Osteoporosis is a common bone disease， whose incidence is still on the rise， posing great challenges to patients and society. This review mainly studies the pathogenesis of osteoporosis from the aspects of oxidative stress， inflammatory response， and glucolipotoxicity-induced injury and clarifies the efficacy and mechanism of some active ingredients of traditional Chinese medicine against osteoporosis through the integration of in vitro and in vivo experiments. The experimental results suggest that some active ingredients can improve bone resorption markers and maintain bone homeostasis by modulating inflammation， oxidative stress， etc. These active ingredients regulate osteoporosis through the receptor activator of nuclear transcription factor-κB （NF-κB） ligand （RANKL） pathway， osteoprotegerin （OPG） pathway， Wnt/β-catenin pathway， NF-κB pathway， mitogen-activated protein kinase （MAPK） pathway， adenosine monophosphate （AMP）-activated protein kinase （AMPK）/mammalian target of rapamycin （mTOR） pathway， and oxidative stress pathway. This review provides ideas for the progress of the prevention and treatment of osteoporosis with the active ingredients of traditional Chinese medicine， aiming to provide new potential lead compounds and reference for the development of innovative drugs and clinical therapy for the treatment of osteoporosis.

ObjectiveTo preliminarily explore the active components and target pathways of Angelicae Sinensis Radix-Polygonati Rhizoma （ASR-PR） herb pair in the treatment of simple obesity through network pharmacology and molecular docking， and to verify and investigate its mechanism of action via animal experiments. MethodsThe chemical constituents and targets of ASR and PR were predicted using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）. Targets related to simple obesity were identified by retrieving the GeneCards， Online Mendelian Inheritance in Man （OMIM）， Pharmacogenomics Knowledgebase （PharmGKB）， and DisGeNET databases. The intersection of drug and disease targets was used to construct an active component-target network using Cytoscape software. This network was imported into the STRING database to construct a protein-protein interaction （PPI） network， and topological analysis was conducted to identify core genes. Gene Ontology （GO） analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis and mapping were performed using the DAVID database and the Microbioinformatics platform. AutoDock 1.5.7 software was used to perform molecular docking between the top five active components and core targets. An animal model of simple obesity was established by feeding C57BL/6J mice a high-fat diet. The mice were administered ASR （2.06 g·kg^-1）， PR （2.06 g·kg^-1）， or ASR-PR （4.11 g·kg^-1） for 10 weeks， while the model group received an equal volume of purified water by gavage. After the administration period， the mice were sacrificed to measure body fat weight and serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein （HDL）， and low-density lipoprotein （LDL）. Hematoxylin-eosin （HE） staining was used to observe histopathological sections of liver and adipose tissue. Serum levels of leptin， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） were determined by enzyme-linked immunosorbent assay （ELISA）， and the mRNA expression levels of epidermal growth factor receptor （EGFR） and signal transducer and activator of transcription 3 （STAT3） in liver tissue were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsNetwork pharmacology and molecular docking results indicated that the treatment of simple obesity by ASR-PR may involve the regulation of protein expression of core targets EGFR and STAT3 by its main components MOL009760 （Siberian glycoside A_qt）， MOL003889 （methyl protodioscin_qt）， MOL009766 （resveratrol）， MOL006331 （4′，5-dihydroxyflavone）， and MOL004941 （baicalin）， thereby modulating the PI3K/Akt and JAK/STAT signaling pathways. The animal experiment results showed that compared with the normal group， the model group had significantly increased body weight， body fat weight， and serum levels of TG， TC， TNF-α， IL-6， and leptin （P<0.01）. EGFR mRNA expression was significantly elevated （P<0.05）， while STAT3 mRNA expression was significantly decreased （P<0.01）. Histological analysis revealed disordered hepatic architecture in the model group， with pronounced lipid vacuoles， cytoplasmic loosening， lipid accumulation， and steatosis. Adipocytes in white adipose tissue （WAT） and brown adipose tissue （BAT） of the model group exhibited markedly increased diameters， reduced cell counts per unit area， and irregular morphology. Compared with the model group， the ASR-PR group significantly reduced body weight， body fat weight， serum TC， IL-6， TNF-α， leptin levels， and EGFR mRNA expression （P<0.01）. TG levels were also significantly decreased （P<0.05）， while STAT3 mRNA expression was significantly increased （P<0.01）. Histopathological improvements included reduced size and number of hepatic lipid vacuoles and restoration of liver cell morphology toward that of the normal group. The diameter of adipocytes significantly decreased， and the number of adipocytes per unit area increased. ConclusionASR-PR may regulate the expression of key target proteins such as EGFR and STAT3 via its core active components， modulate the PI3K/Akt and JAK/STAT signaling pathways， repair damaged liver and adipose tissues， and thereby alleviate the progression of obesity in mice.

ObjectiveTo preliminarily explore the active components and target pathways of Angelicae Sinensis Radix-Polygonati Rhizoma （ASR-PR） herb pair in the treatment of simple obesity through network pharmacology and molecular docking， and to verify and investigate its mechanism of action via animal experiments. MethodsThe chemical constituents and targets of ASR and PR were predicted using the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform （TCMSP）. Targets related to simple obesity were identified by retrieving the GeneCards， Online Mendelian Inheritance in Man （OMIM）， Pharmacogenomics Knowledgebase （PharmGKB）， and DisGeNET databases. The intersection of drug and disease targets was used to construct an active component-target network using Cytoscape software. This network was imported into the STRING database to construct a protein-protein interaction （PPI） network， and topological analysis was conducted to identify core genes. Gene Ontology （GO） analysis and Kyoto Encyclopedia of Genes and Genomes （KEGG） pathway enrichment analysis and mapping were performed using the DAVID database and the Microbioinformatics platform. AutoDock 1.5.7 software was used to perform molecular docking between the top five active components and core targets. An animal model of simple obesity was established by feeding C57BL/6J mice a high-fat diet. The mice were administered ASR （2.06 g·kg^-1）， PR （2.06 g·kg^-1）， or ASR-PR （4.11 g·kg^-1） for 10 weeks， while the model group received an equal volume of purified water by gavage. After the administration period， the mice were sacrificed to measure body fat weight and serum levels of total cholesterol （TC）， triglycerides （TG）， high-density lipoprotein （HDL）， and low-density lipoprotein （LDL）. Hematoxylin-eosin （HE） staining was used to observe histopathological sections of liver and adipose tissue. Serum levels of leptin， interleukin-6 （IL-6）， and tumor necrosis factor-α （TNF-α） were determined by enzyme-linked immunosorbent assay （ELISA）， and the mRNA expression levels of epidermal growth factor receptor （EGFR） and signal transducer and activator of transcription 3 （STAT3） in liver tissue were detected by real-time quantitative polymerase chain reaction （Real-time PCR）. ResultsNetwork pharmacology and molecular docking results indicated that the treatment of simple obesity by ASR-PR may involve the regulation of protein expression of core targets EGFR and STAT3 by its main components MOL009760 （Siberian glycoside A_qt）， MOL003889 （methyl protodioscin_qt）， MOL009766 （resveratrol）， MOL006331 （4′，5-dihydroxyflavone）， and MOL004941 （baicalin）， thereby modulating the PI3K/Akt and JAK/STAT signaling pathways. The animal experiment results showed that compared with the normal group， the model group had significantly increased body weight， body fat weight， and serum levels of TG， TC， TNF-α， IL-6， and leptin （P<0.01）. EGFR mRNA expression was significantly elevated （P<0.05）， while STAT3 mRNA expression was significantly decreased （P<0.01）. Histological analysis revealed disordered hepatic architecture in the model group， with pronounced lipid vacuoles， cytoplasmic loosening， lipid accumulation， and steatosis. Adipocytes in white adipose tissue （WAT） and brown adipose tissue （BAT） of the model group exhibited markedly increased diameters， reduced cell counts per unit area， and irregular morphology. Compared with the model group， the ASR-PR group significantly reduced body weight， body fat weight， serum TC， IL-6， TNF-α， leptin levels， and EGFR mRNA expression （P<0.01）. TG levels were also significantly decreased （P<0.05）， while STAT3 mRNA expression was significantly increased （P<0.01）. Histopathological improvements included reduced size and number of hepatic lipid vacuoles and restoration of liver cell morphology toward that of the normal group. The diameter of adipocytes significantly decreased， and the number of adipocytes per unit area increased. ConclusionASR-PR may regulate the expression of key target proteins such as EGFR and STAT3 via its core active components， modulate the PI3K/Akt and JAK/STAT signaling pathways， repair damaged liver and adipose tissues， and thereby alleviate the progression of obesity in mice.

Insulin resistance （IR） is an important pathological and physiological mechanism of type 2 diabetes （T2DM）， and the treatment of IR has become the key to the prevention and treatment of T2DM. IR is a state of insensitivity or reduced sensitivity of insulin-stimulated tissue cells to glucose， resulting in cells that are unable to efficiently take up glucose in the bloodstream and thus causing hyperglycemia. Adenosine monophosphate-activated protein kinase （AMPK） is an energy-sensing enzyme that can regulate multiple metabolic pathways and maintain the stability of adenosine triphosphate （ATP） in the cell. In recent years， traditional Chinese medicine （TCM） has played an increasingly important role in the prevention and treatment of T2DM. The research on exploring the AMPK signaling pathway of TCM intervention in the progress of T2DM has gradually increased. Many pharmacological studies have shown that TCM has advantages such as safety and high efficiency in the prevention and treatment of T2DM. AMPK signaling pathway is one of the key pathways for the active ingredients of TCM and TCM extracts to improve IR. Active ingredients such as phenols， flavonoids， polysaccharides， alkaloids， and saponins， as well as other herbal extracts can improve IR by activating the AMPK signaling pathway cascade response， thereby improving IR by regulating glucolipid metabolism， inhibiting inflammatory response， anti-oxidative stress and maintaining mitochondrial homeostasis. Based on this， this paper reviews the pharmacological and experimental research results of TCM intervening the AMPK signaling pathway to improve IR in recent years， expecting to provide reference for further research， development and application of TCM in intervening IR and treating T2DM.

Diabetic nephropathy （DN） is a chronic microvascular complication in diabetic patients and the main cause of end-stage renal disease （ESRD）. Studies have shown that nuclear factor kappa-B （NF-κB） signaling pathway is involved in the pathological process of DN by activating pathological mechanisms such as inflammation， oxidative stress， fibrosis， apoptosis， autophagy， and pyroptosis. Therefore， blocking the transduction of NF-κB signaling pathway can help prevent and treat DN. Currently， western medical treatment involves strategies such as lowering blood sugar， blood pressure， and lipids， as well as using endothelin receptor antagonists， mineralocorticoid receptor antagonists， aldosterone synthase inhibitors， and other drugs， but they still cannot block the pathological process of DN. Traditional Chinese medicine （TCM） offers a simpler and more cost-effective approach that addresses both the symptoms and underlying causes of DN. Recent research has shown promising results in managing DN with TCM， and NF-κB， as a key factor， plays an important role in the prevention and treatment of DN. This article summarized the research results of TCM based on the NF-κB signaling pathway for the treatment of DN in the past five years. It described a variety of TCM extracts， such as polysaccharides， terpenes， phenols， flavonoids， saponins， and alkaloids， as well as TCM compound prescriptions such as Huaiqihuang granules， Astragalus mongholicus Bunge and Panax notoginseng formula， and Danzhi Jiangtang capsules， which regulated the NF-κB signaling pathway and its upstream and downstream factors to block the pathological process of DN. This inhibition aims to prevent renal pathological damage caused by DN and slow down the deterioration of renal function. The article aims to provide new ideas and references for the research and development of drugs for the prevention and treatment of DN.

Objective To apply PDCA(plan,do,check and action)cycle to optimize management and shorten the turnaround time(TAT)of five sex hormone tests for improving clinical efficiency and patient satisfaction.Methods A PDCA management team was established to retrospectively analyze the current status of sex hormone TAT in 2021.In 2022,PDCA tools were utilized,including fishbone diagrams for cause analysis,Pareto charts for root cause identification,formulation and implementation of corresponding im-provement measures and monitoring of TAT changes before and after PDCA.Results Through the corrective measures,such as staff personnel training,increasing testing equipment,optimization process and other improvement measures,the median TAT of sex hor-mone samples in 2022(post-PDCA improvement)was 54 minutes which was significantly lower than 61 minutes in 2021(pre-PDCA)(P＜0.05).Conclusion PDCA cycle management effectively shortened the TAT of sex hormone samples,enhanced clinical diagnostic efficiency and patient experience,improved doctor-patient relationships,while also elevated the quality management standards of labo-ratories.

As a chronic metabolic disease,type 2 diabetes poses a significant threat to human health with increasing incidence.An increasing number of studies confirm that the pathogenesis of diabetes is closely related with alterations in multiple cellular signaling pathways.Although numerous studies have reported that traditional Chinese medicine compounds prevent diabetes by modulating cell signaling pathways,asystematic review of the mechanism of action of traditional Chinese medicine compounds in modulating cell signaling pathways is still lacking.Therefore,this paper summarizes the research of type 2 diabetes prevention and treatment,which was found mainly related to the signaling pathways such as PI3K/AKT,AMPK,MAPK,NF-κB,PPAR,TGF-β.This family of signaling pathways can treat type 2 diabetes by inhibiting pancreatic islet cell apoptosis,protecting pancreatic β-cell function,ameliorating insulin resistance,inhibiting hepatic gluconeogenesis,promoting glycogen synthesis,attenuating inflammation,and resisting oxidative stress.At the same time,we analyze the problems in current research and the future development trend,in order to provide a scientific theoretical basis for the drug development and clinical application of traditional Chinese medicine compound in the prevention and treatment of diabetes.

OBJECTIVE: To evaluate the long-term prognosis of patients with ST-segment elevation myocardial infarction (STEMI) treated with different reperfusion strategies in Chinese county-level hospitals. METHODS: A total of 2,514 patients with STEMI from 32 hospitals participated in the China Acute Myocardial Infarction registry between January 2013 and September 2014. The success of fibrinolysis was assessed according to indirect measures of vascular recanalization. The primary outcome was 2-year mortality. RESULTS: Reperfusion therapy was used in 1,080 patients (42.9%): fibrinolysis ( n= 664, 61.5%) and primary percutaneous coronary intervention (PCI) ( n= 416, 38.5%). The most common reason for missing reperfusion therapy was a prehospital delay > 12 h (43%). Fibrinolysis [14.5%, hazard ratio ( HR): 0.59, 95% confidence interval ( CI) 0.44-0.80] and primary PCI (6.8%, HR= 0.32, 95% CI: 0.22-0.48) were associated with lower 2-year mortality than those with no reperfusion (28.5%). Among fibrinolysis-treated patients, 510 (76.8%) achieved successful clinical reperfusion; only 17.0% of those with failed fibrinolysis underwent rescue PCI. There was no difference in 2-year mortality between successful fibrinolysis and primary PCI (8.8% vs. 6.8%, HR = 1.53, 95% CI: 0.85-2.73). Failed fibrinolysis predicted a similar mortality (33.1%) to no reperfusion (33.1% vs. 28.5%, HR= 1.30, 95% CI: 0.93-1.81). CONCLUSION In Chinese county-level hospitals, only approximately 2/5 of patients with STEMI underwent reperfusion therapy, largely due to prehospital delay. Approximately 30% of patients with failed fibrinolysis and no reperfusion therapy did not survive at 2 years. Quality improvement initiativesare warranted, especially in public health education and fast referral for mechanical revascularization in cases of failed fibrinolysis.
Humans ; ST Elevation Myocardial Infarction/therapy* ; Percutaneous Coronary Intervention ; East Asian People ; Treatment Outcome ; Myocardial Reperfusion ; Myocardial Infarction ; Registries ; Hospitals

Objective:To investigate the significance of Th1/Th2 cytokines in prognostic stratification of acute myeloid leukemia (AML).Methods:A total of 83 patients with newly diagnosed AML from June 2017 to April 2019 in the First People's Hospital of Yunnan Province were collected. According to the Chinese guidelines for diagnosis and treatment of adult acute myeloid leukemia (non-acute promyelocytic leukemia) (2017 edition), AML patients were divided into poor prognosis group (45 cases), moderate prognosis group (19 cases), and good prognosis group (19 cases); moderate prognosis plus poor prognosis was treated as the not good prognosis. Mann-Whitney U test and Kruskal-Wallis H test were used to compare the expression differences of Th1/Th2 cytokines in peripheral blood of different prognosis groups; cytokines with statistical differences among different prognosis groups were selected, and the cut-off value of AML patients with different prognostic stratification distinguished by cytokines was determined by using receiver operating characteristic (ROC) curve. Finally, patients were divided into ≥ cut-off value group and 0.05).The cut-off value of TNF-β was 3.23 pg/ml in good prognosis group and moderate prognosis group, the area under the ROC curve was 0.866 (95% CI 0.753-0.978, P < 0.05); among 26 patients with TNF-β≥ 3.23 pg/ml, 25 (96.2%) patients had not good prognosis. The cut-off value was 3.62 pg/ml for distinguishing between moderate prognosis group and poor prognosis group, the area under the ROC curve was 0.747 (95% CI 0.610-0.884, P = 0.02); 18 (100%) patients with TNF-β≥ 3.62 pg/ml had not good prognosis. The cut-off value was 2.19 pg/ml for distinguishing between good prognosis group and not good prognosis group, the area under the ROC curve was 0.719 (95% CI 0.595-0.842, P = 0.04); among 53 patients with TNF-β≥2.19 pg/ml, 46 (86.8%) patients had not good prognosis. Conclusions:The high expression of TNF-β may indicate that the prognosis of AML patients is not good. When the level of TNF-β was equal or greater than 3.62 pg/ml, it may contribute to the prognostic stratification of AML patients.

Objective::To study the protective effect and mechanism of Qidong Yixin oral liquid on doxorubicin-induced myocardial toxicity in mice. Method::Ninety male ICR mice were randomly divided into normal group, model(DOX) group, DOX+ Qidong Yixin oral liquid group (9.55, 23.88, 47.75 g·kg^-1) and high dose group (47.75 g·kg^-1) with 15 mice in each group. The normal group and model group were given pure water by gavage, and each dose group of Qidong Yixin oral liquid was given different doses of Qidong Yixin oral liquid once a day for 21 days. On the seventh day, normal saline was injected into the abdominal cavity of the normal group and the high dose group of Qidong Yixin oral liquid. Doxorubicin was injected into the abdominal cavity of the other groups (15 mg·kg^-1). After 21 days, the weight and heart weight of mice were weighed and cardiac index was calculated. Serum was taken for the detection of lactate dehydrogenase (LDH), creatine kinase (CK), aspartate aminotransferase (AST). Heart was taken for hematoxylin-eosin (HE) staining, superoxide dismutase (SOD), glutathione peroxidase (GSH-PX), catalase (CAT) in myocardial tissue were detected. The expression of nuclear factor NF-E2 related factor (Nrf2) and heme oxygenase-1 (HO-1) were detected by Western blot. Result::Compared with normal group, adriamycin could significantly reduce the body weight of mice (P<0.01), increase the activities of LDH, CK and AST in serum(P<0.01), and decrease the activities of antioxidant enzymes (P<0.01). Compared with DOX group, high dose Qidong Yixin oral liquid could significantly increase the weight of mice (P<0.05, P<0.01), decrease the level of myocardial three enzymes(P<0.01), increase the activity of antioxidant enzymes(P<0.05, P<0.01), and increase the expression of Nrf2 and HO-1(P<0.01). Conclusion::Qidong Yixin oral liquid has a good protective effect on doxorubicin myocardial toxicity. Its mechanism may be related to activating Nrf2/HO-1 signaling pathway and alleviating oxidative stress injury.