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右美托咪定对脂多糖刺激后大鼠肾上腺嗜铬细胞瘤细胞的保护作用及机制
Protective role and mechanism of dexmedetomidine on the LPS-stimulated PC12 cells

作  者: (周俊杰); ; (童华生); (苏磊);

机构地区: 暨南大学

出  处: 《解放军医学杂志》 2018年第4期289-293,共5页

摘  要: 目的探讨右美托咪定DEX对脂多糖(LPS)刺激后的PC12细胞的作用及其可能机制。方法以400μg/ml LPS刺激PC12细胞3、6、12h后,检测细胞活力,测定上清中炎症因子白介素6(IL-6)和肿瘤坏死因子α(TNF-α)的浓度,以及Toll样受体4(TLR4)、髓样分化因子88(My D88)、p-p65表达水平,选取峰值对应的时间点(即LPS刺激后6h)作为后续实验检测点。实验分为对照组(给予常规培养)、LPS组(给予400μg/ml LPS刺激)、DEX组(仅给予100μmol/L DEX)和LPS+DEX组(同时给予400μg/ml LPS及100μmol/L DEX)4组,再次检测上述指标。结果 LPS刺激后细胞活力明显下降,细胞上清中IL-6、TNF-α水平明显上升,3、6、12h组与对照组比较差异均有统计学意义(P<0.05),在6h达到高峰;PC12细胞中TLR4/MyD88/NF-κB通路活化,在LPS刺激6h后达到高峰。与LPS组比较,LPS+DEX组PC12细胞凋亡率明显下降,上清中IL-6、TNF-α水平下降,同时TLR4、MyD88、p-p65表达下降,差异均有统计学意义(P<0.05)。结论 DEX可通过抑制炎症反应对抗LPS引起的PC12细胞损伤。 Objective To explore the effect of dexmedetomidine on the lipopolysaccharide(LPS) stimulated PC12 cells and its potential mechanism. Methods PC12 cells were treated by LPS with a concentration of 400μg/ml. The cell viability, the concentrations of interleukin-6(IL-6) and tumor necrosis factor α(TNF-α) in the cell culture supernatant were measured after 3-, 6-, or 12-h treatment. The expressions of toll-like receptor 4(TLR4), myeloid differentiation factor 88(My D88) and phosphorylated p65(p-p65) were measured. In the second part, PC12 cells were cultured under four different treatments, that is, normal culture media in first group, 400μg/ml LPS in second group, 100μmol/L dexmedetomidine in third group, 400μg/ml LPS and100μmol/L dexmedetomidine in fourth group. The indexes mentioned above were measured 6 hours after LPS and DEX treatments. Results The cell viability was decreased after LPS treatment, and the concentrations of IL-6 and TNF-α were increased significantly. Compared with control group, the concentrations in 3-, 6-, 12-h groups showed statistically significant differences(P〈0.05), especially after 6 hours. The TLR4/MyD88/NF-κB pathway was activated after LPS stimuli and reached the peak value. Compared with LPS treatment group, PC12 cell apoptosis rate, the concentrations of IL-6 and TNF-α and the expressions of TLR4, MyD88 and p-p65 were decreased. The differences between LPS+DEX group and LPS group was statistically significant(P〈0.05). Conclusion Dexmedetomidine has a protective effect on LPS stimulated PC12 cells via the inhibition of inflammatory response.

关 键 词: 脂多糖 右美托咪定 细胞 样受体

领  域: [医药卫生—麻醉学] [医药卫生—外科学] [医药卫生—临床医学]

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