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Fig. 6 | Journal of Neuroinflammation

Fig. 6

From: Neuronal aldosterone elicits a distinct genomic response in pain signaling molecules contributing to inflammatory pain

Fig. 6

Aldosterone synthase inhibitor FAD286 reversed the elevated aldosterone content as well as enhanced expression of pain signaling molecules TRPV1, CGRP, Nav1.8, and trkA mRNA in nociceptive dorsal root ganglia (DRG) neurons with inflammatory pain. a, b Determination of aldosterone-immunoreactive (IR) DRG neurons of FCA rats treated with i.t. aldosterone synthase inhibitor FAD286. Note, the number of aldosterone-IR DRG neurons of FCA rats was increased by approximately 2.2-fold compared to controls which was reversed following continuous i.t. aldosterone synthase inhibitor FAD286 treatment over 5 days (b) (P > 0.05, two-tailed independent Student’s t test; n = 7–11). c Determination of aldosterone content in DRG of FCA rats treated with i.t. aldosterone synthase inhibitor FAD286 by a fluorometric enzyme-linked immunoassay. Note, aldosterone content in DRG of FCA rats was increased by approximately 2.6-fold compared to control which was reversed following i.t. adosterone synthase inhibitor FAD286 treatment (P < 0.05, two-tailed independent Student’s t test; n = 7,8). eh Long-lasting i.t. aldosterone synthase inhibitor FAD286 to rats with Freund’s complete adjuvant (FCA)-induced inflammation reversed the enhanced expression of pain signaling molecules TRPV1 (e), CGRP (f), Nav1.8 (g), and trkA (h) mRNA. (P < 0.05, two-tailed independent Student’s t test; n = 5). Data are expressed as means ± SD

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