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Lnc-NEAT1 induces cell apoptosis and inflammation but inhibits proliferation in a cellular model of hepatic ischemia/reperfusion injury

机译:LNC-Neat1诱导细胞凋亡和炎症,但抑制肝脏缺血/再灌注损伤的细胞模型中的增殖

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Objective We aimed to investigate the effect of long non-coding RNA nuclear-enriched abundant transcript 1 (lnc-NEAT1) on regulating hepatocyte proliferation, apoptosis, and inflammation during hepatic ischemia/reperfusion (I/R) injury. Methods Human liver cells (HL-7702) were cultured under glucose-free and oxygen-free conditions to construct the I/R injury model. Expression of lnc-NEAT1 was detected in this model and in normal cells. Plasmids of control overexpression [NC(+)], lnc-NEAT1 overexpression [NEAT1(+)], control short hairpin (sh)RNA [NC(?)], and lnc-NEAT1 shRNA [NEAT1(?)] were transfected into HL-7702 cells and subsequently subjected to I/R treatment. Cell proliferation, apoptosis, apoptosis-related proteins, and inflammatory cytokines were assessed. Results Lnc-NEAT1 expression was elevated in the I/R group compared with the normal group. Cell proliferation was decreased in the NEAT1(+) group compared with the NC(+) group but increased in NEAT1(?) compared with NC(?). The apoptosis rate increased in the NEAT1(+) group compared with the NC(+) group but decreased in NEAT1(?) compared with NC(?). Western blot assay (detection of apoptosis-related proteins) showed similar results. Expression of interleukin-1β, interleukin-6, and tumor necrosis factor-α increased in the NEAT1(+) group compared with NC(+) but decreased in NEAT1(?) compared with NC(?). Conclusion Lnc-NEAT1 is overexpressed, induces cell apoptosis and inflammation, and inhibits proliferation during hepatic I/R injury.
机译:目的我们旨在探讨长期非编码RNA核富含丰富成绩单1(LNC-Neat1)对调节肝细胞增殖,细胞凋亡和炎症的影响/再灌注(I / R)损伤。方法将人肝细胞(HL-7702)在无葡萄糖和无氧条件下培养以构建I / R损伤模型。在该模型和正常细胞中检测到LNC-Neat1的表达。对照过表达的质粒[nc(+)],LNC-neat1过表达[neat1(+)],对照短发夹(sh)RNA [nc(α)]和LNC-neat1 shRNA [neat1(Δ)]被转染HL-7702细胞随后进行I / R处理。评估细胞增殖,细胞凋亡,凋亡相关蛋白和炎症细胞因子。结果与正常组相比,I / R组在I / R组中升高了LNC-Neat1表达。与NC(+)基团相比,细胞增殖在Neat1(+)组中降低,但与NET1(α)增加,与NC(α)增加。与NC(+)组相比,Neat1(+)组中凋亡率增加,但与NET1(α)减少,与NC(α)减少。 Western印迹测定(检测凋亡相关蛋白质)显示出类似的结果。与NC(+)相比,Neat1(+)组中白细胞介素-1β,白细胞介素-6和肿瘤坏死因子-α的表达增加,但与NC(α)相比,NET1(α)减少。结论LNC-Neat1过表达,诱导细胞凋亡和炎症,抑制肝脏I / R损伤期间的增殖。

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