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Mixture of Ivy Leaves and Coptidis rhizoma Suppresses Pulmonary Inflammation Induced by Air Particles- and Lipopolysaccharide-induced Chronic Obstructive Pulmonary Disease in Mice
Yakhak Hoeji 2019;63(2):95-102
Published online April 30, 2019
© 2019 The Pharmaceutical Society of Korea.

Yeo Yeong Yoon, Won Seok Choi, Ki Cheol Gil, Ye Won Park, Ji Soo Lee, Hyun Seong Youn, Ji Yun Lee, and Kwang Woo Hwang#

College of Pharmacy, Chung-Ang University
Correspondence to: #Kwang Woo Hwang, College of Pharmacy, Chung-Ang University, 84 Heukseok-ro, Dongjak-gu, Seoul 06974 Republic of Korea, Tel: +82-2-820-5597, Fax: +82-2-823-5597, E-mail: khwang@cau.ac.kr
Received February 27, 2019; Revised April 1, 2019; Accepted April 4, 2019.
Abstract
Chronic obstructive pulmonary disease (COPD) is characterized by an elevated number of immune cells and inflammatory cytokines leading to inflammation of the lungs. Air particles including fine dust and sand dust cause respiratory problems and severe inflammation along with lipopolysaccharide (LPS) to induce COPD. HHCR consists of hederacoside C of Ivy leaf dry extract (HH) and berberine of Coptidis rhizoma dry extract (CR). Also, HHCR is a herbal product approved in Republic of Korea for the relief of cough and sputum formation due to acute respiratory infection and inflammation. Although the mechanism of action of hederacoside C and berberine are known, details of the therapeutic effect of their mixture (HHCR) in COPD are not known. Therefore, we aimed to clarify the effect of HHCR on LPSinduced COPD in a mouse model co-exposed to air particles (LPS/air particle-induced COPD mouse model). We used western blotting, ELISA and PCR analyses to quantify the inflammatory proteins that were involved in these effects. Air particles caused significant inflammation in the airway and pathological changes in the lung tissue in mice by activating of NF-κB signaling proteins such as IκB and p65. In contrast, HHCR significantly decreased the infiltration of immune cells into the lung and NF-κB signaling proteins, thereby suppressing inflammation. These data suggest that HHCR has anti-inflammatory effect on COPD mouse model through inactivation of NF-κB signaling.
Keywords : COPD, air particle, HHCR, pro-inflammatory cytokine, inflammation, NF-κB signaling


April 2019, 63 (2)
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