Figure 8

TSG reduces the induction of inducible nitric oxide (iNOS) in lipolysaccharide (LPS)-stimulated primary microglia and protects the hippocampal neurons from primary microglia conditioned medium-induced cell injury. (A) Representative images showing that TSG treatment (30 minutes, 50 μM) inhibited iNOS expression in primary microglia. (B) Quantitative analysis of the iNOS expression in primary microglia in LPS/TSG-treated cells (n = 5, **P < 0.01 versus control or the LPS alone-treated group). (C) Quantitative analysis of NO content in LPS/TSG-treated cells (n = 5, **P < 0.01 versus control; *P < 0.05 versus the LPS alone-treated group). (D) TSG treatment (30 minutes, 50 μM) inhibited the increase in apoptotic nuclei in hippocampal neurons induced by primary microglia-derived conditioned medium. (E) Quantitative analysis of apoptotic nuclei in LPS/TSG-treated cells (n = 5, **P < 0.01 versus control; *P < 0.05 versus the LPS alone-treated group). (F) Quantitative analysis showing that the LPS-induced increase in the binding of nuclear factor -κB (NF-κB) to its DNA element in primary microglia was attenuated by TSG treatment at the concentrations of 10 and 50 μM (n = 5, *P < 0.05 versus the LPS alone-treated group). NS, no significance; GAPDH, glyceraldehyde-3-phosphate dehydrogenase. All data were shown as mean ± standard error.