Objective To investigate the effect of simulated microgravity on the tissue structure and the mRNA and pro-tein expression of HSP70 in lungs of rhesus macaques .Methods Fifteen healthy young male rhesus monkeys were randomly divided into 3 groups:control group (group A, n=5), 6 weeks′simulated microgravity group (group B, n=5) and recovery for 4 weeks after 6 weeks of simulated microgravity group (group C, n=5).-10 degree head-down-tilt was used to simulate microgravity .HE staining and transmission electron microscopy were used to observe the histopathological and ultrastructural changes in pulmonary tissues .The expression and location of HSP 70 in lung tissues were observed by immunohistochemistry (IHC) method.The mRNA and protein expression of HSP70 in lung tissues were detected by quan-titative real-time PCR ( Q-PCR) and Western blotting .Results Compared with group A , histopathological examination re-vealed alveolar septal thickening , partial fusion of pulmonary alveoli and alveolar and interstitial lymphocytic infiltration in groups B and C .Ultrastructure examination showed smaller and irregular nuclei of alveolar epithelial cells , an increased number and volume of the lamellar bodies , enhanced evacuation , part of vacuolar degeneration and mitochondrial swelling in groups B and C .IHC results showed that HSP 70 was expressed in bronchial epithelial cells , vascular endothelial cells and alveolar epithelial cells of pulmonary tissues in each group , either in cytoplasm or in nucleus .In addition , the alveolar interstitial and alveolar exudates in groups B and C also showed positive signals .Q-PCR and Western blotting results showed that HSP70 was expressed in all of the three groups , but no significant difference was found between any two groups (P>0.05).Conclusion Medium or long-term simulated microgravity can cause damage to the lung tissue of rhesus mon-keys, but it has no effect on the expression of HSP 70 in the lung tissue.

Objective To investigate the effect of simulated weightlessness on the mRNA and protein expression of chemokine CCL20 and it′s receptor CCR6 in lung of rhesus macaque. Methods Fifteen healthy young male rhesus monkeys were randomly divided into 3 groups:control group, simulated group and recovery group. HE staining was used to observe the histopathological structure changes of pul-monary tissues. And the mRNA and protein expres-sion of CCR6 and CCL20 in lung tissue were detected by immunohistochemistry and quantitative real-time PCR( Q-PCR) . Results Compared with the control group, histopathological examination revealed alveolar septal thicken-ing, and alveolar and interstitial lymphocytic infiltration in simulated group and recovery group, and the pathologi-cal changes in recovery group were lighter than those in simulated group. The expressions of CCL20 mRNA in simu-lated group and the recovery group were higher than that in the control group, but there was no significant differ-ence;the expression of CCR6 mRNA in simulated group was significantly higher than that in the control group and the recovery group(P<0. 01), but there was no significant difference between the control group and the recovery group. Immunohistochemistry results showed that CCL20 and CCR6 were expressed in the lung tissues of each group, but the expression of CCL20 was weak. The positive cells were found mainly in the cytopl-asm of bronchial and alveolar epithelial cells and vascular endothelial cells. The protein expression of CCL20 and CCR6 in simulated group were significantly higher than that in the control group and the recovery group(P<0. 05). Conclusion Me-dium or long term simulated weightlessness can induce the destruction of lung tissue structure and infiltration of lymphocytes, and it can also significantly enhance the mRNA and protein expression of CCL20 and its receptor CCR6 in lung tissues.

Matrix metalloproteinases,a large family of zinc-dependent endopeptidases,are the main function to degrade the extracellular matrix.Acute respiratory distress syndrome(ARDS),a syndrome of acute respiratory failure,is characterized by refractory hypoxemia,noncardiogenic pulmonary edema and dysregulated and excessive inflammation.Matrix metalloproteinases can promote the occurrence and development of ARDS by proteolytic processing,including cytokines and chemical factors activation and release,destruction of the integrity of alveolar-epithelial barrier and activation of the protein tyrosine kinase signaling pathway.