Effects of corydalis decumbens isocorydine on LPS-induced inflammatory factors and TLR2/NF-κB/MYD88 pathway in bovine pulmonary microvascular endothelial cells
The aim of this study was to investigate the effects of corydalis decumbens isocorydine(ICD)on lipopolysaccharide(LPS)-induced inflammatory factor and toll-like receptor 2/myeloid differentiation factor 88/nuclear transcription factor-KB(TLR2/MYD88/NF-κB)pathways in bovine pulmonary microvascular endothelial cells(CPA 47).The CPA 47 were divided into five groups and seeded into six-well plates with four replicates per well.The control group received only 1640 medium,while the LPS group was treated with LPS to establish an inflammatory model.The ICD high-dose group was treated with 20 mg/L ICD+50 μg/L LPS,the ICD medium-dose group with 15 mg/L ICD+50 μg/L LPS,and the ICD low-dose group with 10 mg/L ICD+50 μg/L LPS.ELISA assays were employed to quantify the concentrations of inflammatory factors in each group.Real-time quantitative PCR was used to detect the mRNA expression of key genes in the TLR2/MYD88/NF-κB pathway,and Western blot analysis was conducted to assess the protein levels within this pathway.The results indicated that compared to the control group,both the LPS-treated group and the ICD low-dose group exhibited significantly elevated levels of inflammatory cytokines IL-1β,IL-6,IL-8,and TNF-α(P＜0.05),as well as increased mRNA expression and protein content of TLR2,NF-κB,and MYD88(P＜0.05).Compared to the LPS group,the ICD high-dose and medium-dose groups showed markedly reduced levels of the inflammatory cytokines IL-1β,IL-6,IL-8,and TNF-α(P＜0.05),along with decreased mRNA expression and protein content of TLR2,NF-κB and MYD88(P＜0.05).This study indicates that 15-20 mg/L ICD can alleviate the inflammatory response induced by LPS in bovine lung microvascular endothelial cells and inhibit the activation of the TLR2/MYD88/NF-κB inflammatory pathway triggered by LPS.
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