Q Y Shen1, L Fang, H M Wu, L Wu, F He, R Y Liu. 1. Department of Anesthesiology, First Affiliated Hospital, Anhui Medical University, Hefei 230022, China.
Abstract
OBJECTIVE: To investigate the effect of Toll-like receptor 2 (TLR2) on the inhibition role of sevoflurane on airway inflammation in asthmatic mice. METHODS: The lung tissue samples of C(57) BL/6 mice used in this study were from previous research, including control group, asthma group and sevoflurane group, 8 samples in each group. Twenty-four specific pathogen free female TLR2 gene deletion (TLR2(-/-)) mice were randomly assigned to control group, asthma group and sevoflurane group, with 8 mice in each group. Asthma group and sevoflurane group were then sensitized and challenged with ovalbumin (OVA) to establish asthma model, combined with repeated inhalation of 3% sevoflurane in sevoflurane group. In C(57) mice, expression levels of TLR2 were detected using Western blotting analyses. In TLR2(-/-) mice, numbers of differential inflammatory cells were investigated; levels of tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10) in bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay (ELISA); lung tissue inflammation was detected with HE staining. RESULTS: In lung tissues from C(57) mice, levels of protein expression of TLR2 in asthma group (0.547±0.042) were higher than those in control group (0.312±0.023) (P=0.023) and sevoflurane group (0.287±0.033) (P=0.020). In TLR2(-/-) mice, the number of total cells ((83.13±19.43)×10(3)/ml), numbers of differential inflammatory cells and TNF-α level ((546±16) pg/ml) in BALF in sevoflurane group were lower than those in asthma group ((206.43±41.82)×10(3)/ml, (732±41) pg/ml), but still higher than those in control group ((44.64±7.17)×10(3)/ml, (380±24) pg/ml) (all P<0.05); lung tissue inflammation was inhibited in sevoflurane group than in asthma group, but still more obvious than that in control group. CONCLUSION: Toll like receptor 2 involved in the anti-inflammatory effect of sevoflurane on asthmatic airway inflammation in mice.
OBJECTIVE: To investigate the effect of Toll-like receptor 2 (TLR2) on the inhibition role of sevoflurane on airway inflammation in asthmatic mice. METHODS: The lung tissue samples of C(57) BL/6 mice used in this study were from previous research, including control group, asthma group and sevoflurane group, 8 samples in each group. Twenty-four specific pathogen free female TLR2 gene deletion (TLR2(-/-)) mice were randomly assigned to control group, asthma group and sevoflurane group, with 8 mice in each group. Asthma group and sevoflurane group were then sensitized and challenged with ovalbumin (OVA) to establish asthma model, combined with repeated inhalation of 3% sevoflurane in sevoflurane group. In C(57) mice, expression levels of TLR2 were detected using Western blotting analyses. In TLR2(-/-) mice, numbers of differential inflammatory cells were investigated; levels of tumor necrosis factor-alpha (TNF-α) and interleukin-10 (IL-10) in bronchoalveolar lavage fluid (BALF) were measured by enzyme linked immunosorbent assay (ELISA); lung tissue inflammation was detected with HE staining. RESULTS: In lung tissues from C(57) mice, levels of protein expression of TLR2 in asthma group (0.547±0.042) were higher than those in control group (0.312±0.023) (P=0.023) and sevoflurane group (0.287±0.033) (P=0.020). In TLR2(-/-) mice, the number of total cells ((83.13±19.43)×10(3)/ml), numbers of differential inflammatory cells and TNF-α level ((546±16) pg/ml) in BALF in sevoflurane group were lower than those in asthma group ((206.43±41.82)×10(3)/ml, (732±41) pg/ml), but still higher than those in control group ((44.64±7.17)×10(3)/ml, (380±24) pg/ml) (all P<0.05); lung tissue inflammation was inhibited in sevoflurane group than in asthma group, but still more obvious than that in control group. CONCLUSION:Toll like receptor 2 involved in the anti-inflammatory effect of sevoflurane on asthmatic airway inflammation in mice.