Dec 27, 2019

Neuroprotection of dihydrotestosterone via suppression of the toll-like receptor 4/nuclear factor-kappa B signaling pathway in high glucose-induced BV-2 microglia inflammatory responses

Lei YangRen-Yuan Zhou


Hyperglycemia is considered to induce neuronal apoptosis via activating microglia inflammatory responses, thus involving in the development and progression of diabetic encephalopathy and neurodegenerative disorders. Increasing evidences suggest that androgen exerts neuroprotective functions including antiapoptosis, anti-inflammation and antioxidative stress. In this study, we investigate the anti-inflammatory role of dihydrotestosterone (DHT) in high glucose (HG)-induced neuroinflammatory response in BV-2 microglia. Our results revealed that DHT significantly inhibited HG-induced production of nitric oxide and prostaglandin E2 through suppressing the expression of corresponding regulatory enzymes - inducible NO synthase and cyclooxygenase-2. Also, DHT inhibited HG-induced expression of TNF-α and IL-1β. Moreover, DHT suppressed the toll-like receptor 4 (TLR4)/nuclear factor-kappa B (NF-κB) signaling pathway. Furthermore, when SH-SY5Y neurons were cultured in HG-treated BV-2 microglial supernatant, DHT pretreatment significantly increased neuronal survival, indicating the neuroprotective role of DHT. Collectively, these results suggest that DHT could protect SH-SY5Y neurons from HG-mediated BV-2 microglia inflammatory damage thro...Continue Reading

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Mentioned in this Paper

Nitric Oxide
TNFSF11-mediated Signaling Pathway
Antioxidant Activity
Interleukin-1 beta
Disease Progression
Cognition Disorders

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Apoptosis is a specific process that leads to programmed cell death through the activation of an evolutionary conserved intracellular pathway leading to pathognomic cellular changes distinct from cellular necrosis