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   <subfield code="a">Paeoniflorin protects against lipopolysaccharide-induced acute lung injury in mice by alleviating inflammatory cell infiltration and microvascular permeability</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Haiqiang Zhou, Difei Bian, Xiaolan Jiao, Zhifeng Wei, Haofang Zhang, Yufeng Xia, Yisheng He, Yue Dai]</subfield>
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   <subfield code="a">Objective: The present study aims to explore the effects of paeoniflorin (PF), a monoterpene glycoside isolated from the roots of Paeonia lactiflora Pallas, on acute lung injury (ALI) and the possible mechanisms. Materials and method: ALI was induced in mice by an intratracheal instillation of lipopolysaccharide (LPS, 1mg/kg), and PF was injected intraperitoneally 30min prior to LPS administration. After 24h, lung water content, histology, microvascular permeability and proinflammatory cytokines in the bronchoaveolar lavage fluid were evaluated. Results: It was shown that PF (50, 100mg/kg) could alleviate LPS-induced ALI, evidenced by reduced pulmonary edema, improved histological changes, and attenuated inflammatory cell accumulation in the interstitium and alveolar space as well as microvascular permeability. It also markedly down-regulated the expressions of proinflammatory cytokines interleukin (IL)-1β and tumor necrosis factor (TNF)-α at both transcription and protein levels. Additionally, PF inhibited the phosphorylations of p38 MAP kinase (p38) and c-Jun NH2-terminal kinase (JNK) but not extracellular signal-regulated kinase (ERK), and prevented the activation of nuclear factor-kappa B (NF-κB) in the lung tissues. Conclusion: The findings suggest that PF is able to alleviate ALI, and the underlying mechanisms are probably attributed to decreasing the production of proinflammatory cytokines through down-regulation of the activation of p38, JNK and NF-κB pathways in lung tissues.</subfield>
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   <subfield code="a">Springer Basel AG, 2011</subfield>
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   <subfield code="a">Paeoniflorin</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Acute lung injury</subfield>
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   <subfield code="a">Proinflammatory cytokines</subfield>
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   <subfield code="a">Permeability</subfield>
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   <subfield code="a">Signaling pathway</subfield>
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   <subfield code="a">Zhou</subfield>
   <subfield code="D">Haiqiang</subfield>
   <subfield code="u">Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, 210009, Nanjing, China</subfield>
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   <subfield code="a">Bian</subfield>
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   <subfield code="u">Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, 210009, Nanjing, China</subfield>
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   <subfield code="a">Jiao</subfield>
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   <subfield code="u">Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, 210009, Nanjing, China</subfield>
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   <subfield code="a">Wei</subfield>
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   <subfield code="u">Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, 210009, Nanjing, China</subfield>
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   <subfield code="a">Zhang</subfield>
   <subfield code="D">Haofang</subfield>
   <subfield code="u">Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, 210009, Nanjing, China</subfield>
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   <subfield code="u">Department of Chinese Materia Medica Analysis, China Pharmaceutical University, 24 TongJia Xiang, 210009, Nanjing, China</subfield>
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   <subfield code="u">Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, 210009, Nanjing, China</subfield>
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   <subfield code="u">Department of Pharmacology of Chinese Materia Medica, China Pharmaceutical University, 24 Tong Jia Xiang, 210009, Nanjing, China</subfield>
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   <subfield code="t">Inflammation Research</subfield>
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   <subfield code="g">60/10(2011-10-01), 981-990</subfield>
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