The pathogenesis of visual dysfunction in
stroke remains unclear. The objective of this study was to explore
retinal damage in
stroke spontaneously hypertensive rats (SHR) and evaluate the role of
curcumin in the
retinal injury after
stroke. Mature male SHR were used as the animal model for
hypertension and age-matched male Wistar-Kyoto (WKY) rats as the normotensive controls. The rat model of
stroke was made by bilateral vertebral artery
electrocoagulation combined with transient bilateral common carotid artery
ligation. The animals were randomly divided into
sham group,
ischemia/reperfusion group,
solvent control group, and
curcumin treatment group. Each group was subdivided into 2 h, 6 h, 24 h, 72 h, and 7 day after reperfusion. Blood pressure was measured in SHR and WKY rats. Eye fundus was examined in living animals, and then, tissue specimens were collected for histologic examination,
terminal deoxynucleotidyl transferase-mediated
2'-deoxyuridine 5'-triphosphate nick end labeling, and immunohistochemistry. Retinopathy, induced by I/R, was more serious in rats with
hypertension than that in normotensive rats (
retinal thickness index, p = 0.004). The number of apoptosis in
retinal capillary cells and neurons reduced significantly in the
curcumin-treated groups.
Curcumin treatment inhibited phosphorylated
c-Jun N-terminal kinase (JNK) expression in SHR after
retinal I/R injury. Thus,
hypertension aggravated
retinal I/R injury after
stroke.
Curcumin, a specific inhibitor of JNK, can prevent the development of
hypertensive retinopathy after I/R injury by inhibiting apoptosis in
retinal capillary cells and neurons.