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.
作者
周俊杰
肖伟
何璇
彭娜
童华生
苏磊
ZHOU Jun-jie;XIAO Wei;HE Xuan;PENG Na;TONG Hua-sheng;SU Lei(Department of Intensive Care Unit, Heyuan People＇s Hospital Affiliated to Jinan University, Heyuan, Guangdong 517000, China;Department of Intensive Care Unit, Guangzhou General Hospital of Guangzhou Military Area Command, Guangzhou 510010, China)
出处
《解放军医学杂志》
CAS
CSCD
北大核心
2018年第4期289-293,共5页
Medical Journal of Chinese People's Liberation Army
基金
广东省自然科学基金博士启动项目(2016A030310288)~~
