Skip to main content


Springer Nature is making SARS-CoV-2 and COVID-19 research free. View research | View latest news | Sign up for updates

Fig. 9 | Journal of Neuroinflammation

Fig. 9

From: HSP60 critically regulates endogenous IL-1β production in activated microglia by stimulating NLRP3 inflammasome pathway

Fig. 9

Downregulation of HSP60 reduces JEV-induced microglial inflammation. The left panel shows the effect of HSP60 knockdown with specific eSiRNA on JEV-induced microglial inflammation in N9 cells, while the right panel shows the effect of HSP60 knockdown using HSP60 vivo-morpholino in JEV-infected mice brains. a, b Western blots of iNOS and COX2 after HSP60 knockdown during JEV infection in N9 cells and mice brain respectively. Protein levels of iNOS and COX2 were normalized with the β-actin levels. The blots are representative of three independent experiments. c–h CBA of pro-inflammatory markers was performed to assess the role of HSP60 in JEV-induced microglial inflammation. Bar graphs show quantification of the cytokines levels in N9 cells (c–e) and in mice brains (f–h). Cytokine bead array was performed in triplicates for each experiment. For animal experiments, at least three mice were used in each group. Data represented as mean ± SD of three independent experiments (n = 3). *p < 0.05, **p < 0.01 in comparison to control values. ##p < 0.01 with respect to JEV-infected values

Back to article page