Potential mechanism of Qinggong Shoutao pill alleviating age-associated memory decline based on integration strategy.

CONTEXT: Qinggong Shoutao Wan (QGSTW) is a pill used as a traditional medicine to treat age-associated memory decline (AAMI). However, its potential mechanisms are unclear. OBJECTIVE: This study elucidates the possible mechanisms of QGSTW in treating AAMI. MATERIALS AND METHODS: Network pharmacology and molecular docking approaches were utilized to identify the potential pathway by which QGSTW alleviates AAMI. C57BL/6J mice were divided randomly into control, model, and QGSTW groups. A mouse model of AAMI was established by d-galactose, and the pathways that QGSTW acts on to ameliorate AAMI were determined by ELISA, immunofluorescence staining and Western blotting after treatment with d-gal (100 mg/kg) and QGSTW (20 mL/kg) for 12 weeks. RESULTS: Network pharmacology demonstrated that the targets of the active components were significantly enriched in the cAMP signaling pathway. AKT1, FOS, GRIN2B, and GRIN1 were the core target proteins. QGSTW treatment increased the discrimination index from -16.92 ± 7.06 to 23.88 ± 15.94% in the novel location test and from -19.54 ± 5.71 to 17.55 ± 6.73% in the novel object recognition test. ELISA showed that QGSTW could increase the levels of cAMP. Western blot analysis revealed that QGSTW could upregulate the expression of PKA, CREB, c-Fos, GluN1, GluA1, CaMKII-α, and SYN. Immunostaining revealed that the expression of SYN was decreased in the CA1 and DG. DISCUSSION AND CONCLUSIONS: This study not only provides new insights into the mechanism of QGSTW in the treatment of AAMI but also provides important information and new research ideas for the discovery of traditional Chinese medicine compounds that can treat AAMI.

Effect and mechanism of Tangzhiqing in improving cardiac function in mice with hyperlipidaemia complicated with myocardial ischaemia.

Purpose: Tangzhiqing formula (TZQ) is a traditional Chinese medicine prescribed to treat lipid metabolism disorders, atherosclerosis, diabetes and diabetic cardiomyopathy. However, some challenges and hurdles remain. TZQ showed promising results in treating diabetes and hyperlipidaemia. However, its effect on and mechanism of action in hyperlipidaemia complicated with myocardial ischaemia (HL-MI) remain unknown. Methods: In this study, a network pharmacology-based strategy integrating target prediction was adopted to predict the targets of TZQ relevant to the treatment of HL-MI and to further explore the involved pharmacological mechanisms. Results: A total of 104 potential therapeutic targets were obtained, including MMP9, Bcl-2, and Bax, which may be related to the apoptosis and PI3K/AKT signalling pathways. Then, we confirmed these potential targets and pathways with animal experimentation. TZQ reduced lipid levels, increased the expression levels of Bcl-2, decreased Bax, caspase-3 and caspase-9 expression levels, and activated the PI3K/AKT signalling pathway. Conclusion: In conclusion, this study provides new insights into the protective mechanisms of TZQ against HL-MI through network pharmacology and pharmacological approaches.