Objective To investigate the inhibitory effect of baicalein on mycoplasma pneumonia and its the protective mecha -nism in body , and to provide scientific experimental basis for prevention and treatment of mycoplasma pneumoniae infection .Methods The mycoplasma pneumoniae and baicalein treated BALB /c mice lung tissues were stained with hematoxylin eosin (HE), and his-topathological grading .Minimum inhibitory concentration ( MIC) of baicalein on mycoplasma pneumonia was determined by real-time quantitative polymerase chain reaction ( PCR) .The expression of P 1 adhesion molecules mRNA and protein in lung tissue of BALB /c mice was determined with reverse transcription-PCR and Western blot .The expression of epidermal growth factor ( EGF) mRNA and protein in lung tissue was detected by quantitative RT-PCR and immunofluorescence .Results Baicalein significantly reduced the my-coplasma treated mice's lung tissue pathological score .The minimal inhibitory concentration of baicalein was 32 μg/ml.Baicalein sig-nificantly downregulated P 1 gene transcription and protein translation , and upregulated EGF gene transcription and protein expression . Conclusions Baicalein shows significant resistance to mycoplasma pneumoniae , and can protect the body against mycoplasma damage by inhibiting the expression of P 1 protein and promoting the expression of EGF protein .

Results of experimental studies with guinea pig showed that a strong blast may produce concussion of the vestibular apparatus. The parts injured include saccule and utricle and their maculas, semicircular canals and their cristas,and the nerves related to these organs.The most common pathological changes were hemorrhage, detachment of sensorial epithelium, collapse of membranous labyrinth, loss of oto-liths and degeneration of sensorial epithelial cells.The authors believe that these vestibular damages are produced by the combined action of strong noise and shock wave, being transmitted through the oral and round windows into the inner ear, producing a violent fluctuation of endolymph.

Objective:To understand and determine the biological properties of Chlamydia pneumonia (Cpn) hypothetical protein Cpn0423 and the mechanisms of which involved in Cpn0423-induced inflammatory response. Methods:The biological properties of Cpn0423 gene were analyzed using bioinformatic software. The subcellular localization of nucleotide-binding oligomerization domain-like receptor 2 (NOD2) in bone marrow-derived macrophages (BMDMs) was detected by confocal microscope. NOD2-siRNA was used to inhibit the expression of NOD2 at mRNA level. Cpn0423-induced macrophage inflammatory protein 2 (MIP-2) and IL-6 production in BMDMs were detected by ELISA. PCR was performed to detect Cpn0423 DNA in bronchoalveolar lavage fluid (BALF) of Cpn-positive patients.Results:The homology between Cpn0423 and other type Ⅲ secretion system effector proteins of Chlamydia ranged from 85% to 93%. NOD2-siRNA could effectively inhibit the expression of NOD2 at mRNA level in BMDMs ( P<0.001). Moreover, Cpn0423-induced production of MIP-2 [(920.5±99.1) pg/ml vs (130.1±11.5) pg/ml, P<0.001] and IL-6 [(266.2±58.4) pg/ml vs (165.7±21.5) pg/ml, P<0.001] in BMDMs were decreased following NOD2-siRNA pre-treatment. Cpn0423 DNA was detected in the BAlF of 83.3% (10/12) of Cpn-positive cases, but not in Cpn-negative cases. Conclusions:Cpn0423 induced inflammatory response in host cells through NOD2 pathway, which was closely related to the chronic inflammatory injury caused by Cpn.