Combined Bacopa, Phosphatidylserine, and Choline Protect Against Stress-Induced Neurotoxicity.

Background/

Objectives

Chronic stress leads to sustained elevations in cortisol levels, which promote neuronal damage and impair memory. Prolonged stress also enhances proinflammatory signaling. Adaptogens are plant-derived compounds associated with the ability to increase the body's resistance to stress, thereby improving mental and physical performance. To identify potential interventions capable of attenuating stress-related memory alterations, this study investigated a formulation combining the adaptogen Bacopa monnieri L. with phosphatidylserine and choline (BPC).

Methods

An in vitro model of stress-related neuroinflammation was established by exposing BV2 microglial cells to corticotropin-releasing hormone (CRH, 100 nM). SH-SY5Y cells exposed to conditioned medium from CRH-stimulated BV2 cells or to iron(II) sulfate and L-ascorbic acid (Fe/Asc) were used as models of neurotoxicity.

Results

BPC attenuated CRH-induced proinflammatory microglial morphology, as well as the reduction in cell viability and cell number. BPC treatment restored the levels of stress-related markers, including SIRT-1, Nrf-2, and phosphorylated JNK (p-JNK). Furthermore, BPC protected against neurotoxicity induced by CRH and Fe/Asc and promoted cholinergic activation by restoring basal acetylcholinesterase (AChE) levels. The combined BPC formulation showed superior efficacy compared with its individual components across all experimental assays.

Conclusions

Collectively, these findings indicate that the BPC formulation developed in this study effectively attenuates stress-related neuroinflammation and neurotoxicity. BPC may represent a promising strategy to help limit the progression of early cognitive dysfunction under conditions of prolonged stress.