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Activated microglia producing reactive nitrogen species, inflammatory factors,reactive oxygen species (ROS) and other neurovirulent factors, can lead to thedevelopment of neurodegenerative diseases. Certain compounds can inhibit the activationof microglia. However, the mechanisms remain unclear. In the present study, weinvestigated the inhibitory effect of geniposide on the production of ROS andinducible nitric oxide synthase (iNOS) in lipopolysaccharide (LPS)-stimulatedN9 murine microglial cells through the p38, ERK1/2 and nuclear factor-κB (NF-κB)signaling pathways. After the N9 cells were pre-treated with the vehicle or geniposideand exposed to LPS for the time indicated, the MTT conversion test was used toassess cell viability. Suitable concentrations were chosen and adjusted accordingto the experiments. Extracellular nitric oxide (NO) release was measured by Griessreaction. The formation of ROS and intracellular NO was evaluated by fluorescenceimaging. NOS activities were determined using commercially available kits. Themorphology of the N9 cells was examined by hematoxylin and eosin staining. Theexpression of iNOS mRNA was examined by RT-PCR. The protein levels of iNOS, p38mitogen-activated protein kinase (MAPK), ERK1/2 and NF-κB, inhibitory factor-κB-α(IκB-α) were determined by western blot analysis. The results showed that geniposideattenuated the activation of N9 cells and inhibited the overproduction of NO,intracellular ROS and the expression of iNOS induced by LPS in the cells. In addition,geniposide blocked the phosphorylation of p38, ERK1/2 and inhibited the drop-offof IκB induced by LPS in the cells. These data indicate that geniposide has therapeuticpotential for the treatment of neurodegenerative diseases, and that it exertsits effects by inhibiting inflammation.

LPS-induced iNOS expression in N9 microglial cells is suppressed by geniposide via ERK, p38 and nuclear factor-κB signaling pathways