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Figure 10 | Journal of Neuroinflammation

Figure 10

From: Telmisartan directly ameliorates the neuronal inflammatory response to IL-1β partly through the JNK/c-Jun and NADPH oxidase pathways

Figure 10

Proposed pathways involved in the neuroprotective effects of telmisartan. The pro-inflammatory effects of interleukin-1 beta (IL-1β) in neurons are the consequence of binding to its IL-1R1 receptor, which in turn increases NADPH oxidase activation, reactive oxygen species (ROS) formation, c-Jun N-terminal kinase (JNK) and c-Jun activation, and IL-1 receptor 1 (IL-1R1) gene expression. This results in enhanced expression of COX-2 and prostaglandin E2 (PGE2). Telmisartan abrogates these pro-inflammatory effects of IL-1β by mechanisms involving inhibition of NADPH oxidase activation and the JNK/c-Jun pathway.

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Journal of Neuroinflammation

ISSN: 1742-2094