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Fig. 5 | Journal of Neuroinflammation

Fig. 5

From: Anti-neuroinflammation ameliorates systemic inflammation-induced mitochondrial DNA impairment in the nucleus of the solitary tract and cardiovascular reflex dysfunction

Fig. 5

Minocycline prevented mitochondrial DNA damage in the NTS induced by LPS peritoneal infusion. a Mitochondrial 8-OHdG levels detected by ELISA and representative gels (inset) and densitometric analysis from Western blot showed the mitochondrial protein expression of b γ-H2AX, c UNG, d APE1, and e RAD51 in the NTS after peritoneal infusion with saline or LPS for 7 days with additional intracisternal (IC) infusion of saline or mino. Prohibitin was used as the internal control for mitochondrial protein expression. f A representative schematic diagram and microscopy images of 8-OHdG (green), NeuN (red), and DAPI (blue) triple immunofluorescent staining in the NTS. Values are the mean ± SEM of 6 to 8 animals in each group. *P < 0.05, **P < 0.01 versus the control (C) group and ##P < 0.01 versus the LPS group according to post hoc Tukey’s multiple range analysis. AP, area postrema; APE1, the apurinic/apyrimidinic endonuclease; C, control, infused with saline; cc, central canal; ELISA, enzyme-linked immunosorbent assay; L, LPS, lipopolysaccharides; mino, minocycline; sol, solitary tract; UNG, uracil-DNA glycosylase. Scale bar, 20 μm

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