Background: Idiopathic pulmonary fibrosis (IPF) is a challenging refractory interstitial lung disease, and acute exacerbation of idiopathic pulmonary fibrosis (AE-IPF) is a significant contributor to rapid clinical deterioration and mortality associated with IPF. The clinical application of Qingluo Yin can obviously improve the symptoms of wheezing and dyspnea in patients with AE-IPF, but its therapeutic mechanism of clearing heat and detoxifying, eliminating phlegm and dredging channels in the treatment of AE-IPF needs to be further explored. This study aimed to elucidate the therapeutic mechanisms of Qingluo Yin by examining its regulatory effect on miR-let-7d, impacting the transforming growth factor-β1 (TGF-β1)/Smads signaling pathway and inhibiting epithelial-mesenchymal transformation in AE-IPF through animal experiments. Methods: An AE-IPF rat model was established through secondary bleomycin administration. Model effectiveness was evaluated through blood gas analysis and tissue staining. Lung CT and lung function assessments were used to assess lung volume and hypoxia status. The wet-dry weight ratio and lung coefficient were used to observe pulmonary tissue edema and fibrosis. Western blot analysis was used to determine protein expression levels of N-cadherin, alpha-smooth muscle actin (α-SMA), and E-cadherin in rat lung tissue to determine the degree of epithelial-mesenchymal transformation. Real-time Polymerase Chain Reaction (Real-time PCR) and Western blot were used to detect the levels of TGF-β1, Smad2, phosphorylation Smad2 (p-Smad2), Smad3, p-Smad3, high mobility group protein 2 (HMGA2), and miR-let-7d in rats to evaluate the impact of Qingluo Yin on AE-IPF. Results: Histopathological analysis revealed that Qingluo Yin could significantly improve the degree of alveolar inflammation and interstitial fibrosis in rats, alleviate the low partial pressure of arterial blood oxygen and decrease extracellular matrix deposition. Western blot analysis demonstrated that Qingluo Yin could significantly upregulate the expression level of E-cadherin protein and inhibit epithelial-mesenchymal transformation (EMT) (p < 0.05). Real-time PCR and Western blot revealed significant regulatory effects on the TGF-β1/Smads and key molecule miR-let-7d associated with the EMT pathway (p < 0.05). This intervention reduced the expression and transcription levels of TGF-β1, Smad2, Smad3, and HMGA2 proteins (p < 0.05) while targeting the regulation of miR-let-7d to inhibit AE-IPF. Conclusion: Qingluo Yin exhibits the potential to upregulate miR-let-7d, downregulate the expression of transcription factor HMGA2, inhibit the TGF-β1/Smads signaling pathway, and inhibit EMT, thereby presenting a promising therapeutic approach for treating AE-IPF.