, Busan 47227, South Korea
[3] Kosin Univ, Dept Parasitol & Genet, Coll Med, Busan 49104, South Korea
[4] Pusan Natl Univ, Korea Nanobiotechnol Ctr, Busan 46241, South Korea
[5] Dong Eui Univ, Coll Liberal Studies, Div Basic Sci, Busan 47340, South Korea
[6] Kosin Univ, Coll Med, Dept Med Life Sci, Busan 49104, South Korea
[7] Mokpo Natl Univ, Dept Pharm, Jeonnam 58554, South Korea
[8] Tongmyong Univ, Dept Food Sci & Nutr, Busan 48520, South Korea
[9] Pusan Natl Univ, Dept Biol Sci, Coll Nat Sci, Busan 46241, South Korea
[10] Marine Bioproc Co Ltd, Ocean Fisheries & Biol Ctr, Busan 46048, South Korea
[11] Pusan Natl Univ, Inst Funct Mat, Ctr Proteome Biophys & Chem, Dept Chem,Coll Nat Sci, Busan 46241, South Korea
[12] Jeju Natl Univ, Dept Marine Life Sci, Jeju 63243, South Korea
关键词
fermented sea tangle; osteoblast; ROS; apoptosis; Nrf2/HO-1; ROSMARINIC ACID; EXTRACTS; ETHANOL; DAMAGE;
D O I
10.3390/foods10112807
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
The purpose of the present study was to explore the efficacy of fermented extract of sea tangle (Laminaria japonica Aresch, FST) with Lactobacillus brevis on DNA damage and apoptosis in hydrogen peroxide (H2O2)-stimulated osteoblastic MC3T3-E1 cells and clarify related signaling pathways. Our results showed that exposure to FST significantly improved cell viability, inhibited apoptosis, and suppressed the generation of reactive oxygen species (ROS) in H2O2-stimulated cells. In addition, H2O2 triggered DNA damage in MC3T3-E1 cells was markedly attenuated by FST pretreatment. Moreover, H2O2-induced mitochondrial dysfunctions associated with apoptotic events, including loss of mitochondrial membrane potential (MMP), decreased Bcl-2/Bcl-2 associated x-protein (Bax) ratio, and cytosolic release of cytochrome c, were reduced in the presence of FST. FST also diminished H2O2-induced activation of caspase-3, which was associated with the ability of FST to protect the degradation of poly (ADP-ribose) polymerase. Furthermore, FST notably enhanced nuclear translocation and phosphorylation of nuclear factor erythroid 2-related factor 2 (Nrf2) in the presence of H2O2 with concomitant upregulation of heme oxygenase-1 (HO-1) expression. However, artificial blockade of this pathway by the HO-1 inhibitor, zinc protoporphyrin IX, greatly abolished the protective effect of FST against H2O2-induced MC3T3-E1 cell injury. Taken together, these results demonstrate that FST could protect MC3T3-E1 cells from H2O2-induced damage by maintaining mitochondrial function while eliminating ROS along with activation of the Nrf2/HO-1 antioxidant pathway.
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页数:15
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