1.Expert Consensus on Clinical Application of Qinbaohong Zhike Oral Liquid in Treatment of Acute Bronchitis and Acute Attack of Chronic Bronchitis
Jian LIU ; Hongchun ZHANG ; Chengxiang WANG ; Hongsheng CUI ; Xia CUI ; Shunan ZHANG ; Daowen YANG ; Cuiling FENG ; Yubo GUO ; Zengtao SUN ; Huiyong ZHANG ; Guangxi LI ; Qing MIAO ; Sumei WANG ; Liqing SHI ; Hongjun YANG ; Ting LIU ; Fangbo ZHANG ; Sheng CHEN ; Wei CHEN ; Hai WANG ; Lin LIN ; Nini QU ; Lei WU ; Dengshan WU ; Yafeng LIU ; Wenyan ZHANG ; Yueying ZHANG ; Yongfen FAN
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(4):182-188
The Expert Consensus on Clinical Application of Qinbaohong Zhike Oral Liquid in Treatment of Acute Bronchitis and Acute Attack of Chronic Bronchitis (GS/CACM 337-2023) was released by the China Association of Chinese Medicine on December 13th, 2023. This expert consensus was developed by experts in methodology, pharmacy, and Chinese medicine in strict accordance with the development requirements of the China Association of Chinese Medicine (CACM) and based on the latest medical evidence and the clinical medication experience of well-known experts in the fields of respiratory medicine (pulmonary diseases) and pediatrics. This expert consensus defines the application of Qinbaohong Zhike oral liquid in the treatment of cough and excessive sputum caused by phlegm-heat obstructing lung, acute bronchitis, and acute attack of chronic bronchitis from the aspects of applicable populations, efficacy evaluation, usage, dosage, drug combination, and safety. It is expected to guide the rational drug use in medical and health institutions, give full play to the unique value of Qinbaohong Zhike oral liquid, and vigorously promote the inheritance and innovation of Chinese patent medicines.
2.Effects of jaceosidin on inflammatory injury in osteoarthritis rats by regulating AMPK/NLRP3 signaling pathway
Chao WEI ; Jiang YU ; Guanyun SHENG ; Yi CAI
China Pharmacy 2025;36(4):421-426
OBJECTIVE To investigate the effects of jaceosidin on osteoarthritis (OA) of rats by regulating adenosine monophosphate-activated protein kinase (AMPK)/NOD-like receptor protein 3 (NLRP3) pathway. METHODS Rats were randomly separated into OA group, jaceosidin group (33.33 mg/kg), AMPK inhibitor (Compound C, 20 mg/kg) group, jaceosidin (33.33 mg/kg)+Compound C (20 mg/kg) group, and sham operation group, with 12 rats in each group. Except for the sham operation group, the OA model was induced with modified Hulth method in all other groups. After successful modeling, they were given a relevant dose of jaceosidin or normal saline intragastrically, and Compound C or normal saline intraperitoneally, once a day, for consecutive 8 weeks. Twenty-four h after the last medication, the degree of knee joint swelling in rats from each group was measured. The pathological changes of the articular cartilage tissue in the knee joints, and the Mankin score were assessed. The levels of tumor necrosis factor-α (TNF-α), interleukin-18 (IL-18), and IL-6, as well as the protein expressions of collagen Ⅱ, aggrecan (ACAN), and a disintegrin and metalloproteinase with thrombospondin 5 (ADAMTS5), phosphorylated AMPK (p-AMPK), AMPK, NLRP3, cleaved-caspase-1, and cleaved-IL-1β were detected in the articular cartilage tissue of rats’ knees. RESULTS Compared with OA group, the cartilage tissue defect of jaceosidin group was relieved, the cartilage matrix staining was deepened, and the number of chondrocytes was increased. Knee swelling, Mankin score, the levels of TNF- α, IL-18 and IL-6, and protein expressions of ADAMTS5, NLRP3, cleaved-caspase-1 and cleaved-IL-1β in knee cartilage were significantly decreased or down-regulated. Protein expressions of collagen Ⅱ, ACAN and phosphorylation level of AMPK were significantly increased or up-regulated (P<0.05). Compound C significantly reversed the improvement effects of jaceosidin on the above indexes of OA rats (P<0.05). CONCLUSIONS Jaceosidin may inhibit inflammation and extracellular matrix degradation in OA rats by regulating the AMPK/NLRP3 signaling pathway.
3.Research progress on the anti-tumor effects of traditional Chinese medicine through intervention in the Nrf2/GPX4 signaling pathway
Jie HUANG ; Si LIN ; Chunjuan JIANG ; Ling WEI
China Pharmacy 2025;36(4):507-512
Nuclear factor-erythroid 2-related factor 2 (Nrf2)/glutathione peroxidase 4 (GPX4) signaling pathway plays a key role in the occurrence and development of tumors, and is involved in tumor cell proliferation, apoptosis, ferroptosis, invasion, migration, and drug resistance. Based on the Nrf2/GPX4 signaling pathway, this paper summarizes the research progress of the anti- tumor effects of traditional Chinese medicine. It is found that flavonoids (ginkgetin, luteolin, etc.), terpenoids (atractylenolide, cucurbitacin B, etc.), saponins (polyphyllin Ⅰ, polyphyllin Ⅶ), ester (brusatol) and other effective components, and traditional Chinese medicine extracts (total coumarins in Pileostegia tomentella and total flavonoids of Pterocarya hupehensis Skan), traditional Chinese medicine compounds (Fushao diqin fang, Xiaoai jiedu fang, etc.) can promote ferroptosis in tumor cells by inhibiting Nrf2/GPX4 signaling pathway and the expressions of its upstream and downstream factor proteins, as well as by increasing Fe2+ levels and lipid peroxidation, thereby exerting an antitumor effect.
4.Dynamic Monitoring and Correlation Analysis of General Body Indicators, Blood Glucose, and Blood Lipid in Obese Cynomolgus Monkeys
Yanye WEI ; Guo SHEN ; Pengfei ZHANG ; Songping SHI ; Jiahao HU ; Xuzhe ZHANG ; Huiyuan HUA ; Guanyang HUA ; Hongzheng LU ; Yong ZENG ; Feng JI ; Zhumei WEI
Laboratory Animal and Comparative Medicine 2025;45(1):30-36
ObjectiveThis study aims to investigate the dynamic changes in general body parameters, blood glucose, and blood lipid profiles in obese cynomolgus monkeys, exploring the correlations among these parameters and providing a reference for research on the obese cynomolgus monkey model. Methods30 normal male cynomolgus monkeys aged 5 - 17 years old (with body mass index < 35 kg/m² and glycated hemoglobin content < 4.50%) and 99 spontaneously obese male cynomolgus monkeys (with body mass index ≥35 kg/m² and glycated hemoglobin content < 4.50%) were selected. Over a period of three years, their abdominal circumference, skinfold thickness, body weight, body mass index, fasting blood glucose, glycated hemoglobin, and four blood lipid indicators were monitored. The correlations between each indicator were analyzed using repeated measurement ANOVA, simple linear regression, and multiple linear regression correlation analysis method. Results Compared to the control group, the obese group exhibited significantly higher levels of abdominal circumference, skinfold thickness, body weight, body mass index, and triglyceride (P<0.05). In the control group, skinfold thickness increased annually, while other indicators remained stable. Compared with the first year, the obese group showed significantly increased abdominal circumference, skinfold thickness, body weight, body mass index, triglyceride, and fasting blood glucose in the second year(P<0.05), with this increasing trend persisting in the third year (P<0.05). In the control group, the obesity incidence rates in the second and third years were 16.67% and 23.33%, respectively, while the prevalence of diabetes remained at 16.67%. In the obese group, the diabetes incidence rates were 29.29% and 44.44% in years 2 and 3, respectively. Among the 11-13 year age group, the incidence rates were 36.36% and 44.68%, while for the group older than 13 years, the rates were 28.13% and 51.35%. Correlation analysis revealed significant associations (P<0.05) between fasting blood glucose and age, abdominal circumference, skinfold thickness, body weight, and triglyceride in the diabetic monkeys. Conclusion Long-term obesity can lead to the increases in general physical indicators and fasting blood glucose levels in cynomolgus monkeys, and an increase in the incidence of diabetes. In diabetic cynomolgus monkeys caused by obesity, there is a high correlation between their fasting blood glucose and age, weight, abdominal circumference, skinfold thickness, and triglyceride levels, which is of some significance for predicting the occurrence of spontaneous diabetes.
5.Traditional Chinese Medicine Intervention in Diarrhea-predominant Irritable Bowel Syndrome Based on Gut-brain Axis: A Review
Jinchan PENG ; Jinxiu WEI ; Zhu LIU ; Lijian LIU ; Liqun LI ; Chengning YANG ; Guangwen CHEN ; Jianfeng LI ; Sheng XIE
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(8):311-319
Diarrhea-predominant irritable bowel syndrome (IBS-D) is a common digestive system disease with high prevalence and recurrence rates for years, high treatment costs, and serious impacts on patients' quality of life and economic burden. Therefore, it is important to explore new and safe treatment methods. The pathogenesis of IBS-D is complex, in which the gut-brain axis is a key factor. The gut-brain axis, a bidirectional signaling pathway connecting the gastrointestinal tract and the central nervous system, regulates gastrointestinal motility, secretion, and immune responses, playing a key role in the occurrence and development of IBS-D. Up to now, antidiarrheal agents, probiotics, and neurotransmitter modulators are the main methods for the clinical treatment of IBS-D. Although they can partially curb the progression of this disease, the therapeutic effects remain to be improved. Studies have confirmed that traditional Chinese medicine (TCM) has significant advantages in the treatment of IBS-D since it can regulate the gut-brain axis via multiple pathways and targets to improve the gastrointestinal motility and strengthen immune defenses. However, there is a lack of systematic reviews on the regulation of the gut-brain axis by TCM in the treatment of IBS-D. Based on the review of IBS-D-related articles published in recent years, this paper systematically summarized the relationship between the gut-brain axis and IBS-D and the role of TCM in the treatment, providing new ideas for the treatment of IBS-D.
6.Relationship between screening myopia and physical fitness index in college freshmen without majoring in public safety administration
Chinese Journal of School Health 2025;46(3):431-434
Objective:
To explore the relationship between visual acuity and physical fitness of university freshmen, so as to provide reference for myopia prevention and control for freshmen.
Methods:
From October to November 2022, 2 160 college freshman without majoring in public safety administration, selected from Guangxi Police College in 2022 by using the stratified cluster random sampling method, were reviewed for the results of visual acuity test and physical fitness scores. The physical fitness indices were evaluated by using the Z scores of physical fitness test scores, and the strength of association between the level of physical fitness index and myopia was analyzed by using Logistic regression model.
Results:
Among 2 160 college freshman without majoring in public safety administration, 917 (42.5%) students were diagnosed screening myopia, including 66 (3.1%) cases of high myopia, 383 (17.7%) cases of moderate myopia and 468 (21.7%) cases of mild myopia. The differences in the distribution of visual acuity tests among students with different physical fitness indices, body mass index, and gender were statistically significant ( Z/H=54.50, 49.53, 15.51, P <0.01). Low level and low middle level physical fitness indices were associated with screening myopia among freshmen[ OR (95% CI )=2.81(1.93-4.08),1.87(1.38-2.54)], and low level physical fitness indexes were associated with high myopia [ OR (95% CI )=7.22(2.33-22.32)] ( P <0.01).
Conclusions
Screening myopia among college freshman without majoring in public safety administration is related to physical fitness, and low level and low middle level physical fitness index are risk factors for myopia. Improving the level of physical fitness might be effective in preventing myopia.
7.Effect of Wenpi tongluo kaiqiao formula against neuronal necroptosis in mice with Alzheimer’s disease and its mechanism
Xiaomin ZHU ; Wei CHEN ; Yulan FU ; Guifeng ZHUO ; Yingrui HUANG ; Ying ZHANG ; Lin WU
China Pharmacy 2025;36(9):1046-1051
OBJECTIVE To investigate the effects and mechanism of Wenpi tongluo kaiqiao formula (WPTL) against neuronal necroptosis in Alzheimer’s disease (AD) mice based on the Z-DNA binding protein 1 (ZBP1)/mixed lineage kinase domain-like protein (MLKL) signaling pathway. METHODS Forty APP/PS1 transgenic AD mice were randomly divided into model group, WPTL low-dose (WPTL-L) group (10.4 g/kg, calculated by the raw medicine), WPTL high-dose (WPTL-H) group (20.8 g/kg, calculated by the raw medicine) and donepezil hydrochloride group (3 mg/kg), with 10 mice in each group; another 10 C57BL/6J mice were selected as normal control group. Intragastric administration, once a day, for 30 consecutive days. Twenty-four hours after the last administration, Morris water maze test was performed to evaluate learning and memory abilities; the pathological morphology of hippocampal tissues was observed; the serum levels of tumor necrosis factor-α (TNF-α) and interleukin-4 (IL-4) were determined; the expressions of amyloid precursor protein (APP), Tau protein, and ZBP1/MLKL signaling pathway-related proteins in hippocampal tissues were detected; the positive expression of phosphorylated receptor-interacting protein kinase 3 (p-RIPK3) in the neurons of hippocampal tissues and mRNA expression of ZBP1 were measured in hippocampal tissues. RESULTS Compared with normal control group, the escape latency of mice in model group was prolonged significantly on day 3 to 5 (P<0.05), the times of crossing platform reduced significantly (P<0.05), and obvious pathological changes were observed in the hippocampal tissue. The level of TNF- α, the expressions of APP, p-Tau and ZBP1, the phosphorylation levels of RIPK1, RIPK3 and MLKL, the fluorescence intensity of p-RIPK3 as well as the mRNA expression of ZBP1 were significantly increased (P<0.05), while the serum level of IL-4 was decreased significantly (P<0.05). Compared with model group, above indexes were reversed significantly in administration groups (P<0.05), and pathological damage of hippocampal tissue was alleviated. CONCLUSIONS WPTL can inhibit the ZBP1/MLKL signaling pathway, reduce neuronal necroptosis in AD mice, and inhibit inflammatory responses, thereby improving learning and spatial memory abilities in AD mice.
8.Mahoniae Caulis Alkaloids Ameliorate Depression by Regulating Synaptic Plasticity via cAMP Pathway
Junhui HE ; Chunlian JIA ; Kedao LAI ; Guili ZHOU ; Rongfei ZHOU ; Yi LI ; Dongmei LI ; Jiaxiu XIE ; Guining WEI ; Juying ZHOU
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(13):132-140
ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids (MA) in ameliorating depression by network pharmacology, molecular docking, and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP, Genecards, HPO, DrugBank and OMIM database. The depression targets were collected through TCMIP, Genecards, HPO, DrugBank and OMIM database. Protein-protein interaction (PPI) network was constructed by protein interaction analysis (STRING) database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed through Bioinformatics (DAVID) database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone (CORT) once a day for 35 consecutive days. Sixty mice were randomly allocated into control (0.9% normal saline), model (CORT, 20 mg·kg-1), positive control (fluoxetine hydrochloride, 3.6 mg·kg-1), and MA (10, 5, and 2.5 mg·kg-1) groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling (TUNEL) was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor (BDNF), dopamine (DA), 5-hydroxytryptamine (5-HT), and norepinephrine (NE) in mice. The mRNA levels of cyclic adenosine monophosphate (cAMP) pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 (Cx43). ResultsA total of 434 component targets and 545 depression targets were obtained, including 84 common targets, among which 10 core targets were screened out. GO analysis predicted 34 biological processes, 15 cell components, and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group, CORT prolonged the immobility time of mice in forced swimming and tail suspension tests (P<0.01), lowered the serum levels of NE, BDNF, and 5-HT (P<0.05), up-regulated the mRNA levels of nuclear factor-κB (NF-κB) and interleukin-6 (IL-6) in the brain tissue (P<0.05), and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein (CREB) and BDNF (P<0.05) and the protein levels of protein kinase (PRKACA), phosphorylation (p)-CREB/CREB, BDNF, and Cx43 (P<0.05) in the brain tissue. Compared with the model group, high-dose MA reduced the immobility time of mice in forced swimming (P<0.05) and tail suspension (P<0.01) tests, raised the serum levels of NE, BDNF, and 5-HT (P<0.01), down-regulated the mRNA level of NF-κB (P<0.01), and up-regulated the mRNA level of BDNF (P<0.01) and protein levels of PRKACA, p-CREB/CREB, BDNF, and Cx43 (P<0.05). ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway, improving synaptic plasticity and gap junction function, and reducing neuroinflammation.
9.Mahoniae Caulis Alkaloids Ameliorate Depression by Regulating Synaptic Plasticity via cAMP Pathway
Junhui HE ; Chunlian JIA ; Kedao LAI ; Guili ZHOU ; Rongfei ZHOU ; Yi LI ; Dongmei LI ; Jiaxiu XIE ; Guining WEI ; Juying ZHOU
Chinese Journal of Experimental Traditional Medical Formulae 2025;31(13):132-140
ObjectiveTo explore the mechanisms associated with Mahoniae Caulis alkaloids (MA) in ameliorating depression by network pharmacology, molecular docking, and animal experiments. MethodsThe component targets of MA were obtained through Swiss Target Prediction and TCMIP database. The depression targets were collected through TCMIP, Genecards, HPO, DrugBank and OMIM database. The depression targets were collected through TCMIP, Genecards, HPO, DrugBank and OMIM database. Protein-protein interaction (PPI) network was constructed by protein interaction analysis (STRING) database. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed through Bioinformatics (DAVID) database. The docking of components and targets was performed by AGFR. The mouse model of depression was established by intraperitoneal injection of corticosterone (CORT) once a day for 35 consecutive days. Sixty mice were randomly allocated into control (0.9% normal saline), model (CORT, 20 mg·kg-1), positive control (fluoxetine hydrochloride, 3.6 mg·kg-1), and MA (10, 5, and 2.5 mg·kg-1) groups. Each group was administrated with corresponding medicine or normal saline once a day for 28 consecutive days. The depression-like behavior of mice was observed. The pathological changes of prefrontal cortex in mice were observed by hematoxylin-eosin staining. Terminal deoxynucleotidyl dUTP transferase nick end labeling (TUNEL) was employed to observe the apoptosis of neurons in the prefrontal cortex. Enzyme-linked immunosorbent assay was employed to assess the serum levels of brain-derived neurotrophic factor (BDNF), dopamine (DA), 5-hydroxytryptamine (5-HT), and norepinephrine (NE) in mice. The mRNA levels of cyclic adenosine monophosphate (cAMP) pathway-related factors and inflammatory factors were determined by Real-time PCR. Western blot was employed to determine the expression of cAMP pathway-related factors and connexin 43 (Cx43). ResultsA total of 434 component targets and 545 depression targets were obtained, including 84 common targets, among which 10 core targets were screened out. GO analysis predicted 34 biological processes, 15 cell components, and 11 molecular functions. The KEGG pathways were mainly related to gap junction and cAMP signaling pathway. The core components had good binding affinity with the core targets. The results of animal experiments showed that compared with the control group, CORT prolonged the immobility time of mice in forced swimming and tail suspension tests (P<0.01), lowered the serum levels of NE, BDNF, and 5-HT (P<0.05), up-regulated the mRNA levels of nuclear factor-κB (NF-κB) and interleukin-6 (IL-6) in the brain tissue (P<0.05), and down-regulated the mRNA levels of cyclic adenosine monophosphate effector binding protein (CREB) and BDNF (P<0.05) and the protein levels of protein kinase (PRKACA), phosphorylation (p)-CREB/CREB, BDNF, and Cx43 (P<0.05) in the brain tissue. Compared with the model group, high-dose MA reduced the immobility time of mice in forced swimming (P<0.05) and tail suspension (P<0.01) tests, raised the serum levels of NE, BDNF, and 5-HT (P<0.01), down-regulated the mRNA level of NF-κB (P<0.01), and up-regulated the mRNA level of BDNF (P<0.01) and protein levels of PRKACA, p-CREB/CREB, BDNF, and Cx43 (P<0.05). ConclusionMA alleviates the CORT-induced depressive behavior of mice. It may play an antidepressant role by regulating cAMP signaling pathway and gap junction pathway, improving synaptic plasticity and gap junction function, and reducing neuroinflammation.
10.Impact of Antibody Immune Response and Immune Cells on Osteoporosis and Fractures
Kangkang OU ; Jiarui CHEN ; Jichong ZHU ; Weiming TAN ; Cheng WEI ; Guiyu LI ; Yingying QIN ; Chong LIU
Clinics in Orthopedic Surgery 2025;17(3):530-545
Background:
The immune system plays a critical role in the development and progression of osteoporosis and fractures. However, the causal relationships between antibody immune responses, immune cells, and these bone conditions remain unclear. This study aimed to explore these relationships using Mendelian randomization (MR) analysis.
Methods:
We collected complete blood count data from patients with fractures and healthy individuals and analyzed their differences. Then, we conducted a 2-sample, 2-step MR analysis to investigate the causal effects of antibody immune responses on osteoporosis and fractures, using inverse-variance weighted (IVW) as the primary method. We also explored whether immune cells mediate the pathway between antibodies and osteoporosis or fractures. Finally, we analyzed the functions and expression levels of key genes involved.
Results:
Overall, the fracture group exhibited increased white blood cell count, absolute neutrophil count, absolute monocyte count, platelet count, and their respective proportions, while absolute lymphocyte count, absolute eosinophil count, absolute basophil count, red blood cell count, and their proportions were decreased. We identified 44 causal relationships between antibodies and osteoporosis or fractures, with 7 supported by multiple MR methods, and 5 showing odds ratios significantly deviating from 1 in the IVW analysis. Epstein-Barr virus-related antibodies had a notable impact on osteoporosis and fractures. The human leukocyte antigen (HLA) gene family, particularly HLA-DPB1, emerged as a significant risk factor. However, immune cells were not found to mediate these effects.
Conclusions
This study elucidated the causal relationships between antibody immune responses, immune cells, and osteoporosis or fractures. The HLA gene family plays a crucial role in the interaction between antibodies and these bone conditions, with HLA-DPB1 identified as a key risk gene. Immune cells do not serve as mediators in this process. These findings provide valuable insights for future research.


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