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| Effect of Mongolian medicine Agaru-25 on pulmonary fibrosis in mice#br# |
| JIA Ruo1 WANG Yongqing1 YANG Yumin2 LI Yanhua2 SU Baoke2 LIU Lixin2#br# |
1.Department of Emergency, Traditional Chinese Medicine Hospital of Inner Mongolia Autonomous Region, Inner Mongolia Autonomous Region, Hohhot 010050, China;
2.Department of Geriatrics, Traditional Chinese Medicine Hospital of Inner Mongolia Autonomous Region, Inner Mongolia Autonomous Region, Hohhot 010050, China |
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Abstract Objective The effect of Mongolian medicine Agaru-25 on pulmonary fibrosis in mice. Methods Seventy-two healthy SPF C57BL/6 mice were selected, ten mice were randomly selected as normal group, Bleomycin was injected into the trachea of the other 62 mice after anesthesia to establish pulmonary fibrosis model. On the 28th day of modeling, seven mice died. After successful molding, the mice were divided into model group (n = 10), Western medicine group (n = 9, 13 mg/ml), Mongolian high group (n = 9, 6.5 mg/ml), Mongolian middle group (n = 9, 3.25 mg/ml), Mongolian low group (n = 9), and Chinese medicine group (n = 9) according to random number table method, after eight weeks of intragastric administration, mice in each group were sacrificed for sampling. Immunohistochemical staining and Masson staining were used to observe the pathological changes and fibrosis of lung tissues, Western blot was used to detect the expression of transforming growth factor -β1 (TGF-β1), receptor phosphate cytoplasmic protein (p-Smad3), fibronectin (FN) and, osteopontin (OPN) in lung tissues, and Tunel was used to detect the apoptosis rate. Results Compared with model group, the pathological morphology of lung tissue in Mongolian high group, Mongolian middle group and Mongolian low group was significantly improved, the percentage of collagen fiber area in model group was higher than that in normal group, the percentage of collagen fiber area in each administration group was lower than that in model group, and the percentage of collagen fiber area in Mongolian group was lower than that in other administration groups, and the differences were statistically significant (P ＜ 0.05). The protein expressions of TGF-β1, p-Smad3, FN, and OPN in the treatment group were lower than those in the model group, and the protein expressions of TGF-β1, p-Smad3, FN, and OPN in the Mongolian high group were lower than those in the other Mongolian medicine groups, and Mongolian middle group were lower than Mongolian low group, and the differences were statistically significant (P ＜ 0.05). The apoptosis rate of the each Mongolian medicine groups was lower than that of the model group, and the apoptosis rate of Mongolians group was lower than that of other Mongolian medicine groups, and Mongolian middle group were lower than Mongolian low group, and the differences were statistically significant (P ＜ 0.05). Conclusion The anti-pulmonary fibrosis mechanism of the Mongolian medicine Agaru-25 may be related to the inhibition of the TGF-β/Smad signaling pathway.
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