Background: H1N1 is one of the major subtypes of influenza A virus (IAV) that causes seasonal influenza, posing a serious threat to human health. A traditional Chinese medicine combination called Qingxing granules (QX) is utilized clinically to treat epidemic influenza. However, its chemical components are complex, and the potential pharmacological mechanisms are still unknown. Methods: QX’s effective components were gathered from the TCMSP database based on two criteria: drug-likeness (DL ≥ 0.18) and oral bioavailability (OB ≥ 30%). SwissADME was used to predict potential targets of effective components, and Cytoscape was used to create a “Herb-Component-Target” network for QX. In addition, targets associated with H1N1 were gathered from the databases GeneCards, OMIM, and GEO. Targets associated with autophagy were retrieved from the KEGG, HAMdb, and HADb databases. Intersection targets for QX, H1N1 influenza, and autophagy were identified using Venn diagrams. Afterward, key targets were screened using Cytoscape’s protein–protein interaction networks built using the database STRING. Biological functions and signaling pathways of overlapping targets were observed through GO analysis and KEGG enrichment analysis. The main chemical components of QX were determined by high-performance liquid chromatography (HPLC), followed by molecular docking. Finally, the mechanism of QX in treating H1N1 was validated through animal experiments. Results: A total of 786 potential targets and 91 effective components of QX were identified. There were 5420 targets related to H1N1 and 821 autophagy-related targets. The intersection of all targets of QX, H1N1, and autophagy yielded 75 intersecting targets. Ultimately, 10 core targets were selected: BCL2, CASP3, NFKB1, MTOR, JUN, TNF, HSP90AA1, EGFR, HIF1A, and MAPK3. Identification of the main chemical components of QX by HPLC resulted in the separation of seven marker ingredients within 195 min, which are amygdalin, puerarin, baicalin, phillyrin, wogonoside, baicalein, and wogonin. Molecular docking results showed that BCL2, CASP3, NFKB1, and MTOR could bind well with the compounds. In animal studies, QX reduced the degenerative alterations in the lung tissue of H1N1-infected mice by upregulating the expression of p-mTOR/mTOR and p62 and downregulating the expression of LC3, which inhibited autophagy. Conclusions: According to this study’s network pharmacology analysis and experimental confirmation, QX may be able to treat H1N1 infection by regulating autophagy, lowering the expression of LC3, and increasing the expression of p62 and p-mTOR/mTOR.

Introduction: The incidence of diabetes is rising annually, significantly impacting public health and imposing a substantial economic burden on society. Ophiopogonin D (Op D) exhibits certain hypoglycemic effects; however, its mechanisms remain unclear.Methods: β-cell dedifferentiation, distinct from β-cell apoptosis, is a pathogenic mechanism we aim to explore regarding Op D’s regulatory effects. We established an animal model of β-cell dedifferentiation to assess Op D’s impact on glucose tolerance, blood glucose levels, and insulin secretion. We employed immunohistochemistry and immunofluorescence to analyze the expression levels of dedifferentiation-related proteins. Additionally, we created an in vitro β-cell dedifferentiation model using INS-1 cells to evaluate Op D’s influence on insulin secretion and dedifferentiation. Transcriptomic analysis was conducted to explore potential mechanisms by which Op D ameliorates dedifferentiation, with further validation via Western blotting and immunofluorescence. Flow cytometry, fluorescence microscopy, and related assays were used to assess Op D’s effects on oxidative stress. Endoplasmic reticulum (ER) tracing agents marked the ER, and laser confocal microscopy examined ER morphology, with ER stress inducers and inhibitors employed to clarify Op D’s mechanisms.Results: Results indicated that Op D reduced blood glucose levels, improved glucose tolerance, enhanced insulin secretion, mitigated pancreatic atrophy, and increased PDX1 and FOXO1 expression levels. Furthermore, Op D inhibited ER stress, decreased GRP78 expression, reduced NGN3 levels, elevated PDX1, NKX6.1, and MAFA expression, and decreased oxidative stress-related products (ROS, MDA) while increasing SOD and GSH levels.Discussion: These findings demonstrate that Op D can improve β-cell dedifferentiation by modulating the GRP78/ROS/PDX1 pathway to inhibit ER stress.

Review question / Objective: Would meditation programs affect fasting blood glucose levels and HbA(1c) of patients with type 2 diabetes mellitus? Would meditation programs intervention be of benefit for remission of depression and anxiety level? Would meditation programs improve quality of life of individuals with type 2 diabetes？ Do meditation programs affect body mass index (BMI), serum lipid levels and level of blood pressure? Which type of meditation programs is better for type 2 diabetes patients? Are there any differences of efficacy among different meditation programs? To provide valid evidence for the effect of meditation programs for type 2 diabetes by synthesizing and comparing outcomes from clinical trials. Main outcome(s): The outcomes include fasting blood glucose levels and HbA(1c).