Effects of Sodium Houttuyfonate on Pulmonary Inflammation in COPD Model Rats
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ORIGINAL ARTICLE
Effects of Sodium Houttuyfonate on Pulmonary Inflammation in COPD Model Rats Zhonghua Wu,1,2 Bo Tan,3 Haiying Zhang,1 Yinuo Guo,1 Yanjie Tu,1 Furong Qiu,3,4 and Aidong Yang1,4
Abstract—The anti-inflammatory effect of sodium houttuyfonate (SH), an herbal-originated drug that used in China clinically, was investigated on chronic obstructive pulmonary disease (COPD) inflammatory model rats induced by combination usage of cigarette smoke (CS) and lipopolysaccharide (LPS). The morphology of the lung tissue, the expression levels of cytokines in the bronchoalveolar lavage fluid (BALF), the protein levels of TLR4, NF-κB p65, and SIGIRR, and the mRNA levels of TLR4, MyD88, NF-κB p65, and SIGIRR in lung tissues were investigated, respectively. After treated by SH (24.3 mg/ kg), the abnormal morphology changes of lung tissues in COPD rats, such as neutrophil infiltration and airway obstruction, were considerably alleviated, as well as both proinflammatory cytokines, TNF-α and IL-1β, significantly decreased in BALF. The mRNA level of TLR4, MyD88, and NF-κB p65 and protein expression of TLR4 and NF-κB p65 in lung tissues decreased significantly after SH treatment, while both SIGIRR mRNA and protein levels increased significantly. These results suggest that SH markedly attenuated the pulmonary inflammation induced by CS and LPS and protected the lung tissue in COPD model rat. The anti-inflammatory effects were related to suppress the TLR4/NF-κB pathway dependent on MyD88. TIR8/SIGIRR might contribute to the protective effects of SH on pulmonary inflammation. KEY WORDS: pulmonary inflammation; sodium houttuyfonate; COPD; TLR4; NF-κB; TIR8/SIGIRR.
INTRODUCTION Chronic obstructive pulmonary disease (COPD) is the third leading cause of death throughout the world [4]. Zhonghua Wu and Bo Tan are authors who have contributed equally to this work. 1
Department of Febrile Disease, Basic Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China 2 Department of Experiment Center for Science and Technology, Shanghai University of Traditional Chinese Medicine, Shanghai, China 3 Clinical Pharmacokinetic Laboratory, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China 4 To whom correspondence should be addressed to Furong Qiu at Clinical Pharmacokinetic Laboratory, Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine, Shanghai, China. E-mail: [email protected]; and Aidong Yang at Department of Febrile Disease, Basic Medical College, Shanghai University of Traditional Chinese Medicine, Shanghai, China. E-mail: [email protected]
COPD is defined as an inflammatory disease characterized by progressive decline in lung function and irreversible airflow obstruction [3]. Cigarette smoke (CS) exposure is the major risk factor for the development of COPD [3]. Several mechanisms regarding inflammatory response are involved in the pathophysiology of COPD [5]. Toll-like receptor 4 (TLR4) signaling pathway is recognized as one of
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