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Abstract：
OBJECTIVE: To observe the effect of Shenqi Chongcao (SQCC) Formula on the ASS1/src/STAT3 signaling pathway in a rat model of lung fibrosis and explore its therapeutic mechanism.
METHODS: A total of 120 male SD rats were divided equally into 5 groups, including a blank control group with saline treatment and 4 groups of rat models of idiopathic pulmonary fibrosis induced by intratracheal instillation of bleomycin. One day after modeling, the rat models were treated with daily gavage of 10 mL/kg saline, SQCC decoction (0.423 g/kg), pirfenidone (10 mL/kg), or intraperitoneal injection of arginine deiminase (ADI; 2.25 mg/kg, every 3 days) for 28 days. After the treatments, the lung tissues of the rats were collected for calculating the lung/body weight ratio, observing histopathology using HE and Masson staining, and analyzing the inflammatory cells in BALF using Giemsa staining. Serum chemokine ligand 2 (CCL2) and transforming growth factor-β1 (TGF-β1) levels were measured with ELISA. The protein expressions of src, p-srcTry529, STAT3, and p-STAT3Try705 and the mRNA expressions of ASS1, src and STAT3 in the lung tissues were detected using Western blotting and RT-qPCR.
RESULTS: The neutrophil, macrophage and lymphocyte counts and serum levels of CCL2 and TGF-β1 were significantly lower in SQCC, pirfenidone and ADI treatment groups than in the model group at each time point of measurement (P < 0.05). P-srcTry529 and p-STAT3Try705 protein expression levels and ASS1, src, and STAT3 mRNA in the lung tissues were also significantly lower in the 3 treatment groups than in the model group (P < 0.05).
CONCLUSIONS: SQCC Formula can alleviate lung fibrosis in rats possibly by activating the ASS1/src/STAT3 signaling pathway in the lung tissues.
METHODS: A total of 120 male SD rats were divided equally into 5 groups, including a blank control group with saline treatment and 4 groups of rat models of idiopathic pulmonary fibrosis induced by intratracheal instillation of bleomycin. One day after modeling, the rat models were treated with daily gavage of 10 mL/kg saline, SQCC decoction (0.423 g/kg), pirfenidone (10 mL/kg), or intraperitoneal injection of arginine deiminase (ADI; 2.25 mg/kg, every 3 days) for 28 days. After the treatments, the lung tissues of the rats were collected for calculating the lung/body weight ratio, observing histopathology using HE and Masson staining, and analyzing the inflammatory cells in BALF using Giemsa staining. Serum chemokine ligand 2 (CCL2) and transforming growth factor-β1 (TGF-β1) levels were measured with ELISA. The protein expressions of src, p-srcTry529, STAT3, and p-STAT3Try705 and the mRNA expressions of ASS1, src and STAT3 in the lung tissues were detected using Western blotting and RT-qPCR.
RESULTS: The neutrophil, macrophage and lymphocyte counts and serum levels of CCL2 and TGF-β1 were significantly lower in SQCC, pirfenidone and ADI treatment groups than in the model group at each time point of measurement (P < 0.05). P-srcTry529 and p-STAT3Try705 protein expression levels and ASS1, src, and STAT3 mRNA in the lung tissues were also significantly lower in the 3 treatment groups than in the model group (P < 0.05).
CONCLUSIONS: SQCC Formula can alleviate lung fibrosis in rats possibly by activating the ASS1/src/STAT3 signaling pathway in the lung tissues.
摘要：
目的：观察参芪重草方对肺纤维化大鼠ASS1/src/STAT3信号通路的影响，并探讨其治疗机制。
方法:将120只雄性SD大鼠平均分为5组,空白对照组加生理盐水治疗，气管内滴注博莱霉素致特发性肺纤维化大鼠模型4组。建模后的一天，大鼠模型每日灌胃10mL/kg生理盐水,SQCC汤（0.423g/kg），吡非尼酮(10mL/kg),或腹膜内注射精氨酸脱亚胺酶（ADI；2.25mg/kg，每3天)持续28天。治疗后,收集大鼠的肺组织用于计算肺/体重比，用HE和Masson染色观察组织病理学，并使用Giemsa染色分析BALF中的炎症细胞。ELISA法测定血清趋化因子配体2(CCL2)和转化生长因子β1(TGF-β1)水平。src的蛋白质表达，采用Westernblotting和RT-qPCR检测肺组织中p-srcTry529、STAT3和p-STAT3Try705以及ASS1、src和STAT3mRNA的表达。
结果：中性粒细胞，SQCC中巨噬细胞和淋巴细胞计数以及血清CCL2和TGF-β1水平显着降低，吡非尼酮和ADI治疗组在各时间点的测量均优于模型组（P<0.05）。P-srcTry529和p-STAT3Try705蛋白表达水平与ASS1、src、3个治疗组大鼠肺组织中STAT3mRNA表达水平也显著低于模型组(P<0.05)。
结论：SQCC方可能通过激活肺组织ASS1/src/STAT3信号通路减轻大鼠肺纤维化。
方法:将120只雄性SD大鼠平均分为5组,空白对照组加生理盐水治疗，气管内滴注博莱霉素致特发性肺纤维化大鼠模型4组。建模后的一天，大鼠模型每日灌胃10mL/kg生理盐水,SQCC汤（0.423g/kg），吡非尼酮(10mL/kg),或腹膜内注射精氨酸脱亚胺酶（ADI；2.25mg/kg，每3天)持续28天。治疗后,收集大鼠的肺组织用于计算肺/体重比，用HE和Masson染色观察组织病理学，并使用Giemsa染色分析BALF中的炎症细胞。ELISA法测定血清趋化因子配体2(CCL2)和转化生长因子β1(TGF-β1)水平。src的蛋白质表达，采用Westernblotting和RT-qPCR检测肺组织中p-srcTry529、STAT3和p-STAT3Try705以及ASS1、src和STAT3mRNA的表达。
结果：中性粒细胞，SQCC中巨噬细胞和淋巴细胞计数以及血清CCL2和TGF-β1水平显着降低，吡非尼酮和ADI治疗组在各时间点的测量均优于模型组（P<0.05）。P-srcTry529和p-STAT3Try705蛋白表达水平与ASS1、src、3个治疗组大鼠肺组织中STAT3mRNA表达水平也显著低于模型组(P<0.05)。
结论：SQCC方可能通过激活肺组织ASS1/src/STAT3信号通路减轻大鼠肺纤维化。
