5.Mechanism of Yupingfeng granules for recurrent respiratory tract infections in children based on network pharmacology
Qiuyue HONG ; Qi KUANG ; Jun WU
China Pharmacist 2024;28(9):12-19
Objective To analyze the molecular mechanism of Yupingfeng granules(YPFG)in the treatment of recurrent respiratory tract infection(RRTI),and provide a pharmacological basis for the diagnosis and treatment of RRTI in traditional Chinese medicine.Methods The TCMSP database and SwissTargetPredication database were used to screen the active ingredients and active ingredient targets of YPFG.All pathogenic targets of RRTI were obtained using the DisGeNET dataBase,DrugBank database,GeneCards database,and OMIM database.Drug-disease target-compound networks and protein-protein interaction networks were established to explore the main drugs,compounds,and target proteins.GO enrichment analysis and KEGG signaling pathway enrichment analysis were used to explore the main molecular mechanisms of YPFG in the treatment of RRTI.Results The main active ingredients of YPFG screened include three main active ingredients,including daylily lignans A,peucedanum praeruptorum B,and wogonin,which mainly target SRC and COX-2.Enrichment analysis showed that phosphorylation(biological process),cytoplasm perinuclear region(cellular component),and phosphotransferase activity(molecular function)were the main GO enrichment items.The signaling pathways mainly involve tumor signaling pathways,relaxin signaling pathways,Th17 signaling pathways,and so on.Conclusion YPFG mainly treats RRTI by participating in the signal transduction of certain key nodes in tumor signaling pathways,relaxin signaling pathways,Th17 signaling pathways,etc.It has a direct or indirect impact on multiple signaling pathways and has the characteristics of multi-component,multi-target,and multi-channel effects.
6.Immunotherapy for endometrial carcinoma based on molecular typing
Qiuyue XU ; Xianmei MA ; Qi YUE
Journal of International Oncology 2022;49(11):700-704
Endometrial cancer has been identified by The Cancer Genome Atlas program with four molecular subtypes by genome sequence analysis. Clinical trials to select suitable immunotherapeutic agents based on the different immune characteristics of each subtype have been conducted in several countries and have made important progress. The main clinical applications of immune checkpoint inhibitors include anti-programmed cell death protein-1/programmed death-ligand 1 antibodies and poly ADP-ribose polymerase inhibitors. Optimizing drug selection and drug combination based on the target characteristics of different immune checkpoint inhibitors may provide new opportunities for immunotherapy of endometrial cancer and bring new light to improve survival rates.
7.MondoA Is Required for Normal Myogenesis and Regulation of the Skeletal Muscle Glycogen Content in Mice
Hui RAN ; Yao LU ; Qi ZHANG ; Qiuyue HU ; Junmei ZHAO ; Kai WANG ; Xuemei TONG ; Qing SU
Diabetes & Metabolism Journal 2021;45(3):439-451
Skeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear. We generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle. MAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake. MondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.
9.MondoA Is Required for Normal Myogenesis and Regulation of the Skeletal Muscle Glycogen Content in Mice
Hui RAN ; Yao LU ; Qi ZHANG ; Qiuyue HU ; Junmei ZHAO ; Kai WANG ; Xuemei TONG ; Qing SU
Diabetes & Metabolism Journal 2021;45(3):439-451
Skeletal muscle is the largest tissue in the human body, and it plays a major role in exerting force and maintaining metabolism homeostasis. The role of muscle transcription factors in the regulation of metabolism is not fully understood. MondoA is a glucose-sensing transcription factor that is highly expressed in skeletal muscle. Previous studies suggest that MondoA can influence systemic metabolism homeostasis. However, the function of MondoA in the skeletal muscle remains unclear. We generated muscle-specific MondoA knockout (MAKO) mice and analyzed the skeletal muscle morphology and glycogen content. Along with skeletal muscle from MAKO mice, C2C12 myocytes transfected with small interfering RNA against MondoA were also used to investigate the role and potential mechanism of MondoA in the development and glycogen metabolism of skeletal muscle. MAKO caused muscle fiber atrophy, reduced the proportion of type II fibers compared to type I fibers, and increased the muscle glycogen level. MondoA knockdown inhibited myoblast proliferation, migration, and differentiation by inhibiting the phosphatase and tensin homolog (PTEN)/phosphoinositide 3-kinase (PI3K)/Akt pathway. Further mechanistic experiments revealed that the increased muscle glycogen in MAKO mice was caused by thioredoxin-interacting protein (TXNIP) downregulation, which led to upregulation of glucose transporter 4 (GLUT4), potentially increasing glucose uptake. MondoA appears to mediate mouse myofiber development, and MondoA decreases the muscle glycogen level. The findings indicate the potential function of MondoA in skeletal muscle, linking the glucose-related transcription factor to myogenesis and skeletal myofiber glycogen metabolism.
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