ABSTRACT
AIM:
To investigate the effects and mechanisms of
curcumin on
apoptosis of
retinal ganglion cells(RGCs)in chronic
ocular hypertension rats.
METHODS:
A total of 21 Spraque-Dawley(SD)
rats were randomly divided into 3 groups with 7
rats in each group. The
rat models of chronic
ocular hypertension were established by
cauterization of the superior scleral
veins in the high
intraocular pressure model group and the
curcumin treatment group, and the sham operation group only cut the
conjunctiva without the
cauterization of the superior scleral
veins; the
rats in the
curcumin treatment group were intragastrically treated with
curcumin at a
dose of 4mL/kg, and the
rats in the sham operation group and the high
intraocular pressure model group were treated with
pure water at a
dose of 4mL/kg for 3wk. After 3wk, HE
staining was used to observe the morphological and pathological changes of
retina, the number of RGCs and the thickness of
ganglion cell layer(GCL)in each group of
rats;
TUNEL staining was used to observe the
apoptosis of RGCs and
retinal cells in each group of
rats; the expression levels of
glutamate-cysteine ligase modifier subunit(GCLM)and
heme oxygenase-1(HO-1)in the
retina of each group of
rats were detected by real-
time fluorescence quantitative
PCR, immunohistochemical
staining and
Western blot.
RESULTS:
Compared with the sham operation group, the
retinal morphology of
rats in the high
intraocular pressure model group and the
curcumin treatment group was disorganized, the number of RGCs was reduced, the GCL was thinner, the
apoptosis rate of RGCs and
retinal cells increased, and the expression levels of GCLM and HO-1 increased. Compared with the high
intraocular pressure model group, the
retinal morphology of
rats in the
curcumin treatment group was basically normal, the number of RGCs increased, the GCL thickened, the
apoptosis rate of RGCs and
retinal cells decreased, and the expression levels of GCLM and HO-1 increased.
CONCLUSION:
Curcumin can inhibit the
apoptosis of RGCs in the
rat model of chronic
ocular hypertension by up-regulating the expression of
antioxidant genes GCLM and HO-1.