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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. 4. Angiotensin II-induced Nox2 and Nox4 gene expression was reduced by treatment with B1R antagonist in primary hypothalamic neurons.

Fig. 4.

Angiotensin II treatment induced oxidative stress by increased gene expression of (A) Nox2 and (B) Nox4. This increase was attenuated or prevented by pre-treatment with R715. The cultured primary neurons are pre-treated with a specific B1R antagonist (R715, 10 μM) for 1 hour, followed by treatment with angiotensin II (Ang II, 300 nM) for 6 hours. The gene expression was measured using real time RT-PCR in triplicates. (n=4 independent cultures/group). Statistical significance: One-way ANOVA followed by Tukey’s multiple comparisons test. *p<0.05 compared to vehicle, †p<0.05 compared to Ang II.