OBJECTIVE To understand the development status and existing problems of traditional Chinese medicine（TCM） pharmacists in public TCM hospitals in China， aiming to provide suggestions for the competent departments to formulate management policies for TCM pharmacists and promote the healthy development of TCM. METHODS The data on the number and professional titles of TCM pharmacists in public TCM hospitals in China from 2019 to 2023 were collected. Descriptive analysis was employed to analyze the number， distribution and professional titles of TCM pharmacists in public TCM hospitals across the country， and to measure the quantity shortfalls of the number of TCM pharmacists in these hospitals. RESULTS From 2019 to 2023， the number of TCM pharmacists in public TCM hospitals in China grew slowly， with an average annual growth rate of 2.56%. However， the proportion of TCM pharmacists to the total number of pharmacists in public TCM hospitals gradually decreased， with an average annual growth rate of －0.65%. In terms of hospital grades， the number of TCM pharmacists in tertiary public TCM hospitals showed positive growth， while those in secondary and primary public TCM hospitals showed negative growth. In terms of hospital types， the average annual growth rate of TCM pharmacists in TCM hospitals was 2.22%， in integrated Chinese and Western medicine hospitals it was 7.97%， and in ethnic minority medicine hospitals it was 2.74%. The development of TCM pharmacists in different provinces was uneven. The annual growth rate of TCM pharmacists in Guizhou exceeded 10%， while the growth rate in Hunan and Heilongjiang was negative. In 2023， the number of TCM pharmacists per thousand population in public TCM hospitals was 0.03， indicating a relatively low staffing level. The professional titles of TCM pharmacists in public TCM hospitals were mainly primary and E-mail：601907549@qq.com intermediate， with a total of 67.33%. According to the calculation that the proportion of TCM pharmacists to pharmacists was not less than 60%， public TCM hospitals and hospitals of integrated TCM and Western medicine should be reconfigured with TCM pharmacists 6 212 and 1 288 people， respectively. CONCLUSIONS The number of TCM pharmacists in public TCM hospitals is growing slowly， with insufficient staffing levels， relatively low professional titles， and uneven distribution and development across provinces. It is suggested that relevant competent departments strengthen policy guidance， increase the attention given by the state level to TCM pharmacists， strengthen the construction of the talent team for TCM pharmacists， improve the quality and optimize the allocation of TCM pharmacist talents in order to promote the high-quality development of TCM services.

This study investigated the effect of Wuling San on transforming growth factor-β1(TGF-β1)-induced fibrosis, inflammation, and oxidative stress in human renal tubular epithelial cells(HK-2) and its mechanism of antioxidant stress injury. HK-2 cells were cultured in vitro and divided into a control group, a TGF-β1 model group, and three treatment groups receiving Wuling San-containing serum at low(2.5%), medium(5.0%), and high(10.0%) doses. TGF-β1 was used to establish the model in all groups except the control group. CCK-8 was used to analyze the effect of different concentrations of Wuling San on the activity of HK-2 cells with or without TGF-β1 stimulation. The expression of key fibrosis molecules, including actin alpha 2(Acta2), collagen type Ⅰ alpha 1 chain(Col1α1), collagen type Ⅲ alpha 1 chain(Col3α1), TIMP metallopeptidase inhibitor 1(Timp1), and fibronectin 1(Fn1), was detected using qPCR. The expression levels of inflammatory cytokines, including tumor necrosis factor-α(TNF-α), interleukin-1β(IL-1β), interleukin-6(IL-6), interleukin-8(IL-8), and interleukin-4(IL-4), were measured using ELISA kits. Glutathione peroxidase(GSH-Px), malondialdehyde(MDA), catalase(CAT), and superoxide dismutase(SOD) biochemical kits were used to analyze the effect of Wuling San on TGF-β1-induced oxidative stress injury in HK-2 cells, and the expression of nuclear factor E2-related factor 2(Nrf2), heme oxygenase 1(HO-1), and NAD(P)H quinone oxidoreductase 1(NQO1) was analyzed by qPCR and immunofluorescence. The CCK-8 results indicated that the optimal administration concentrations of Wuling San were 2.5%, 5.0%, and 10.0%. Compared with the control group, the TGF-β1 model group showed significantly increased levels of key fibrosis molecules(Acta2, Col1α1, Col3α1, Timp1, and Fn1) and inflammatory cytokines(TNF-α, IL-1β, IL-6, IL-8, and IL-4). In contrast, the Wuling San administration groups were able to dose-dependently inhibit the expression levels of key fibrosis molecules and inflammatory cytokines compared with the TGF-β1 model group. Wuling San significantly increased the activities of GSH-Px, CAT, and SOD enzymes in TGF-β1-stimulated HK-2 cells and significantly inhibited the level of MDA. Furthermore, compared with the control group, the TGF-β1 model group exhibited a significant reduction in the expression of Nrf2, HO-1, and NQO1 genes and proteins. After Wuling San intervention, the expression of Nrf2, HO-1, and NQO1 genes and proteins was significantly increased. Correlation analysis showed that antioxidant stress enzymes(GSH-Px, CAT, and SOD) and Nrf2 signaling were significantly negatively correlated with key fibrosis molecules and inflammatory cytokines in the TGF-β1-stimulated HK-2 cell model. In conclusion, Wuling San can inhibit TGF-β1-induced fibrosis in HK-2 cells by activating the Nrf2 signaling pathway, improving oxidative stress injury, and reducing inflammation.
Humans ; Oxidative Stress/drug effects* ; Transforming Growth Factor beta1/metabolism* ; Fibrosis/genetics* ; Cell Line ; Drugs, Chinese Herbal/pharmacology* ; Epithelial Cells/immunology* ; Inflammation/metabolism*

The traditional Chinese medicine(TCM) industry is a crucial part of China's pharmaceutical sector and plays a strategic role in ensuring public health and promoting economic and social development. In response to the practical demand for high-quality development of the TCM industry, this paper focused on the bottlenecks encountered during the digital and intelligent transformation of TCM production systems. Specifically, it explored technical strategies and methodologies for constructing the best TCM production mode. An innovative artificial intelligence(AI)-centered technical architecture for TCM production was proposed, focusing on key aspects of production management including process modeling, state evaluation, and decision optimization. Furthermore, a series of critical technologies were developed to realize the best TCM production mode. Finally, a novel AI-driven TCM production mode characterized by a closed-loop system of "measurement-modeling-decision-execution" was presented through engineering case studies. This study is expected to provide a technological pathway for developing new quality productive forces within the TCM industry.
Artificial Intelligence ; Drugs, Chinese Herbal ; Medicine, Chinese Traditional/methods* ; Humans

OBJECTIVE: To investigate the effects of acupuncture on the neurotransmitter levels and gut microbiota in a mouse model of Tourette syndrome (TS). METHODS: Thirty-six male C57/BL6 mice were randomly divided into 4 groups using a random number table method: 3,3'-iminodipropionitrile (IDPN) group, control group, acupuncture group, and tiapride group, with 9 mice in each group. In the IDPN group, acupuncture group, and tiapride group, mice received daily intraperitoneal injections of IDPN (300 mg/kg body weight) for 7 consecutive days to induce stereotyped behaviors. Subsequently, in the acupuncture intervention group, standardized acupuncture treatment was administered for 14 consecutive days to IDPN-induced TS model mice. The selected acupoints included Baihui (DU 20), Yintang (DU 29), Waiguan (SJ 5), and Zulinqi (GB 41). In the tiapride group, mice were administered tiapride (50 mg/kg body weight) via oral gavage daily for 14 consecutive days. The control group, IDPN group, and acupuncture group received the same volume of saline orally for 14 consecutive days. Stereotypic behaviors were quantified through behavioral assessments. Neurotransmitter levels, including dopamine (DA), glutamate (Glu), and aspartate (ASP) in striatal tissue were measured using enzyme-linked immunosorbent assay. Dopamine transporter (DAT) expression levels were additionally quantified through quantitative polymerase chain reaction (qPCR). Gut microbial composition was analyzed through 16S ribosomal RNA gene sequencing, while metabolic profiling was conducted using liquid chromatography-mass spectrometry (LC-MS). RESULTS: Acupuncture administration significantly attenuated stereotypic behaviors, concurrently reducing striatal levels of DA, Glu and ASP concentrations while upregulating DAT expression compared with untreated TS controls (P<0.05 or P<0.01). Comparative analysis identified significant differences in Muribaculaceae (P=0.001), Oscillospiraceae (P=0.049), Desulfovibrionaceae (P=0.001), and Marinifilaceae (P=0.014) following acupuncture intervention. Metabolomic profiling revealed alterations in 7 metabolites and 18 metabolic pathways when compared to the TS mice, which involved various amino acid metabolisms associated with DA, Glu, and ASP. CONCLUSIONS Acupuncture demonstrates significant modulatory effects on both central neurotransmitter systems and gut microbial ecology, thereby highlighting its dual therapeutic potential for TS management through gut-brain axis regulation.
Animals ; Tourette Syndrome/metabolism* ; Gastrointestinal Microbiome ; Neurotransmitter Agents/metabolism* ; Acupuncture Therapy ; Male ; Mice, Inbred C57BL ; Mice

Objective To explore the mechanism of action of jolkinolide B in the treatment of gastric cancer by network pharmacology combined with molecular docking technique.Methods The SwissTargetPrediction database was used to obtain the targets of the active compounds.Search Genecards,OMIM,Drugbank,TTD,and PharmGKB databases to obtain targets for gastric cancer.The intersection between the targets of jolkinolide B and those of gastric cancer was identified pinpoint potential targets for jolkinolide B in treating gastric cancer.The String database was utilized construct a protein-protein interaction(PPI)network.Bioconductor bioinformatics packages with R software was employed conduct Gene Ontology(GO)functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG)pathway enrichment analysis on the shared targets.This process revealed significant regulatory pathways crucial for jolkinolide B's efficacy in treating gastric cancer.Cytoscape 3.7.1 software was utilized create the core network of"Potential Targets of Triptolide B in Gastric Cancer Treatment",and SYBYL-X2.1.1 software was employed conduct molecular docking validation of the selected main active ingredients and critical targets.Results Jolkinolide B may target multiple proteins,including MAPK1,glycogen synthase kinae-3β(GSK-3β),and JUN,impacting the proliferation,invasion,and metastasis of gastric cancer,ultimately inhibiting its growth.Conclusion We predicted the possible molecular mechanism of jolkinolide B in the treatment of gastric cancer to provide guide information for the subsequent experimental research and clinical application.

Objective To investigate the role of G protein signal regulator 2(RGS2)in regulating the formation of angiotensin Ⅱ(Ang Ⅱ)-induced aortic dissection.Methods C57BL/6 mice were divided into 3 groups:control group(n=10),Ang Ⅱ group(n=20),Ang Ⅱ+sh-RGS2 group(n=20).The Ang Ⅱ group and Ang Ⅱ+sh-RGS2 group established an aortic dissection model.The incidence of aortic dissection was evaluated in vivo,and the phenotypic transformation of VSMC was evaluated in vitro and in vivo.Results Knockdown of RGS2 largely coun-teracted Ang Ⅱ-induced inhibition of αSMA,ACTA2 and MYH11,and suppressed Ang Ⅱ-induced SPP1 and Vim-entin in VSMC.The incidence of aortic dissection in Ang Ⅱ group and Ang Ⅱ+sh-RGS2 group were 45％(9/20)and 10％(2/20),respectively.Fewer elastic lamina thickening,aortic rupture,and aortic wall collagen fiber con-tent were observed in Ang Ⅱ+sh-RGS2 group compared to Ang Ⅱ group.In addition,compared with the Ang Ⅱgroup,the maximum diameter of the aorta in the Ang Ⅱ+sh-RGS2 group was significantly reduced(P＜0.05).In addition,the ACTA2 and MYH11 proteins in the aorta of the Ang Ⅱ+sh-RGS2 group were significantly higher than those in the Ang Ⅱ group(P＜0.01),while the RGS2,SPP1,and Vimentin proteins significantly decreased(P＜0.01).Conclusion Knockdown of RGS2 inhibits the transformation of Ang Ⅱ-induced VSMC from a contractile phenotype to a synthetic phenotype,thereby reducing the incidence of aortic dissection formation.

Objective To explore the effect of behavioral vision training on post-stroke ocular motility disorders(PSOMD). Methods From August to Octobor,2023,a total of 21 PSOMD patients in Beijing Bo'ai Hospital were selected.They re-ceived behavioral vision training,including brain-based visual training and visual fusion training,for four weeks.Visual function was assessed with Snellen eye chart,strabismus prism and Titmus near stereopia. Results The vision of both right and left eyes improved after training(Z right eye=-3.601,Z left eye=3.012,P<0.01),while the strabismus prism reduced significantly(t=8.930,P<0.001).But Titmus near stereopia showed no difference(P>0.05). Conclusion Behavioral vision training could improve vision and strabismus after stroke.

The assessment of adverse drug events is an important basis for clinical safety evaluation and post-marketing risk control of drugs,and its causality assessment is gaining increasing attention.The existing methods for assessing the causal relationship between drugs and the occurrence of adverse reactions can be broadly classified into three categories:global introspective methods,standardized methods,and probabilistic methods.At present,there is no systematic introduction of the operational details of the various methods in the domestic literature.This paper compares representative causality assessment methods in terms of definition and concept,methodological steps,industry evaluation and advantages and disadvantages,clarifies the basic process of determining the causality of adverse drug reactions,and discusses how to further improve the adverse drug reaction monitoring and evaluation system,with a view to providing a reference for drug development and pharmacovigilance work in China.

ObjectiveHuman Ku70 protein mainly involves the non-homologous end joining (NHEJ) repair of double-stranded DNA breaks (DSB) through its DNA-binding properties, and it is recently reported having an RNA-binding ability. This paper is to explore whether Ku70 has RNA helicase activity and affects miRNA maturation. MethodsRNAs bound to Ku protein were analyzed by RNA immunoprecipitation sequencing (RIP-seq) and bioinfomatic anaylsis. The expression relationship between Ku protein and miRNAs was verified by Western blot (WB) and quantitative reverse transcriptase-polymerase chain reaction (qRT-PCR) assays. Binding ability of Ku protein to the RNAs was tested by biolayer interferometry (BLI) assay. RNA helicase activity of Ku protein was identified with EMSA assay. The effect of Ku70 regulated miR-124 on neuronal differentiation was performed by morphology analysis, WB and immunofluorescence assays with or without Zika virus (ZIKV) infection. ResultsWe revealed that the Ku70 protein had RNA helicase activity and affected miRNA maturation. Deficiency of Ku70 led to the up-regulation of a large number of mature miRNAs, especially neuronal specific miRNAs like miR-124. The knockdown of Ku70 promoted neuronal differentiation in human neural progenitor cells (hNPCs) and SH-SY5Y cells by boosting miR-124 maturation. Importantly, ZIKV infection reduced the expression of Ku70 whereas increased expression of miR-124 in hNPCs, and led to morphologically neuronal differentiation. ConclusionOur study revealed a novel function of Ku70 as an RNA helicase and regulating miRNA maturation. The reduced expression of Ku70 with ZIKV infection increased the expression of miR-124 and led to the premature differentiation of embryonic neural progenitor cells, which might be one of the causes of microcephaly.