Rui Zhou1, Fen Luo1, Hui Lei2, Kai Zhang3, Jingyan Liu1, He He1, Jin Gao1, Xiayun Chang1, Ling He4, Hui Ji4, Tianhua Yan5, Tong Chen6. 1. Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing 210009, China. 2. Pharmaceutical Animal Experiment Center of China Pharmaceutical University, Nanjing 211198, China. 3. Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, Nanjing 210009, China. 4. Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, China. 5. Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing 210009, China. Electronic address: yantianhuabest@126.com. 6. Department of Physiology and Pharmacology, China Pharmaceutical University, Nanjing 210009, China; Department of Pharmacology, China Pharmaceutical University, Nanjing 210009, China. Electronic address: tongchencpu@163.com.
Abstract
ETHNOPHARMACOLOGICAL RELEVANCE: Liujunzi Tang is a traditional herbal medicine widely used in East Asia and clinically applied to treat Phlegm-Heat Syndrome. The purpose of the present study was to investigate the protective effects of Liujunzi Tang on cigarette smoke-induced (CS) mouse model of chronic obstructive pulmonary disease (COPD) and explore its potential molecular mechanism. MATERIALS AND METHODS: The mice received 1h of cigarette smoke for 8 weeks. The serum levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 were determined by enzyme-linked immunosorbent assay (ELISA) kits. Superoxide dismutase (SOD) and malondialdehyde (MDA) were tested by biochemical methods. Histopathological alteration was observed by hematoxylin-eosin (H&E) staining. Additionally, the expressions of nuclear transcription factor-κB (NF-κBp65) and (inhibitor of NF-κB)IκB-α were determined by western blot and immunohistochemistry analysis. RESULTS: Liujunzi Tang enhanced the activities of antioxidant enzymes and attenuated the levels of lipid oxidative production, meanwhile significantly inhibited the generations of inflammatory cytokines by inhibiting the phosphorylation of IκB-α and NF-κB. CONCLUSION: Our findings indicated that Liujunzi Tang exhibited the protective effect on cigarette smoke-induced COPD mice by anti-inflammatory and anti-oxidative properties through the inhibition of NF-κB activation.
ETHNOPHARMACOLOGICAL RELEVANCE: Liujunzi Tang is a traditional herbal medicine widely used in East Asia and clinically applied to treat Phlegm-Heat Syndrome. The purpose of the present study was to investigate the protective effects of Liujunzi Tang on cigarette smoke-induced (CS) mouse model of chronic obstructive pulmonary disease (COPD) and explore its potential molecular mechanism. MATERIALS AND METHODS: The mice received 1h of cigarette smoke for 8 weeks. The serum levels of tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 were determined by enzyme-linked immunosorbent assay (ELISA) kits. Superoxide dismutase (SOD) and malondialdehyde (MDA) were tested by biochemical methods. Histopathological alteration was observed by hematoxylin-eosin (H&E) staining. Additionally, the expressions of nuclear transcription factor-κB (NF-κBp65) and (inhibitor of NF-κB)IκB-α were determined by western blot and immunohistochemistry analysis. RESULTS: Liujunzi Tang enhanced the activities of antioxidant enzymes and attenuated the levels of lipid oxidative production, meanwhile significantly inhibited the generations of inflammatory cytokines by inhibiting the phosphorylation of IκB-α and NF-κB. CONCLUSION: Our findings indicated that Liujunzi Tang exhibited the protective effect on cigarette smoke-induced COPDmice by anti-inflammatory and anti-oxidative properties through the inhibition of NF-κB activation.