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Emodin protects H9c2 cells from hypoxia-induced injury by up-regulating miR-138 expression
Zhang, Xuezhi; Qin, Qiaoji; Dai, Hongyan; Cai, Shanglang; Zhou, Changyong; Guan, Jun.
  • Zhang, Xuezhi; Affiliated Hospital of Qingdao University. Department of Emergency Internal Medicine. Qingdao. CN
  • Qin, Qiaoji; Affiliated Hospital of Qingdao University. Department of Emergency Internal Medicine. Qingdao. CN
  • Dai, Hongyan; Qingdao Municipal Hospital. Department of Cardiology. Qingdao. CN
  • Cai, Shanglang; Affiliated Hospital of Qingdao University. Department of Cardiology. Qingdao. CN
  • Zhou, Changyong; Affiliated Hospital of Qingdao University. Department of Emergency Internal Medicine. Qingdao. CN
  • Guan, Jun; Qingdao Municipal Hospital. Department of Cardiology. Qingdao. CN
Braz. j. med. biol. res ; 52(3): e7994, 2019. graf
Article in English | LILACS | ID: biblio-984040
ABSTRACT
Myocardial infarction (MI) is a common presentation for ischemic heart disease, which is a leading cause of death. Emodin is a Chinese herbal anthraquinone used in several diseases. However, the effect of emodin in hypoxia-induced injury in cardiomyocytes has not been clearly elucidated. Our study aimed to clarify the functions of emodin in hypoxia-induced injury in rat cardiomyocytes H9c2 and explore the underlying mechanism. The effects of emodin on cell viability and apoptosis were analyzed by the Cell counting kit-8 assay and flow cytometry assay, respectively. The cell proliferation- and cell apoptosis-related proteins were detected by western blot. qRT-PCR was used to determine the relative expression of miR-138. Cell transfection was performed to alter miR-138 and MLK3 expression. miR-138 target was performed by dual luciferase activity assay. Sirt1/AKT and Wnt/β-catenin pathways-related factors phosphorylation were analyzed by western blot. Emodin inhibited hypoxia-induced injury in H9c2 cells by promoting cell viability and reducing cell apoptosis. miR-138 was down-regulated by hypoxia treatment but up-regulated by emodin. Up-regulation of miR-138 alleviated hypoxia-induced cell injury. Down-regulation of miR-138 attenuated the growth-promoting effect of emodin on hypoxia-induced injury, whereas up-regulation of miR-138 enhanced the growth-promoting effects of emodin. The underlying mechanism might be by inactivating Sirt1/AKT and Wnt/β-catenin pathways. MLK3 was negatively regulated by miR-138 expression and inactivated Sirt1/AKT and Wnt/β-catenin pathways. Emodin alleviated hypoxia-induced injury in H9c2 cells via up-regulation of miR-138 modulated by MLK3, as well as by activating Sirt1/AKT and Wnt/β-catenin pathways.
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Full text: Available Index: LILACS (Americas) Main subject: Cell Hypoxia / Cell Survival / Emodin / Myocytes, Cardiac / Cell Proliferation / Hypoxia Limits: Animals Language: English Journal: Braz. j. med. biol. res Journal subject: Biology / Medicine Year: 2019 Type: Article Affiliation country: China Institution/Affiliation country: Affiliated Hospital of Qingdao University/CN / Qingdao Municipal Hospital/CN

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Full text: Available Index: LILACS (Americas) Main subject: Cell Hypoxia / Cell Survival / Emodin / Myocytes, Cardiac / Cell Proliferation / Hypoxia Limits: Animals Language: English Journal: Braz. j. med. biol. res Journal subject: Biology / Medicine Year: 2019 Type: Article Affiliation country: China Institution/Affiliation country: Affiliated Hospital of Qingdao University/CN / Qingdao Municipal Hospital/CN