Effect and mechanism of Shenziling capsules on silica-induced pulmonary fibrosis in rats
Objective To observe the improvement effect of Shenziling capsules on silica-induced pulmonary fibrosis in rats and to explore its mechanism.Methods Totally 120 male SD rats were randomly divided into 5 groups:a control group,a model group,a low-dose Shenziling capsule group,a medium-dose Shenziling capsule group,and a high-dose Shenziling capsule group,with 24 rats in each group.Except for the normal group,the other groups used a single non-exposure silica tracheal instillation method to create a silicosis model.On the second day after successful modeling,the control group and model group were given 10 mL/(kg·d)normal saline by oral administration,and the high-,medium-,and low-dose Shenziling capsule groups were given 0.60,0.30,and 0.15 g/(g·d)Shenziling capsules by oral administration for 28 consecutive days.The body weight gain,lung organ coefficient,liver organ coefficient,and spleen organ coefficient of the rats were measured.HE staining was used to observe pathological changes in lung tissue.ELISA kits were used to detect the levels of IFN-γ,IL-17,IL-4,and CD25 in the serum of each group of rats.Results Compared with the model group,there was no significant difference in body weight gain,lung organ coefficient,liver organ coefficient,and spleen organ coefficient among the control group,low-dose Shenziling capsule group,medium-dose Shenziling capsule group,and high-dose Shenziling capsule group(P＞0.05).The alveolar cavity of rats in the model group was filled with secretions and exudates,and inflammatory infiltration increased significantly.After the treatment with Shenziling capsules,the inflammatory damage of lung tissue was significantly reduced,and the levels of IFN-γ,IL-17,and CD25 in the serum were significantly decreased(P＜0.05,P＜0.01),while the level of IL-4 increased significantly(P＜0.05,P＜0.01).Conclusion Shenziling capsules can improve inflammatory damage in the lung tissue,and its mechanism may be related to inhibiting the release of IFN-γ,IL-17,and CD25 factors and increasing the expression level of IL-4.
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