Effect of Tanshinone II A on Cytokines of Rats with Severe Acute Pancreatitis Lung Injury.
- Author:
Ming-dong LIU
;
Yong-hua SHEN
- Publication Type:Journal Article
- MeSH: Acute Lung Injury; drug therapy; Animals; Cytokines; metabolism; Diterpenes, Abietane; pharmacology; therapeutic use; Intercellular Adhesion Molecule-1; Interleukin-1beta; Lung; Pancreatitis; drug therapy; Peroxidase; Rats; Rats, Sprague-Dawley; Taurocholic Acid; Tumor Necrosis Factor-alpha
- From: Chinese Journal of Integrated Traditional and Western Medicine 2015;35(11):1361-1366
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo explore the effect of Tanshinone II A on severe acute pancreatitis (SAP) lung injury (ALI) rats and its possible mechanism.
METHODSSD rats were injected with sodium taurocholate to induce SAP group, and then intervened with sodium tanshinone II A sulfonate ( STS group). Simultaneously a sham-operation group (SO group) was set up. There were 24 rats in each group. The survival state and wet-to-dry weight ratio of lung tissues were observed. Activities of myeloperoxidase (MPO) in lung were determined by MPO reagent kit. Pathologic changes of lung tissues were determined by Hofbuaer method. Expression levels of three cytokines, TNF-alpha, IL-1beta, and intercellular cell adhesion molecule-1 (ICAM-1) were detected by ELISA.
RESULTSThe survival state of rats in the SAP group was deteriorated. The wet-to-dry weight ratio, MPO activities, pathologic changes in lung tissues, and expression levels of TNF-alpha, IL-1beta, and ICAM-1 increased significantly more in the SAP group than in the SO group (P < 0.05). Compared with those in the SAP group, the survival state of rats in the STS group was improved; the wet-to-dry weight ratio, MPO activities, pathologic changes in lung tissues, and expression levels of TNF-alpha, IL-1beta, and ICAM-1 obviously decreased in the STS group (P < 0.05).
CONCLUSIONTanshinone II A had remarkable effect on SPA LI rats, which might be associated with changing cytokines levels and attenuating infiltration of lung inflammatory cells.