Progesterone restores mitochondrial bioenergetic function in streptozotocin- and amyloid-β-challenged HT-22 hippocampal cells: An in vitro model of Alzheimer's disease
Seema Yousuf, Fahim Atif, Donald G. SteinBackground
Mitochondrial dysfunction contributes to Alzheimer's disease (AD) by promoting bioenergetic failure and neuronal loss.
Objective
We investigated whether progesterone (P4) protects against mitochondrial impairment in two
Methods
Mouse hippocampal HT-22 cells were exposed to amyloid-β (Aβ) or streptozotocin (STZ) and treated with P4. Mitochondrial respiration was assessed using Seahorse extracellular flux analysis.
Results
Both Aβ and STZ significantly reduced basal and maximal respiration, spare respiratory capacity, and ATP-linked respiration (ATP production rate), while increasing proton leak and cell death. P4 treatment restored mitochondrial respiratory parameters and improved cell viability.
Conclusions
These findings suggest progesterone preserves mitochondrial bioenergetic function under AD-related stress conditions.