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. Author manuscript; available in PMC: 2021 May 11.
Published in final edited form as: Cell Mol Neurobiol. 2019 Dec 21;40(5):845–857. doi: 10.1007/s10571-019-00778-1

Fig 7. Angiotensin II-induced neuroinflammation and oxidative stress are mediated by kinin B1R.

Fig 7.

Mouse neonatal primary hypothermic neurons express both B1R and AT1R. Ang II stimulation of neurons increased expression of B1R, which in turn increased resulted in upregulation of Nox2 and Nox4 expression, and NF-κB activation, and ultimately leading to expression of pro-inflammatory cytokine production. Treatment with R715, the specific B1R antagonist blunted angiotensin II-induced neuroinflammation and oxidative stress by reducing Nox gene expression and attenuating NF-κB activation.