Abstract
Objective The study aimed to explore the effect of total flavonoids of Oxytropis falcata Bunge (FOFB) on the expression of p-JAK1/p-STAT1 and SOCS3 proteins in idiopathic pulmonary fibrosis (IPF). Methods Rats model with IPF was established by one-off intratracheal injection of bleomycin (BLM, 5 mg/kg). After 14 days, the same volume of low dose (100 mg/kg), medium dose (200 mg/kg), and high dose (400 mg/kg) of FOFB and prednisolone acetate (20 mg/kg) as positive control drugs, as well as normal saline, were orally administered to rats once a day for 28 consecutive days. Subsequently, the degree of fibrosis and alveolitis in rat lung tissue was observed, respectively, by HE and Masson staining. Further more, observing the ultrastructure of lung tissue by transmission electron microscopy (TEM), the detection of JAK/STAT pathway related indicators including p-JAK1, p-STAT1, and SOCS3 with immunohistochemistry and SOCS3 with real-time PCR (RT-PCR) was performed. Results Compared with the BLM group, the degree of alveolitis and fibrosis improved significantly, and the expression of p-JAK1 and p-STAT1 decreased; conversely, the expression of SOCS3 increased in the treatment group. Conclusion IPF causes high expression of p-JAK1 and p-STAT1 and low expression of SOCS3. FOFB can play a role in the treatment of IPF via upregulating SOCS3 and downregulating p-JAK1 and p-STAT1.
Highlights
Idiopathic pulmonary fibrosis (IPF), characterized by progressive dyspnea, is a chronic progressive interstitial lung disease [1]
Sixty adult specific pathogen-free animal (SPF) Sprague Dawley (SD) rats in half genders (200 ± 20 g) were provided by the Experimental Animal Center of Gansu University of Chinese Medicine. e environmental temperature was controlled at 25 ± 2°C, humidity was maintained at 45%–55%, and circadian rhythm was 12:12 h dark/light
Studies have shown that JAK1 and STAT1 are abnormally expressed in the lung tissue of IPF mice [8]
Summary
Idiopathic pulmonary fibrosis (IPF), characterized by progressive dyspnea, is a chronic progressive interstitial lung disease [1]. Without a lung transplant, the median survival rate is 3–5 years, and the patient eventually dies from respiratory failure [2]. The specific etiology and pathogen are still unknown [3]. Most studies suggest that the occurrence of IPF is characterized by repeated subclinical damage to the alveolar epithelium [4,5,6]. After the lung tissue is damaged, the alveolar epithelium cell is activated. Chemokines are released to recruit fibroblasts (FB)
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