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Mechanism of Huoshan large-leaf yellow tea in treatment of diabetic cognitive dysfunction based on bioinformatics and
1Anhui Medical College (Anhui Academy of Medical Sciences), 15 Yonghong Road, Hefei 230061, China.
Background:
Diabetic cognitive dysfunction (DCD) is a prevalent complication of diabetes, characterized by progressive cognitive decline. Current pharmacological interventions have limited therapeutic efficacy in managing this condition. Huoshan large - leaf yellow tea (HLYT), derived from Camellia sinensis leaves, has demonstrated dual pharmacological properties in both glycemic regulation and cognitive enhancement, suggesting its potential as a preventive and therapeutic agent for DCD.
Purpose:
The main purpose of this study was to clarify the regulatory effect of HLYT on DCD and explore its underlying mechanisms.
Study Design:
The research encompassed a comprehensive multi-phase investigation. Network pharmacological analysis identified HLYT's key target genes for DCD. Molecular docking screened hub target genes, which were further verified by molecular dynamic (MD) simulations. High-performance liquid chromatography (HPLC) quantified HLYT's active components for setting animal experiment dosages. A DCD model was established in rats by feeding them a high - fat diet and injecting streptozotocin (STZ). Subsequently, HLYT was administered to the rats via intragastric gavage for intervention. The results of this intervention were then verified through relevant animal experiments.
Results:
Utilizing an integrated approach of network pharmacology and molecular docking, five pivotal target genes (Adora2a, Mapk8, Stat3, Vcam1, Edn1) were identified as the primary molecular targets of HLYT in DCD pathogenesis. Quercetin, kaempferol, caffeine, theobromine, and EGCG in HLYT exhibited significant binding affinities with these targets. The results of animal experiment have shown that HLYT can alleviate neuronal damage and cognitive dysfunction, reduce the levels of IL-6 and IL-1β in the serum and brain tissue in DCD rats. Furthermore, it can also inhibit the expression of Adora2a, Mapk8, Stat3, Vcam1, and Edn1 mRNA as well as the expression of STAT3, ADORA2A, JNK1, ET1, and VCAM1 proteins.
Conclusion:
HLYT has a significant protective effect on DCD in rats by regulating Adora2a, Mapk8, Stat3, Vcam1, and Edn1 genes, suggesting that it has remarkable clinical potential in the treatment of DCD.
