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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. 3. B1R antagonist treatment reduced angiotensin II induced reactive oxygen species (ROS) production in primary hypothalamic neurons.

Fig. 3.

(A). Representative photomicrographs showing dihydroethidium (DHE) stained primary hypothalamic neurons. (B). DHE staining quantified as corrected total cell fluorescence shows increased superoxide generation by treatment with angiotensin II (Ang II), which was attenuated by R715 treatment. (n=8/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 (C). ROS production measured by microplate DHE assay indicates that Ang II-induced a significant increase in total ROS production indicating increased oxidative stress, and treatment with R715 prevented this Ang II-induced ROS production. (n=6 independent culture wells/group). Treatment with antimycin A (Ani-A), an inhibitor of complex III of the mitochondrial electron transport chain, is used as a positive control for ROS generation and treatment with N-Acetyl-L-Cysteine (NAC) is used as an antioxidant control. 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.