2018Jiefangjun yixue zazhiRequires access

Protective role and mechanism of dexmedetomidine on the LPS-stimulated PC12 cells

Junjie Zhou, Wei Xiao, Xuan He, Na Peng, Huasheng Tong, Lei Su

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Abstract

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 400?g/ml. The cell viability, the concentrations of interleukin-6 (IL-6) and tumor necrosis factor ? (TNF-?) 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 (MyD88) 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, 400?g/ml LPS in second group, 100?mol/L dexmedetomidine in third group, 400?g/ml LPS and100?mol/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-? 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-?B 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-? 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. DOI: 10.11855/j.issn.0577-7402.2018.04.04

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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 400?g/ml. The cell viability, the concentrations of interleukin-6 (IL-6) and tumor necrosis factor ? (TNF-?) 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 (MyD88) 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, 400?g/ml LPS in second group, 100?mol/L dexmedetomidine in third group, 400?g/ml LPS and100?mol/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-? 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-?B 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-? 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. DOI: 10.11855/j.issn.0577-7402.2018.04.04

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Available abstract

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 400?g/ml. The cell viability, the concentrations of interleukin-6 (IL-6) and tumor necrosis factor ? (TNF-?) 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 (MyD88) 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, 400?g/ml LPS in second group, 100?mol/L dexmedetomidine in third group, 400?g/ml LPS and100?mol/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-? 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-?B 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-? 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. DOI: 10.11855/j.issn.0577-7402.2018.04.04

Key concepts: Dexmedetomidine, TLR4, Lipopolysaccharide, Tumor necrosis factor alpha, Apoptosis, Viability assay, Chemistry, Pharmacology

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