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Objective: To investigate the mechanism of the effects of Radix isatidis on lung inflammation in tuberculosis rats through TLR4-NF-κB pathway. Methods: Forty-five SD rats were randomly divided into three groups (n=15 in each group): control group, model group, and isatis root polysaccharide group. Through the tail vein injection of H37RV Mycobacterium tuberculosis model, the rats in the isatis root polysaccharide group received the intervention of Radix isatidis polysaccharides on the second day of infection. The serum inflammatory factors and the expression levels of TLR4-NF-κB pathway and inflammatory factors in lung tissue of each group were detected and compared.Results: A large number of Mycobacterium tuberculosis infection in the lung tissue of the model group, and clustered outside the cell. In the isatis root polysaccharide group, the CFU level was significantly lower compared with the model group, and the number of Mycobacterium tuberculosis was less than that of the model group (P＜0.05), mainly distributed in tuberculous nodules and giant cells. The level of serum inflammatory factors in the model group was significantly higher than that in the control group (P＜0.05). The levels of IL-1β, IL-6 and IFN-γ in the serum of the isatis root polysaccharide group were significantly lower than those in the model group and significantly higher than those in the control group (P＜0.05). The TLR4-NF-κB pathway and inflammatory factor mRNA levels in the lung tissue of the model group were significantly higher than those of the control group (P＜0.05). The levels of TLR4, NF-κB, IL-1β, IL-6 and IFN-γ in the lung tissue of the isatis root polysaccharide group were significantly lower than those of the model group and significantly higher than those of the control group (P＜0.05). The expression level of TLR4-NF-κB pathway was significantly up-regulated in the lung tissue of model rats (P＜0.05). The levels of TLR4 and NF-κB in the lung tissue of the isatis root polysaccharide group were significantly lower than those of the model group and significantly higher than those of the control group (P＜0.05). Conclusion: Radix isatidis can alleviate lung inflammation caused by Mycobacterium tuberculosis infection by regulating TLR4-NF-κB pathway. |
