17 β-Estradiol Oxidative Stress Attenuation and Autophagy-Induced
Degeneration of dopaminergic neurons in the substantia nigra of the brain stem is the main pathological aspect of Parkinson’s disease (PD). 17 β-estradiol (E2) has neuroprotective effects on substantia nigra, however, the underlined mechanism is not well-known. In this study, we evaluated the neuroprotective effects of E2 in the ovariectomized 6-hydroxydopamine- (6-OHDA) rat model of PD.
Materials and Methods
In this experimental study, all animals were ovariectomized to avoid any further bias in E2 levels
and then these ovariectomized rats were randomly assigned into three experimental groups (10 rats in each group):
ovariectomized control group (OCG), ovariectomized degeneration group receiving 25 μg of 6-OHDA into the left corpus
striatum (ODG), and ovariectomized E2 pretreatment group pretreated with 0.1 mgkg-1of 17 β-estradiol for three days prior
to the destruction of corpus striatum with 6-OHDA (OE2PTG). The apomorphine behavioral test and Nissl staining were
performed in all experimental groups. The expressions of Sequestosome-1 (
E2 administration reduced the damages to the dopaminergic neurons of the substantia nigra. The motor
behavior, the number of rotations, and histological tests in the treatment group showed the cell survival improvement in
comparison with the control groups indicating that E2 can inhibit the neurodegeneration. P62 and Lc3 were expressed
in all experimental groups while
E2 prevents neurodegeneration in dopaminergic neurons of the midbrain by over-expression of Ulk1 gene and augmenting the induction of autophagy.