Journal of ethnopharmacology · 2026
Jiao-tai-wan alleviates cognitive impairment induced by sleep deprivation through IL33-associated lipid metabolism and PTP1B/SYK/AKT signaling pathway.
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Ma Yujie, Zhang Ting, Tian Yu, Chen Qini, Su Shijie, Lin Yeze, Shi Jiahui, Zou Yutong, Li Shiyin, Liu Shan, Yang Cong, Wang Qi
Аннотация
ETHNOPHARMACOLOGICAL RELEVANCE: Sleep deprivation (SD)-induced cognitive impairment remains a major neurological concern. Although Jiao-tai-wan (JTW) has demonstrated cognitive-enhancing effects in traditional practice, its underlying regulatory network remains undefined.
AIM OF THE STUDY: This study aims to explore the efficacy and mechanism of JTW in mitigating SD-induced cognitive impairment.
MATERIALS AND METHODS: Behavioral tests, Nissl staining, and Golgi staining were employed to evaluate the cognitive improvement induced by JTW in sleep-deprived (SD) mice. Immunofluorescence was performed to detect changes in IL33-related proteins. To examine the contribution of IL33, recombinant mouse IL33 or an IL33-neutralizing antibody was co-administered with JTW. Transcriptomic data analysis and in vitro experiments were conducted to identify key pathways. Single-cell transcriptomic data analysis, combined with scTenifoldKnk virtual knockout, was applied to explore the expression of key genes in microglia of SD mice. Finally, targeted metabolomics analyses and western blotting were utilized to validate the key pathways.
RESULTS: JTW significantly improved the behavioral performance of SD mice and attenuated hippocampal neuronal damage. Additionally, JTW upregulates IL33 expression, enhancing microglial phagocytic capacity while reducing perineuronal net aggregation. Notably, blockade of the IL33 signaling pathway further confirmed the critical role of this molecule in mediating JTW-induced neuroprotection and perineuronal nets (PNNs) remodeling. Lipid metabolism pathways and the Ptpn1-related signaling axis were identified as the key mechanisms underlying IL33-associated modulation of microglial function, as demonstrated by combined DEGs analysis and in vitro experiments. Single-cell transcriptomic analysis further indicated that Ptpn1 was predominantly expressed in microglia and glutamatergic neurons of SD mice. Mechanistic investigations confirmed that JTW modulated the lipid metabolic profile and regulated the PTP1B/SYK/AKT signaling axis in SD mice.
CONCLUSIONS: JTW mitigates neuronal damage and cognitive decline in SD mice via IL33-associated remodeling of PNNs. This protective effect is associated with its dual modulation of lipid metabolism and the PTP1B/SYK/AKT signaling axis.
AIM OF THE STUDY: This study aims to explore the efficacy and mechanism of JTW in mitigating SD-induced cognitive impairment.
MATERIALS AND METHODS: Behavioral tests, Nissl staining, and Golgi staining were employed to evaluate the cognitive improvement induced by JTW in sleep-deprived (SD) mice. Immunofluorescence was performed to detect changes in IL33-related proteins. To examine the contribution of IL33, recombinant mouse IL33 or an IL33-neutralizing antibody was co-administered with JTW. Transcriptomic data analysis and in vitro experiments were conducted to identify key pathways. Single-cell transcriptomic data analysis, combined with scTenifoldKnk virtual knockout, was applied to explore the expression of key genes in microglia of SD mice. Finally, targeted metabolomics analyses and western blotting were utilized to validate the key pathways.
RESULTS: JTW significantly improved the behavioral performance of SD mice and attenuated hippocampal neuronal damage. Additionally, JTW upregulates IL33 expression, enhancing microglial phagocytic capacity while reducing perineuronal net aggregation. Notably, blockade of the IL33 signaling pathway further confirmed the critical role of this molecule in mediating JTW-induced neuroprotection and perineuronal nets (PNNs) remodeling. Lipid metabolism pathways and the Ptpn1-related signaling axis were identified as the key mechanisms underlying IL33-associated modulation of microglial function, as demonstrated by combined DEGs analysis and in vitro experiments. Single-cell transcriptomic analysis further indicated that Ptpn1 was predominantly expressed in microglia and glutamatergic neurons of SD mice. Mechanistic investigations confirmed that JTW modulated the lipid metabolic profile and regulated the PTP1B/SYK/AKT signaling axis in SD mice.
CONCLUSIONS: JTW mitigates neuronal damage and cognitive decline in SD mice via IL33-associated remodeling of PNNs. This protective effect is associated with its dual modulation of lipid metabolism and the PTP1B/SYK/AKT signaling axis.