Soy lysolecithin reduces salt-induced hypertension and cognitive decline

High salt (HS) intake is a major global health concern, closely linked to hypertension and growing evidence of cognitive and emotional decline. Although salt is a routine part of daily diets, long-term overconsumption can negatively impact both the cardiovascular system and the central nervous system, underscoring the need for practical dietary strategies to mitigate these adverse health effects.

Prostaglandins (PGs) are lipid compounds derived from arachidonic acid (AA) that act as potent local hormones. They maintain cardiovascular homeostasis through a delicate balance of vasodilation and vasoconstriction. In the brain, depending on the receptor involved, PGs can promote either neuroprotective or neurotoxic signaling, thereby influencing emotional and cognitive function. LPC70, a soy lysolecithin with lysophosphatidylcholine (LPC) comprising more than 70% phospholipids, has previously been shown to attenuate high-salt diet (HSD)-induced hypertension and cognitive impairment. However, the biological mechanisms, specifically the role of LPC70 in regulating PG signaling, remain unclear.

To address this gap, a team of researchers, led by Professor Akihiro Mouri and Dr. Hisayoshi Kubota, along with Dr. Kazuhiro Kagotani, studied how LPC70 regulates PG signaling and how this attenuates hypertension and behavioral impairments in a mouse model. Dr. Kubota, the first author of the study, made major contributions to the project's execution, including the evaluation of blood pressure, behavioral phenotypes, and PG-related molecular changes. His dedicated work helped reveal the organ-specific effects of LPC70 on HSD-induced cardiovascular and cognitive abnormalities. Prof. Mouri and Dr. Kubota are affiliated with the Department of Regulatory Science for Evaluation and Development of Pharmaceuticals & Devices, Fujita Health University Graduate School of Medical Science, and the International Center for Brain Science (ICBS), Fujita Health University, Japan. Dr. Kagotani is affiliated with Tsuji Oil Mills Co., Ltd, Japan, and Tsuji Health and Beauty Science Laboratory, Mie University, Japan. The results of this study were made available online on May 14, 2026, and will be published in Volume 197 of the Neurochemistry International journal on July 1, 2026.

"We wanted to understand the role of LPC70 in coordinating changes in PG signaling across organ systems," mentioned Prof. Mouri. "Our study originated from a collaborative research project with Tsuji Oil Mills Co., Ltd, a company that develops naturally derived food ingredients," he added.

As anticipated, mice fed the HSD developed elevated blood pressure. They also showed reduced social interaction and impaired object recognition memory, despite no major changes in locomotor activity or anxiety-like behavior. This suggests that HSD selectively affected higher-order behavioral and cognitive functions. LPC70 supplementation attenuated the increased blood pressure and improved both social behavior and object recognition memory in HSD mice.

In the kidney, HSD increased the expression of cyclooxygenase-2 (COX-2) and the PGE2 receptor EP3, both of which are involved in PG signaling and may contribute to HSD-induced hypertension. LPC70 reduced these HSD-associated changes, suggesting that it can help normalize maladaptive PG signaling in the kidney.

In the prefrontal cortex, a region of the brain involved in cognition and social behavior, HSD reduced expression of the PGD2 receptor DP1, which mediates neuroprotective and anti-inflammatory signaling. LPC70 restored DP1 expression without affecting DP2, a receptor associated with neurotoxic signaling. This receptor-specific response suggests that LPC70 may help shift PGD2 signaling toward a more neuroprotective profile, leading to attenuation of behavioral and cognitive impairments.

Another key finding was related to the changes in the levels of circulating AA, the fatty acid precursor for PG production. Despite reduced circulating AA levels in HSD mice, LPC70 increased AA-derived PGs, including PGE2 and PGD2. This suggests that LPC70 enhances AA utilization, thereby promoting AA-derived PG production under HSD conditions.

Together, these findings indicate that LPC70 promotes organ-specific, receptor-dependent PG signaling, suppressing maladaptive pathways in the kidney while restoring neuroprotective signaling in the brain.

LPC70 shows promise as a functional food ingredient for mitigating the negative health impacts of HS intake. It may support cardiovascular and cognitive health, especially in populations with high dietary salt intake.

"Our study elucidates LPC70's role in PG signaling, laying the groundwork for future clinical research and dietary interventions aimed at reducing hypertension-related cognitive decline and promoting healthy aging globally," concluded Prof. Mouri.