**5. Conclusions**

This study investigated that YE counteracted pulmonary emphysema due to the CS challenge and OVA inhalation through blocking pulmonary inflammation. Oral administration of YE diminished CS-elicited induction of pro-inflammatory COX-2, iNOS, and ICAM-1 in airways and leukocytosis in BALF. YE antagonized CS exposure-induced lung tissue damage and emphysematous destruction of proteolytic MMP-12 through inhibiting ROS-triggered apoptosis of alveolar cells due to CSE. In addition, oral supplementation of YE inhibited OVA-prompted pulmonary asthmatic inflammation and alveolar destruction concomitantly with reduced leukocytosis in BALF. Furthermore, YE suppressed LPS-induced alveolar inflammation of TNF-α and MCP-1 via activation of NF-κB signaling. Thus, YE may have a potential benefit in treating pulmonary diseases of COPD and asthma through inhibiting oxidative stress, pulmonary inflammation, and subsequent emphysematous damage. Although YE may serve as an antioxidant and modulator against airway inflammation and alveolar emphysema due to CS and OVA, its dietary role in COPD and asthma remains unclear. Further validation is required to clarify whether an appropriate intake of YE may constitute a dietary treatment for a therapeutically preventive strategy for COPD.

**Author Contributions:** Y.-H.K. (Yun-Ho Kim), Y.-J.C., S.-J.P. and Y.-H.K. (Young-Hee Kang) designed research; Y.-H.K. (Yun-Ho Kim), E.-J.L., M.-K.K., D.Y.K., H.O., S.-I.K., S.Y.O. and K.-H.K., conducted research; Y.-H.K. (Yun-Ho Kim) and Y.-J.C. analyzed data; Y.-H.K. (Yun-Ho Kim) and Y.-H.K. (Young-Hee Kang) wrote the paper; and Y.-H.K. (Young-Hee Kang) had primary responsibility for final content. All authors read and approved the final manuscript.

**Funding:** This work was supported by the Ministry of Small and Medium-sized Enterprises (SMEs) and Startups, Korea (C050162).

**Conflicts of Interest:** The authors declare no conflict of interest.
