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吡咯喹啉醌改善了自然衰老小鼠与增强线粒体生物能量相关的认知相关行为表现

ABSTRACT: We investigated whether pyrroloquinoline quinone (PQQ) could improve cognitive performance in twenty-month-old naturally aged mice and explored the potential mechanisms involved. Results showed that PQQ supplementation improved spatial working memory and recognition memory without inducing anxiety-like behavior, and was associated with better preservation of hippocampal neuronal integrity. In HT-22 hippocampal neuronal cells, PQQ reduced reactive oxygen species (ROS) accumulation, restored mitochondrial membrane potential, and enhanced mitochondrial respiratory capacity. Hippocampal transcriptomic analysis and upstream regulator prediction identified SIRT1 as a major regulator associated with the PQQ-induced transcriptional response, while uncoupling protein 2 (UCP2) emerged as a candidate downstream mitochondrial effector. Consistently, PQQ increased hippocampal SIRT1 protein expression and downregulated UCP2 at both mRNA and protein levels. Pharmacological inhibition of SIRT1 attenuated the PQQ-induced increase in ATP production and partially weakened the regulatory effect of PQQ on UCP2, supporting the involvement of SIRT1 in PQQ-associated mitochondrial bioenergetic regulation. Collectively, these findings indicate that PQQ improves cognitive-related behavioral performance in naturally aged mice and is associated with mitochondrial bioenergetic regulation, and suggest that modulation of a SIRT1–UCP2-associated pathway may contribute to its neuroprotective effects.

ORGANISM(S): Mus musculus

PROVIDER: GSE338219 | GEO | 2026/07/14

REPOSITORIES: GEO

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Project description:Pyrroloquinoline quinone (PQQ) is a naturally occurring compound and known to improve growth and reproductive performance when added to diets of PQQ-deprived rodents. To understand its mechanism action, changes in hepatic gene expression were measured in rats fed diets with or without added PQQ. Gene expression changes for PQQ supplemented (EC50 ~ 3 nmol PQQ/Kg diet) or deficient rats were assayed by expression microarray analysis and compared to those for known transcriptional regulators (epicatechin; Epi; dexamethasone, Dex; clofibrate, Clo; phenobarbital, Pb). Two principal expression clusters were observed; one for Dex and another for Pb, Epi, Clo, and PQQ. Within the latter, a PQQ subcluster containing a unique group of genes for cell signaling and transport functions. Next, short and long term PQQ depletion and repletion protocols (48 or 36 h, respectively) were performed, leading to changes in hepatic gene expression for both time periods. Of the ~10,000 genes and ESTs analyzed, 4.7% of the transcripts were sensitive to changes in PQQ dietary status. PQQ deprivation generally caused down regulation of genes associated with mitochondriogenesis, cell differentiation, and immune function. These gene expression changes provide the basis for most of the previously published functional observations associated with PQQ deficiency and PQQ administered in pharmacological amounts. To assess PQQ’s potential functions, we used gene expression profiling through microarray technology as part of a comprehensive approach to identify potential pathways and mechanisms. Given that the systemic effects of PQQ deprivation are influenced at levels of dietary intake in the micromolar range, highly purified diets were used to reduce expression from other bioactive factors and xenobiotics, such as those found in typical rodent chow diets. To establish if the changes in gene expression in response to PQQ exposure will follow a similar pattern as other xenobiotics, the responses to PQQ exposure were contrasted with those from exposure to epicatechin (Epi), dexamethasone (Dex), clofibrate (Clo), or phenobarbital (Pb). Dietary conditions were also chosen to clarify the response to short- and longer-term PQQ deprivation. A goal was to determine if specific changes in dietary protocol or patterns could be used to identify genes important to the function of PQQ. Because it has been observed that mitochondrial-related functions are influenced by PQQ, we hypothesized that changes in genes important to fatty acid and amino acid metabolism and mitochondrial function would be likewise affected by dietary levels of PQQ. The overall study was carried out using two experiments. In this specific experiment, the gene expression profiles of Sprague Dawley (SD) rats treated with different xenobiotics were compared to the gene expression profile of PQQ treated SD rats.

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吡咯喹啉醌改善了自然衰老小鼠与增强线粒体生物能量相关的认知相关行为表现

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