Effect of TRPV1 activation on lipopolysaccharide-induced lung inflammatory injury in mice

AIM:To investigate the effects of transient receptor potential cation channel subfamily V member 1 (TRPV1) activation by capsaicin on the inflammation and its underlying mechanisms in lipopolysaccharide (LPS)-induced lung injury in mice. METHODS:A total of 108 specific pathogen-free male ICR mice were randomly divided into 6 groups: normal control group, capsaicin (CAP) control group, capsazepine (CAPZ) control group, endotoxemia group, CAP treatment group and CAPZ treatment group. LPS was intraperitoneally injected 30 min after the subcutaneous injection of CAP or CAPZ. After modeling, the levels of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-10, substance P (SP) and calcitonin gene-related peptide (CGRP) in the lung were measured by ELISA. The expression of Toll-like receptor 4 (TLR4) and nuclear factor κB (NF-κB) in the lung tissue was assessed by Western blotting. The pathological changes of the lung tissue were observed under light microscope. RESULTS:The expression of TNF-α, IL-6, IL-10 and NF-κB in the lung tissues at 3 h, 8 h and 16 h was dramatically higher in endotoxemia group than that in normal control group. Compared with endotoxemia group, the levels of TNF-α, IL-6 and nuclear NF-κB in CAP treatment group at 3 h, 8 h and 16 h were obviously decreased, but the level of IL-10 was increased. The changes of the factors mentioned above in CAPZ treatment group were absolutely adverse to those in CAP treatment group. The levels of SP and CGRP were significantly higher in endotoxemia group and CAP control group than those in normal control group, but those in CAPZ control group were lower. Compared with endotoxemia group, SP and CGRP were markedly increased in CAP treatment group and were obviously decreased in CAPZ treatment group. The level of TLR4 in endotoxemia group was distinctly higher than that in normal control group at 3 h, 8 h and 16 h. However, as compared with endotoxemia group, the expression of TLR4 in CAP treatment group and CAPZ treatment group didn’t change much. At 8 h and 16 h after modeling, the degree of lung damage was also decreased in CAP treatment group as compared with endotoxemia group, while that in CAPZ treatment group was aggravated. CONCLUSION: TRPV1 activation obviously inhibits the increase in TNF-α, IL-6 and NF-κB in the lung tissue of endotoxemia mice, and promotes the increase in the anti-inflammatory factor IL-10, as well as the levels of SP and CGRP, but has no effect on the expression of TLR4.