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Polydatin up-regulates clara cell secretory protein to suppress phospholipase A2 of lung induced by LPS in vivo and in vitro

Shu Shiyu1, Ling Zhiyu2, Ye Mao1, Bo Lin1, Wang Lijia3, Zhang Tianbao4, Chen Jie5 and Li Tingyu6*

Author affiliations

1 Department of Anesthesiology, Children's Hospital of Chongqing Medical University, Zhongshan Er Road NO136, Yuzhong District, Chongqing 40 0014, China

2 Department of Cardiology, Second Affiliated Hospital of Chongqing Medical University, Linjiang Road NO74, Yuzhong District, Chongqing 40 0010, China

3 Immunological laboratory, Ministry of Education Key Laboratory of Child Development and Disorders; Zhongshan Er Road NO136, Yuzhong District, Chongqing 40 0014, China

4 Department of Health and Toxicology, Second Military Medical University of PLA, Xiangyin Road NO800, Shanghai 20 0433, China

5 Children Nutrition Research Center, Key Laboratory of Pediatrics in Chongqing, CSTC2009CA 5002, Zhongshan Er Road NO136, Yuzhong District, Chongqing 40 0014, China

6 Chongqing International Science and Technology Cooperation Center for Child Development and Disorders, Zhongshan Er Road NO136, Yuzhong District, Chongqing 40 0014, China

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Citation and License

BMC Cell Biology 2011, 12:31  doi:10.1186/1471-2121-12-31

Published: 25 July 2011



Lung injury induced by lipopolysaccharide (LPS) remains one of the leading causes of morbidity and mortality in children. The damage to membrane phospholipids leads to the collapse of the bronchial alveolar epithelial barrier during acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Phospholipase A2 (PLA2), a key enzyme in the hydrolysis of membrane phospholipids, plays an important traumatic role in pulmonary inflammation, and Clara cell secretory protein (CCSP) is an endogenous inhibitor of PLA2. Our previous study showed that polydatin (PD), a monocrystalline extracted from a traditional Chinese medicinal herb (Polygonum cuspidatum Sieb, et Zucc), reduced PLA2 activity and sPLA2-IIA mRNA expression and mitigated LPS-induced lung injury. However, the potential mechanism for these effects has not been well defined. We have continued to investigate the effect of PD on LPS-induced expression of CCSP mRNA and protein in vivo and in vitro.


Our results suggested that the CCSP mRNA level was consistent with its protein expression. CCSP expression was decreased in lung after LPS challenge. In contrast, PD markedly increased CCSP expression in a concentration-dependent manner. In particular, CCSP expression in PD-pretreated rat lung was higher than in rats receiving only PD treatment.


These results indicated that up-regulation of CCSP expression causing inhibition of PLA2 activation may be one of the crucial protective mechanisms of PD in LPS-induced lung injury.