首页|Effects of compatibility of Scutellaria baicalensis stems and Polygonum cuspidatum on TRPV1 expression and inflammatory cytokines in rats with acute lung injury
Effects of compatibility of Scutellaria baicalensis stems and Polygonum cuspidatum on TRPV1 expression and inflammatory cytokines in rats with acute lung injury
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Objective:The protective effect of Scutellaria baicalensis Stems and Polygonum Cuspidatum compatibility on lipopolysaccharide (LPS)-induced acute lung injury (ALI) in rats was studied by observing the expression of TRPV1 and inflammatory cytokines. Methods: 48 male SD rats were randomly divided into 6 groups: control group, model group, dexamethasone group (5mg / kg) and Scutellaria baicalensis Stems -Polygonum Cuspidatum (3.5, 7 and 14g / kg). The administration group was gavaged for 7 days, and the control group and model group were given the same amount of 0.9% sodium chloride. On the 8th day, except the control group, rats in other groups were injected with 8mg / kg LPS through caudal vein to induce Ali model. Take the rat lung tissue 6 hours after modeling, and calculate the wet/dry weight ratio (W/D) of the rat lung tissue; HE staining to observe the pathological changes of lung tissue; Determine the content of tumor necrosis factor-α (TNF-α) and interleukin-1β (1L-1β) in alveolar lavage fluid (BALF) and the activity of superoxide dismutase (SOD) in serum; Detect the mRNA and protein expression levels of TRPV1 receptor in rat lung tissue. Results: Compared with the model group, Scutellaria baicalensis Stems -Polygonum Cuspidatum can significantly reduce the damage of lung tissue structure and bleeding state, W/D value and TNF- α、 IL-1 β The content of TRPV1 decreased, the level of SOD increased, and the mRNA and protein expression of TRPV1 receptor decreased. Conclusion: The combination of Scutellaria baicalensis Stems -Polygonum has a protective effect on acute lung injury in rats, and its mechanism may be related to down-regulating the expression of TRPV1 and inhibiting the levels of TNF-α and IL-1β in inflammatory cells.