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17β-Estradiol Modulates SIRT1 and Halts Oxidative Stress-Mediated Cognitive Impairment in a Male Aging Mouse Model
Mehtab Khan1, Rahat Ullah1, Shafiq Ur Rehman1
1Division of Life sciences and Applied Life Science (BK 21plus), College of Natural Science, Gyeongsang National University, Jinju 52828, Korea.
Abstract:
Oxidative stress has been considered the main mediator in neurodegenerative disease and in normal aging processes. Several studies have reported that the accumulation of reactive oxygen species (ROS), elevated oxidative stress, and neuroinflammation result in cellular malfunction. These conditions lead to neuronal cell death in aging-related neurodegenerative disorders such as Alzheimer's disease (AD) and Parkinson's disease. Chronic administration of d-galactose (d-gal) for a period of 10 weeks causes ROS generation and neuroinflammation, ultimately leading to cognitive impairment. In this study, we evaluated the estrogen receptor α (ERα)/silent mating type information regulation 2 homolog 1 (SIRT1)-dependent antioxidant efficacy of 17β-estradiol against d-gal-induced oxidative damage-mediated cognitive dysfunction in a male mouse model. The results indicate that 17β-estradiol, by stimulating ERα/SIRT1, halts d-gal-induced oxidative stress-mediated JNK/NF-ҡB overexpression, neuroinflammation and neuronal apoptosis. Moreover, 17β-estradiol ameliorated d-gal-induced AD-like pathophysiology, synaptic dysfunction and memory impairment in adult mouse brains. Interestingly, inhibition of SIRT1 with Ex527 (a potent and selective SIRT1 inhibitor) further enhanced d-gal-induced toxicity and abolished the beneficial effect of 17β-estradiol. Most importantly, for the first time, our molecular docking study reveals that 17β-estradiol allosterically increases the expression of SIRT1 and abolishes the inhibitory potential of d-ga. In summary, we can conclude that 17β-estradiol, in an ERα/SIRT1-dependent manner, abrogates d-gal-induced oxidative stress-mediated memory impairment, neuroinflammation, and neurodegeneration in adult mice.
Insights
17β-estradiol protects against d-galactose-induced cognitive decline by reducing oxidative stress and neuroinflammation. This effect is mediated through the estrogen receptor α (ERα)/silent mating type information regulation 2 homolog 1 (SIRT1) pathway, improving memory and preventing neuronal damage.
Area of Science:
- Neuroscience
- Molecular Biology
- Pharmacology
Background:
- Oxidative stress, reactive oxygen species (ROS), and neuroinflammation are key factors in neurodegenerative diseases like Alzheimer's and Parkinson's.
- Chronic d-galactose (d-gal) administration induces oxidative damage, neuroinflammation, and cognitive impairment, mimicking aging processes.
- Estrogen receptor α (ERα) and SIRT1 are implicated in cellular protection and aging.
Purpose of the Study:
- To investigate the antioxidant and neuroprotective effects of 17β-estradiol in a d-gal-induced mouse model of cognitive dysfunction.
- To elucidate the role of the ERα/SIRT1 pathway in mediating these protective effects.
Main Methods:
- Male mice were treated with d-galactose for 10 weeks to induce oxidative stress and cognitive impairment.
- 17β-estradiol was administered to assess its protective effects.
- SIRT1 inhibition was achieved using Ex527 to evaluate its impact on 17β-estradiol's efficacy.
- Molecular docking studies were performed to analyze interactions between 17β-estradiol and SIRT1.
Main Results:
- 17β-estradiol significantly ameliorated d-gal-induced cognitive deficits, AD-like pathology, and synaptic dysfunction.
- Treatment with 17β-estradiol reduced oxidative stress, neuroinflammation (JNK/NF-κB pathways), and neuronal apoptosis.
- SIRT1 inhibition abolished the beneficial effects of 17β-estradiol, confirming its critical role.
- Molecular docking revealed that 17β-estradiol allosterically enhances SIRT1 expression and counteracts d-galactose's inhibitory effects.
Conclusions:
- 17β-estradiol exerts significant neuroprotective effects against d-galactose-induced cognitive impairment via an ERα/SIRT1-dependent mechanism.
- The ERα/SIRT1 pathway is crucial for mitigating oxidative stress, neuroinflammation, and neurodegeneration.
- 17β-estradiol represents a potential therapeutic agent for age-related cognitive decline and neurodegenerative diseases.
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