PMID- 37308428 OWN - NLM STAT- MEDLINE DCOM- 20230614 LR - 20230614 IS - 1000-6834 (Print) IS - 1000-6834 (Linking) VI - 38 IP - 6 DP - 2022 Nov TI - [Effects of fucoidan inducing impairment of human osteosarcoma cell 143B and its mechanism]. PG - 739-744 LID - 10.12047/j.cjap.6331.2022.135 [doi] AB - Objective: To investigate the effects of fucoidan inducing impairment of human osteosarcoma cell 143B, as well its mechanisms. Methods: After 143B cells were treated with different concentrations of FUC (0, 0.5, 1, 10, 100, 400, 800 mug/ml) for 48 h, the cell viability and dehydrogenase (LDH) level were detected by MTT assay and chemical colorimetry with six multiple wells for each concentration. Based on MTT results, we determined the value of IC(50) was 244.5 mug/ml. The follow-up experiments were divided into control group (without FUC), FUC (10 mug/ml)-treated group, FUC (100 mug/ml)-treated group, FUC (400 mug/ml)-treated group and positive group (resveratrol, 40 mumol/L). There were four multiple wells for each concentration, and each experiment was repeated at least three times. Flow cytometry was performed to detect cell apoptosis and intracellular reactive oxygen species (ROS) level; acridine orange (AO) staining and lyso-tracker red staining were used to observe the autophagolysosome formation; chemical colorimetric analysis was performed to determine malondialdehyde (MDA) content and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px); Western blot was used to detect protein expressions of nuclear factor E2-associated factor 2 (Nrf2), heme oxygenase 1 (HO-1) and autophagy-associated proteins including microtubule-associated light chain protein 3 (LC-3), Atg7, Beclin-1 and p62. Results: Compared with control group, the cell viability was decreased significantly in FUC (100~400 mug/ml)-treated groups (P<0.01); LDH levels in the supernatant (P<0.05 or P<0.01), the percentage of cell apoptosis (P<0.01), intracellular ROS level and MDA content (P<0.01) were increased remarkably; protein expressions of Atg7 and Beclin-1 were upregulated (P<0.05 or P<0.01); the conversion from LC-3I to LC-3II was significant (P<0.01) together with elevation of autophagolysosome formation (P<0.05 or P<0.01); while the activities of SOD and GSH-Px and protein expressions of Nrf2, HO-1 and p62 were decreased remarkably (P<0.05 or P<0.01). Conclusion: FUC (100~400 mug/ml) treatment induces oxidative damage and autophagic death in osteosarcoma 143B cells. FAU - Wang, Qi-Qi AU - Wang QQ AD - College of Medicine, Shaoxing University, Shaoxing 312000, China. FAU - Lin, Qiao AU - Lin Q AD - College of Medicine, Shaoxing University, Shaoxing 312000, China. FAU - Shan, Wei-Yan AU - Shan WY AD - College of Medicine, Shaoxing University, Shaoxing 312000, China. FAU - Zhang, Tao AU - Zhang T AD - College of Medicine, Shaoxing University, Shaoxing 312000, China. FAU - Li, Yu-Rong AU - Li YR AD - College of Medicine, Shaoxing University, Shaoxing 312000, China. FAU - Zhang, Yun AU - Zhang Y AD - College of Medicine, Shaoxing University, Shaoxing 312000, China. LA - chi PT - English Abstract PT - Journal Article PL - China TA - Zhongguo Ying Yong Sheng Li Xue Za Zhi JT - Zhongguo ying yong sheng li xue za zhi = Zhongguo yingyong shenglixue zazhi = Chinese journal of applied physiology JID - 9426407 RN - 9072-19-9 (fucoidan) RN - 0 (Beclin-1) RN - 0 (NF-E2-Related Factor 2) RN - 0 (Reactive Oxygen Species) RN - EC 1.11.1.9 (Glutathione Peroxidase) SB - IM MH - Humans MH - Beclin-1 MH - NF-E2-Related Factor 2 MH - Reactive Oxygen Species MH - *Osteosarcoma MH - Glutathione Peroxidase MH - *Bone Neoplasms OTO - NOTNLM OT - autophagy OT - cell culture OT - fucoidan OT - osteosarcoma 143B cells OT - oxidative damage EDAT- 2023/06/13 01:13 MHDA- 2023/06/14 06:42 CRDT- 2023/06/12 22:03 PHST- 2023/06/14 06:42 [medline] PHST- 2023/06/13 01:13 [pubmed] PHST- 2023/06/12 22:03 [entrez] AID - 10.12047/j.cjap.6331.2022.135 [doi] PST - ppublish SO - Zhongguo Ying Yong Sheng Li Xue Za Zhi. 2022 Nov;38(6):739-744. doi: 10.12047/j.cjap.6331.2022.135.