›› 2014, Vol. 29 ›› Issue (5): 535-539.DOI: 10.3969/j.issn.1673-8640.2014.05.023

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The anti-inflammatory role and mechanism of andrographolide on Pseudomonas aeruginosa-induced lung inflammation in rat model

LI Liyan1, LI Hongchun2, MA Ping2.   

  1. 1.College of Medical Technique, Xuzhou Medical College, Jiangsu Xuzhou 221004, China;
    2. Department of Clinical Laboratory, the Affiliated Hospital of Xuzhou Medical College, Jiangsu Xuzhou 221002, China
  • Received:2013-07-15 Online:2014-05-30 Published:2014-05-27

Abstract: Objective To investigate the anti-inflammatory role and mechanism of andrographolide on Pseudomonas aeruginosa (PA)-induced lung inflammation in rats. Methods The rat′s model of PA-induced lung inflammation was established and classified into different time groups(0, 24, 48, 72 and 96h). The white blood cell count and leukocyte classification were determined in blood and bronchoalveolar lavage fluid. Reverse transcription polymerase chain reaction (PCR) was used to determine the level of Toll-like receptor 4 (TLR4) in lung tissue, a peak time point was selected, and the subjects were classified into infection group, solvent group and treatment group(5, 10, 15 and 20μg/g body weight for andrographolide), and the rat blood, bronchoalveolar lavage fluid and lung tissue at the peak time point were used for testing various indicators. Results After PA inflammation, the white blood cell count decreased in 24 h, then increased and reached the peak point at 48 h . The total cell count in bronchoalveolar lavage fluid reached the peak point at 48 h. The mRNA expressions of TLR4 in white blood cell, bronchoalveolar lavage fluid and lung tissue were higher than the others. After receiving andrographolide, the white blood cell count, the total cell count of bronchoalveolar lavage fluid and TLR4 mRNA decreased to various degrees, and had dose-dependent manner. Conclusions PA-induced lung inflammation is related with TLR4 mRNA expression changes, and andrographolide can effectively suppress lung inflammation induced by PA. Its anti-inflammatory mechanism may be achieved through the regulation of TLR4 mRNA expression.

Key words: Pseudomonas aeruginosa, Lung inflammation, Andrographolide, Toll-like receptor 4

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