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Figure 2 | Journal of Neuroinflammation

Figure 2

From: The anti-inflammatory role of tissue inhibitor of metalloproteinase-2 in lipopolysaccharide-stimulated microglia

Figure 2

Overexpression of tissue inhibitor of metalloproteinase (TIMP)-2 inhibited the production of nitric oxide (NO), TNF-α, IL-1β, and reactive oxygen species (ROS), while increasing anti-inflammatory IL-10 production in lipopolysaccharide (LPS)-stimulated BV2 cells. (A) Control vector and TIMP-2 expression plasmid. (B) Western blot for TIMP-2 in BV2 cells transfected with TIMP-2 or control vector. (C-H) Effects of TIMP-2 on pro- or anti-inflammatory molecules. BV2 cells transfected with TIMP-2 or control vector were treated with LPS (100 ng/ml) for 16 h, and the amounts of NO, TNF-α, IL-1β, IL-6, and IL-10 released into the media, as well as the intracellular ROS level, were measured. (I) BV2 cells transfected with TIMP-2 or control vector were treated with LPS (100 ng/ml) for 6 h, and total RNA was isolated. The mRNA levels of inducible nitric oxide synthase (iNOS) and cytokines were determined by RT-PCR. (J) Quantification of RT-PCR data. Values correspond to the mean ± S.E.M. of three independent experiments. *P <0.05, significantly different from the LPS + control vector group.

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