NLRP3 inflammasome contributes to neurovascular unit damage in stroke.

Recently, a wealth of information has emerged connecting the activation of the NLRP3 (NOD-like receptor family pyrin domain-containing 3) inflammasome to stroke pathogenesis, although the exact influence of the NLRP3 inflammasome on stroke is still in the stage of preliminary study and is awaiting further confirmation. In this paper, we will review the structure, assembly and activation of the NLRP3 inflammasome and its expression in the neurovascular units and will speculate on its possible roles in neurovascular injury post-stroke. Evidence on this topic suggests that targeting NLRP3-mediated inflammation at multiple levels may provide a new therapeutic strategy to prevent the deterioration of neurovascular units after stroke. However, many aspects of the biological link between the NLRP3 inflammasome and stroke remain ill-defined or even completely unknown. As fresh insights come to light regarding the NLRP3 inflammasome, the opportunities to develop new therapeutic strategies for stroke patients are expected to improve accordingly.

[Pulmonary platelet endothelial cell adhesion molecule-1 (PECAM-1) in rabbits after acute paraquat (PQ) poisoning].

OBJECTIVE: To examine the changes in PECAM-1 expression and its correlation to the level of pulmonary tissue injury in the lungs from rabbits exposed to acute PQ poisoning. METHODS: Three groups of New Zealand rabbits (12 each, randomly assigned) were treated with PQ at 8, 16 and 32 mg/kg respectively through gavage. The animals were sacrificed 7 days after the poisoning and the upper lobe of their lungs collected for semi-quantitative microscopic evaluation of tissue injury, pulmonary fibrosis and the expression of PECAM-1 after hematoxylin-eosin (HE), Masson, and immuno-histological staining. The correlation analysis was used for the relationship between the expression of PECAM-1 and lung injury score or fibrosis of lung. RESULTS: The evaluation scores (demonstrated as mean+ standard deviation) in the three treatment groups were found to be (a) 8.33±1.03, 9.83±1.17 and 11.50±1.38 for lung tissue injury, (b) (31.09±2.05)%, (34.37±1.62)% and (36.54±0.44)% for pulmonary fibrosis, and (c) (20.31± 0.70)%, (19.34±0.68)% and (18.37±0.46)% for PECAM-1 expression. Statistically significant difference (P< 0.05) was found between the results from different dose groups for all the indexes examined. Pearson correlation analysis showed that expression of PECAM-1 was negatively correlated to lung injury score ( r = - 0.732, P = 0.001) and fibrosis degree of lung ( r = - 0. 779, P< 0.001). CONCLUSION: (1) The expressions of PECAM-1 in the lungs of PQ treated animals decrease to increased dose of PQ poisoning, (2) such decrease is correlated to the degree of pulmonary tissue injury and fibrosis of lung. It is possible that PECAM-1 expression inhibition be an important factor in the development of lung injury after acute PQ poisoning.