Polydatin up-regulates Clara cell secretory protein to suppress phospholipase A2 of lung induced by LPS in vivo and in vitro.
Polydatin up-regulates Clara cell secretory protein to suppress phospholipase A2 of lung induced by LPS in vivo and in vitro.
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DOI：
10.1186/1471-2121-12-31
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发表时间：
2011-07-25
期刊：
影响因子：
--
通讯作者：
Tingyu L
中科院分区：
文献类型：
--
作者：
Shiyu S;Zhiyu L;Mao Y;Lin B;Lijia W;Tianbao Z;Jie C;Tingyu L
脂多糖（LPS）引起的肺损伤仍然是儿童发病和死亡的主要原因之一。在急性肺损伤（ALI）/急性呼吸窘迫综合征（ARDS）中，膜磷脂的损伤导致支气管肺泡上皮屏障的崩溃。磷脂酶A2（Phospholipase A2，PLA 2）是膜磷脂水解的关键酶，在肺部炎症中起重要的创伤作用，Clara细胞分泌蛋白（Clara cell secretory protein，CCSP）是PLA 2的内源性抑制剂。我们前期的研究表明，虎杖苷（polydatin，PD）能降低LPS诱导的肺损伤大鼠PLA 2活性和sPLA 2-IIA mRNA表达，减轻肺损伤。然而，这些影响的潜在机制尚未得到很好的界定。我们继续在体内和体外研究PD对LPS诱导的CCSP mRNA和蛋白表达的影响。结果表明，CCSP的mRNA表达水平与蛋白表达水平基本一致。LPS刺激后肺组织CCSP表达减少。相反，PD以浓度依赖性方式显著增加CCSP表达。特别是，PD预处理的大鼠肺中CCSP的表达高于仅接受PD治疗的大鼠。这些结果表明，上调CCSP的表达，抑制PLA 2的活化可能是PD在LPS诱导的肺损伤中的重要保护机制之一。
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.
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影响因子：
6.1
作者：
LEVIN, SW;BUTLER, JD;MUKHERJEE, AB
通讯作者：
MUKHERJEE, AB
DOI：
10.1152/ajplung.00404.2001
发表时间：
2002-07-01
影响因子：
4.9
作者：
Kim, S;Shim, JJ;Nadel, JA
通讯作者：
Nadel, JA
DOI：
10.1152/ajplung.00181.2001
发表时间：
2002-04-01
影响因子：
4.9
作者：
Wu, YZ;Singer, M;Touqui, L
通讯作者：
Touqui, L
克拉拉细胞：支气管上皮的祖细胞。
DOI：
10.1016/j.biocel.2009.09.002
发表时间：
2010-01
影响因子：
4
作者：
Reynolds, Susan D.;Malkinson, Alvin M.
通讯作者：
Malkinson, Alvin M.
影响因子：
5.1
作者：
Cunningham, Timothy J.;Yao, Lihua;Lucena, Angel
通讯作者：
Lucena, Angel