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CJAP ›› 2019, Vol. 35 ›› Issue (3): 273-278.doi: 10.12047/j.cjap.5834.2019.057

• ORIGINAL ARTICLES • Previous Articles     Next Articles

Effects of MD2 gene silencing on high glucose-induced proliferation inhibition, apoptosis and inflammation in rat cardiomyocytes

LIN Zhong-min1, CHEN Guo-rong1, ZHANG Quan-bo1, WANG Fang1, XIANG Lan-ting1, CAO Qiong-jie2△   

  1. 1. Department of Pathology, the First Affiliated Hospital, Wenzhou Medical University,
    2. State Key Laboratory of Ophthalmology, Optometry and Vision Science, Eye Hospital of Wenzhou Medical University, Wenzhou 325000, China
  • Online:2019-05-28 Published:2019-06-28

Abstract: Objective: To investigate the effects of myeloid differentiation-2 (MD2) gene silencing on high glucose-induced proliferation inhibition, apoptosis and inflammation in rat cardiomyocytes. Methods: The immortalized rat cardiomyocyte cell line H9C2 were transfected with MD2 small interfering RNA (si-MD2) and negative control for 24 h, then stimulated with high glucose (HG) for 48 h. RT-qPCR was performed to detect the mRNA levels of MD2 and inflammatory factors TNF-α, IL-1β and IL-6. MTS and flow cytometry were used to evaluate cell proliferation, cell cycle and apoptosis rate. Western blot was used to detect protein expression levels and phosphorylation levels. Results: The mRNA and protein levels of MD2 in H9C2 cells were dramatically decreased after transfected with si-MD2 (P<0.01). After stimulation of high glucose, the mRNA levels of inflammatory factors, the cells in G0/G1 phase , the cell apoptosis rate and the protein level of cleaved Caspase-3 were significantly increased, while the cell proliferation ability was decreased (P<0.01). MD2 gene silencing antagonized the effects of high glucose on cell proliferation, cell cycle, cell apoptosis and the mRNA levels of TNF-α, IL-1β , IL-6(P<0.05). Western blot analysis showed that the phosphorylation levels of extracellular signal-regulated kinase(ERK1/2), P38 mitogen-activated protein kinase(P38 MAPK) and C-Jun N-terminal kinase(JNK) protein were increased significantly in H9C2 cells treated with high glucose, which could be reversed by silencing of MD2 (P<0.01). Conclusion: This study demonstrates that MD2 gene silencing reverses high glucose-induced myocardial inflammation, apoptosis and proliferation inhibition via the mechanisms involving suppression of ERK, P38 MAPK, JNK signaling pathway.

Key words: myeloid differentiation 2, rat cardiomyocyte cell, inflammatory factors apoptosis, proliferation

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