Objective To study the influence of active ingredients (ML-HB) of anti-pulmonary fibrosis extracted from Periplaneta Americana on pulmonary fibrosis in rats.
Methods Adult male SD rats were randomly divided into normal group, model group, and ML-HB high-, medium-, and low-dose groups, with thirty-two rats in each group. Except for the normal group, all groups were treated with SiO2 suspension by intratracheal administration; then the rats were intervened with ML-HB at 120, 60, and 30 mg/(kg·d) by intraperitoneal administration on the third day after the SiO2 treatment, the model group was given isodose saline, and the normal group was given no additional treatment. Eight rats in each group were sacrificed on the 30th, 45th, 60th, and 75th days respectively after the intervention, rat lung tissues were observed, the expressions of alpha-smooth muscle actin (α-SMA) and collagen type I (COL-I) were observed by immunohistochemistry, and the concentrations of tumor necrosis factor-α (TNF-α) and transforming growth factor-β1 (TGF-β1) in lung homogenate were detected by ELISA.
Results The model group showed increased lung volume, dark red and uneven lung tissues, gray-white plaque nodules on the surface of the sampled lung tissues, and a sense of sandiness and inelasticity, indicating that the silicosis model was established successfully. The expressions of α-SMA and COL-I and the concentrations of TNF-α and TGF-β1 in the lung tissues of the model group were increased (P < 0.05) at different time points compared with the normal group. The expressions of α-SMA and COL-I in the ML-HB groups were all lower than those in the model group, especially the ML-HB medium-dose group (P < 0.05). The concentrations of TNF-α and TGF-β1 in the ML-HB medium-dose groups were significantly lower than those in the model group (P < 0.05).
Conclusion ML-HB can decrease the expressions of α-SMA, COL-I, TNF-α, and TGF-β1 in lung tissues post SiO2 exposure, delay the inflammatory lesions of lung tissues, and interfere with the deposition of collagen, thus intervene in further development of pulmonary fibrosis.
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