Oxidative Medicine and Cellular Longevity / 2015 / Article / Fig 1

Research Article

Neuroprotective Effect of Dexmedetomidine on Hyperoxia-Induced Toxicity in the Neonatal Rat Brain

Figure 1

Apoptosis caused by hyperoxia is prevented by dexmedetomidine. (a) Representative TUNEL staining images (original magnification ×400) of rat brain frontal cortices (FC), retrosplenial cortices (RSC), hypothalamus (HTH), and thalamus (TH) of P7 control pups in room air without (CON) and with dexmedetomidine administration (DEX1, DEX5, and DEX10, corresponding to the concentrations of 1, 5, and 10 μg/kg) and after 24 h of hyperoxia from P6 to P7 without (HY) and with dexmedetomidine administration (HYDEX1, HYDEX5, and HYDEX10). (b) Quantitation of TUNEL positive cells in the rat brain frontal cortices (FC), retrosplenial cortices (RSC), hypothalamus (HTH), and thalamus (TH) showed that relative to the control (white bars) hyperoxia at 24 h significantly increased these cell counts in cortex and deep grey matter (black bars). These levels were significantly decreased through systemic dexmedetomidine pretreatment (hatched grey bars; DEX 1, 5, and 10 μg/kg). However, dexmedetomidine administration resulted in increased TUNEL positive cells in control rats most profound in TH (grey bars; DEX 1, 5, and 10 μg/kg). Data are expressed relative to the normoxia-exposed control group (white bars, 100%). Bars represent mean + SEM; per group; *, **, and *** versus normoxia/control; ## and ### versus hyperoxia.
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