Abstract

Objective To evaluate the effect of dexmedetomidine on retinal ischemia-reperfusion (I/R) injury in mice. Methods Forty-eight C57BL/6 male mice, aged 8 weeks, weighing 20-24 g, were divided into 3 groups (n=16 each) using a random number table: control group (C group), I/R group and dexmedetomidine group (D group). The model of retinal I/R injury was established by elevating intraocular pressure for 60 min using anterior chamber cannulation followed by 24 h of reperfusion.At 15 min before ischemia and 5 min before reperfusion, dexmedetomidine 25 μg/kg was intraperitoneally injected in group D, and the equal volume of normal saline was intraperitoneally injected in C and I/R groups.Eight mice were sacrificed at 24 h of reperfusion, and the retina was removed for microscopic examination of pathologic changes (with light microscope) after haematoxylin and eosin staining and for determination of cell apoptosis in retinal tissues (by TUNEL). Apoptosis index (AI) was calculated.Eight mice were sacrificed at 24 h of reperfusion, and the retina was removed for determination of the expression of Bcl-2, Bax, caspase-3 and CCAAT/enhancer-binding protein homologous protein (CHOP) in retinal tissues (by Western blot). Bcl-2/Bax ratio was calculated. Results Compared with group C, AI was significantly increased, the expression of Bax, caspase-3 and CHOP was up-regulated, the expression of Bcl-2 was down-regulated, Bcl-2/Bax ratio was decreased (P<0.05), and pathologic changes were found in retinal tissues in group I/R.Compared with group I/R, AI was significantly decreased, the expression of Bax, caspase-3 and CHOP was down-regulated, the expression of Bcl-2 was up-regulated, Bcl-2/Bax ratio was increased (P<0.05), and pathologic changes of retinal tissues were significantly attenuated in group D (P<0.05). Conclusion Dexmedetomidine can reduce retinal I/R injury, and the mechanism may be related to inhibiting cell apoptosis in mice. Key words: Dexmedetomidine; Reperfusion injury; Retina

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