Retinal microcirculatory disorder is a key factor in the occurrence and development of diabetic retinopathy （DR）， and also an important link in the prevention and treatment of DR. The theory of "Gaozhuo" holds that the microcirculatory disorder in DR is based on the deficiency of spleen Qi and is characterized by the obstruction caused by "Gaozhuo" and blood stasis. The deficiency of spleen Qi is an essential precondition for the endogenous formation and accumulation of Gaozhuo， while Gaozhuo invasion is the direct cause of microcirculatory disorders in DR. The deficiency of spleen Qi and the endogenous formation of Gaozhuo mean the process in which glucose metabolism dysfunction induces an excessive production of inflammatory factors and lipid metabolites. The obstruction caused by "Gaozhuo" and blood stasis is the direct pathogenesis of microcirculatory disorders in DR， encompassing two stages： Gaozhuo obstruction and turbidity and stasis stagnation. Gaozhuo obstruction and turbidity and stasis stagnation represent the process in which inflammatory factors and lipid metabolites damage the retinal microcirculation and induce thrombosis， thus mediating microcirculatory disorders. Turbidity and stasis stagnation and blood extravasation outside the vessels reveal the progression to microvascular rupture and hemorrhage resulting from the microcirculatory disorders. According to the pathogenesis evolution of the theory of "Gaozhuo"， microcirculatory disorders in DR can be divided into deficiency of spleen Qi with Gaozhuo obstruction， deficiency of spleen Qi with turbidity and stasis stagnation， and turbidity and stasis stagnation with blood extravasation outside the vessels. Clinically， treatment principles should focus on strengthening the spleen and benefiting Qi， resolving turbidity， and dispersing stasis. Different syndrome patterns should be addressed with tailored therapies， such as enhancing the spleen and benefiting Qi while regulating Qi and reducing turbidity， strengthening the spleen and benefiting Qi while resolving turbidity and dispelling stasis， and strengthening the spleen and resolving turbidity while removing stasis and stopping bleeding. Representative prescriptions include modified Wendantang， modified Buyang Huanwutang， modified Danggui Buxuetang， Zhuixue Mingmu decoction， Tangmuqing， Shengqing Jiangzhuo Tongluo Mingmu prescription， Danhong Huayu decoction， and Yiqi Yangyin Huoxue Lishui formula.

OBJECTIVE To formulate Guidelines for the standardized implementation of pharmacist-managed clinics （ 2026 edition ） in response to the challenges faced by such clinics in China， including uneven development， large discrepancies in service specifications， insufficient patient awareness， and limited medical insurance coverage. METHODS Led by the Pharmaceutical Affairs Professional Committee of the Chinese Hospital Association， the Evidence-based Pharmacy Professional Committee of the Chinese Pharmaceutical Association， and the Hospital Pharmacy Professional Committee of the Cross-strait Medical and Health Exchange Association， a total of 19 domestic hospital pharmacy experts were organized. Through a systematic review of national policies and literature research， current practical experience was summarized. Consensus on the contents of the guidelines was reached after in-depth discussions. RESULTS &CONCLUSIONS The guidelines covered five sections： definition and connotation of pharmacist-managed clinics， establishment requirements， implementation and management， post competency， and practical research. Firstly， the definition and connotation included three operational forms of pharmacist-managed clinics （independent mode， physician-pharmacist joint mode， and online pharmacist-managed clinic mode） and classified service modes （specialty-specific， drug-specific， and disease-specific pharmacist-managed clinics）. The establishment requirements were further refined， covering system construction （pharmaceutical service management system， quality control and assessment mechanism）， personnel qualifications （professional credentials， continuing education and professional training， etc）， service recipients， as well as service venues and facilities. Subsequently， the implementation and management of pharmacist-managed clinics were proposed， involving service procedures， intervention measures， documentation and records， patient education and follow-up， humanistic care， as well as risk management and quality control. Finally， post competency encompassed the competency requirements for pharmacists providing services in pharmacist-managed clinics， as well as the suggestions on teaching methods； practical research encouraged the conduct of high-quality pharmaceutical practice in the setting of pharmacist-managed clinics. The guidelines provide valuable guidance for the standardized implementation of pharmacist-managed clinics in China in terms of establishment， management， teaching， and research， fill the guideline gap in this field， and can promote the high-quality development of pharmacist-managed clinics.

OBJECTIVE To investigate the mechanism of Huangqin decoction in improving ulcerative colitis （UC） through the gut microbiota-tryptophan metabolism-aryl hydrocarbon receptor （AhR） axis. METHODS Mice were randomly divided into normal group （normal saline）， model group （normal saline）， microbiota depletion-model group （normal saline）， microbiota depletion-Huangqin decoction group （9.1 g/kg， by crude drug， similarly hereinafter）， Huangqin decoction group and mesalazine group （positive control group， 0.4 g/kg）， with 6 mice in each group. Microbiota depletion was achieved by providing free access to a mixed antibiotics for 10 days. The UC model was induced by administering 2.5% dextran sulfate sodium solution for 7 days. After successful modeling， each treatment group received corresponding drugs or normal saline intragastrically once daily for 10 days. After the final administration， body weight change ratio， disease activity index （DAI） score， and colon length were evaluated； colon pathological changes were observed； serum levels of interleukin-6 （IL-6）， IL-10， IL-22， and tumor necrosis factor-α （TNF-α） were measured； the expressions of Occludin， zonula occluden-1 （ZO-1）， and AhR in colon tissue were detected； fecal samples were subjected to high-throughput sequencing to analyze targeted tryptophan metabolomics. RESULTS Compared with the model group， Huangqin decoction group showed reduced infiltration of inflammatory cells in the colon tissue and restoration of the intestinal mucosal structure. Body weight change ratio， colon length， serum content of IL-10， the expressions of Occludin， ZO-1 and AhR in colon tissue and the contents of tryptophan metabolites indole-3-propionic acid （IPA）， N -acetylserotonin （NAS） and indole-3-acetic acid （IAA） were all significantly increased （ P ＜0.05）； DAI score， serum levels of IL-6， TNF-α， and IL-22 and the content of tryptophan metabolite indole-3-ethanol were significantly decreased （ P ＜0.05）； gut microbiota structure was improved， with increased relative abundances of beneficial bacteria such as Lactobacillus ， and decreased relative abundances of pathogenic bacteria such as Escherichia-Shigella . However， after antibiotic-induced microbiota depletion， although Huangqin decoction significantly increased the content of NAS in the feces of mice， the expression of AhR protein in colon tissue did not increase concurrently. CONCLUSIONS Huangqin decoction can repair the intestinal mucosal barrier in UC mice by regulating the gut microbiota and promoting the production of IPA and IAA， thereby activating AhR. This suggests that an intact gut microbiota is an important prerequisite for Huangqin decoction to exert its AhR-regulating effects.

Primary biliary cholangitis （PBC） is a cholestatic autoimmune liver disease characterized by the injury of small intrahepatic bile ducts， and at present， the pathogenesis of PBC remains unclear. Recent studies have shown that bile acid metabolism disorder and gut microbiota imbalance play a key role in the development and progression of PBC， and they form a complex and dynamic interaction network via the “gut-liver axis” and regulate core physiopathological processes such as immune response， metabolic homeostasis， and inflammatory response in a synergistic manner. This article systematically elaborates on the abnormal features of bile acid metabolism and gut microbiota in PBC， discusses their synergistic mechanisms in PBC， and then proposes a combined strategy of targeting bile acid receptors and modulating gut microbiota， in order to overcome the limitations of current treatment modalities and provide new insights and directions for the clinical management of PBC.

Objective: To evaluate the methodological quality and reporting quality of clinical practice guidelines or expert consensus on blood transfusion and blood use (BTBU) in China (hereinafter referred to as "guidelines/consensus"), providing reference for the development and updating of future BTBU guidelines/consensus. Methods: A systematic search was conducted in Chinese databases such as China National Knowledge Infrastructure (CNKI), Wanfang Data, VIP Data-base, relevant guideline release platforms, and professional association websites. BTBU-related guidelines/consensus published between January 2006 and December 2025 were included. According to the inclusion and exclusion criteria, after completing literature screening and data extraction, three evaluators independently assessed the quality of the included literature using the Scientificity, Transparency, and Applicability of Guidelines Rating Tool (STAR), the Appraisal of Guidelines for Research and Evaluation Ⅱ (AGREE Ⅱ), and the International Practice Guideline Reporting Standards (RIGHT). Results: A total of 29 documents were included, including 5 guidelines, 22 consensus statements, and 2 protocols. The results of the STAR assessment showed that the total score was (21.7±8.8)%. The domain score ratios for registration, research protocol, funding, working group, conflict of interest, clinical question, evidence, consensus method, recommendation, accessibility and other domains were (2.2±12.1)%, 0, (36.7±25.1)%, (18.3±7.6)%, (19.2±15.3)%, (16.6±23.1)%, (15.1±6.3)%, (9.6±21.2)%, (54.3±18.4)%, (31.7±10.4)% and (10.3±31.0)%, respectively. For the AGREE Ⅱ assessment, the methodological quality of 26 articles was rated Grade B and 3 articles Grade C. The results of the RIGHT assessment indicated that the overall reporting rate of all guidelines/consensuses was (65.3±4.0)%. Conclusion: The methodological and reporting quality of current expert guidelines/consensus on BTBU in China still need improvement, and guidelines and consensus should be strictly formulated and standardized according to the standards of STAR, AGREE II and RIGHT.

Objective To investigated the effects of occupational exposure to N,N-dimethylformamide (DMF) on sterol regulatory element-binding protein (SREBP) and iron metabolism among workers. Methods A total of 20 workers occupationally exposed to DMF were selected as the exposure group, and 15 healthy workers without DMF exposure from the same factory were selected as the control group using the purposive sampling method. DMF exposure levels were assessed in individual samples of the workers. The urinary N-methylformamide (NMF) levels were measured by gas chromatography. The mRNA expression of SREBP-1a, SREBP-1c, and SREBP-2 in peripheral blood was measured by real-time quantitative polymerase chain reaction. Enzyme-linked immunosorbent assay was used to detect serum transferrin, soluble transferrin receptor (sTfR), and ferritin levels. Results The DMF exposure levels among the workers in the control group were below the detection limit, and urinary NMF was undetectable. The median DMF exposure level was 13.30 mg/m³, and the mean urinary NMF level was (9.72±1.78) mg/g Cr among the workers in the exposure group. Compared with the control group, the relative mRNA expression of SREBP-1a, SREBP-1c, and SREBP-2 in peripheral blood of workers in the exposure group increased (all P<0.05), while the levels of transferrin and sTfR decreased (both P<0.01). However, there was no statistically significant difference in serum ferritin levels between the two groups (P>0.05). In the exposure group, urinary NMF level of workers was negatively correlated with the relative mRNA expression level of SREBP-1c in blood [correlation coefficient (r)=-0.50, P=0.03], and positively correlated with the levels of serum transferrin, sTfR, and ferritin (r = 0.63, 0.58, and 0.52, respectively; all P<0.05). Conclusion Occupational exposure to DMF can upregulate the expression of the SREBP family and disrupt iron metabolism, with a potential association between these effects.

Objective: To analyze the etiologic distribution of difficult crossmatching and the characteristics of red blood cell antibodies, to summarize compatible transfusion strategies based on serological abnormalities, and to evaluate red blood cell transfusion efficacy and changes in bilirubin levels before and after transfusion. Methods: A retrospective analysis was conducted on difficult crossmatching cases handled by the Department of Blood Transfusion of our hospital from January 2024 to December 2025. Cases that met the criteria for difficult crossmatching determination and had complete data were included in the analysis of the causes and antibody distribution. Patients who completed red blood cell transfusion and had complete hemoglobin (Hb) data before and within 24 hours after transfusion were included in the exploratory subgroup analysis of transfusion efficacy; among them, those who also had total bilirubin and indirect bilirubin data before and after the corresponding transfusion event were included in the bilirubin analysis. According to the main serological abnormal manifestations before transfusion and the actual compatible transfusion management pathways, the cases included in the exploratory subgroup analysis were divided into three groups: the alloantibody-related difficult crossmatching group, the autoantibody-related or autoantibody combined with alloantibody-related difficult crossmatching group, and the ABO blood group identification abnormality-related difficult crossmatching group. The Hb levels before and after transfusion, the Hb increase after transfusion of each unit of red blood cells, and the changes in bilirubin levels before and after transfusion were compared among the groups. Results: A total of 322 difficult crossmatching cases met the predefined criteria, of which 287 were included in the analysis of causes and antibody distribution. There were 183 cases of alloantibody-related difficult crossmatching (63.76%), 54 cases related to inconsistency between ABO forward and reverse typing (18.82%), 44 cases related to autoantibodies (15.33%), and 6 cases related to interference from anti-CD38 monoclonal antibody drugs (2.09%). Among the 183 alloantibody-related cases, 79 cases had only a single alloantibody detected, among which antibodies of the Rh blood group system accounted for 49.37% (39/79). Among single alloantibodies, anti-E was detected most frequently, with 35 cases (44.30%), followed by anti-M with 19 cases (24.05%) and anti-Le with 13 cases (16.46%). A total of 109 cases were included in the exploratory subgroup analysis of transfusion efficacy, including 76 cases in the alloantibodyrelated difficult crossmatching group, 17 cases in the autoantibody-related or autoantibody combined with alloantibody-related difficult crossmatching group, and 16 cases in the ABO blood group identification abnormality-related difficult crossmatching group. The sex distribution and history of previous transfusion differed between cases included in and not included in this analysis. The Hb levels after transfusion in all three groups were higher than those before transfusion, and the differences were statistically significant (P<0.05). The Hb increase per unit of red blood cells did not differ significantly among the three groups (P=0.086). Among 73 cases with paired total and indirect bilirubin data corresponding to the transfusion events, the comparison of changes in total bilirubin among the three groups showed no statistically significant difference (P=0.864), and the comparison of changes in indirect bilirubin among the three groups also showed no statistically significant difference (P=0.914). Conclusion: Alloantibody-related factors were the main causes of difficult crossmatching in this study. Among single alloantibodies, Rh blood group system antibodies, especially anti-E, were relatively common. In the included exploratory subgroup, after individualized compatible transfusion based on the causes of difficult crossmatching, antibody specificities, and crossmatching results, Hb levels were higher after transfusion than before transfusion in all three groups. Within the scope of this study, the magnitude of bilirubin changes did not differ significantly among the different types of difficult crossmatching.

ObjectiveTo clarify the anti-inflammatory and lung-protective effects of Yantiao prescription on lipopolysaccharide （LPS）-induced acute lung injury （ALI）， and to explore the impact of Yantiao prescription on the metabolic pathways of arachidonic acid （AA） in vivo. MethodsThirty male C57BL/6J mice were randomly divided into the following groups based on body weight： normal group， model group， dexamethasone group （2 mg·kg^-1）， low-dose Yantiao prescription group （18 g·kg^-1）， and high-dose Yantiao prescription group （36 g·kg^-1）， with 6 mice in each group. The ALI mouse model was established by intraperitoneal injection of LPS. The treatment groups received oral gavage once a day for 7 consecutive days， and serum and lung tissue were collected at the end of the experiment. The content of pro-inflammatory cytokines tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） in serum was detected by enzyme-linked immunosorbent assay （ELISA）. Hematoxylin-eosin （HE） staining was used to assess lung tissue pathology. The wet/dry weight ratio （W/D） and myeloperoxidase （MPO） activity in lung tissue were measured. The content of AA metabolites in serum and lung tissue was measured by liquid chromatography triple quadrupole-mass spectrometry （LC-MS/MS）. ResultsCompared with the conditions in the normal group， the content of serum pro-inflammatory cytokines TNF-α， IL-1β， and IL-6 in the model group was significantly increased （P<0.01）. The alveolar structure in mice was severely damaged， with markedly thickened alveolar walls and extensive inflammatory cell infiltration. The W/D ratio and MPO activity in lung tissue were significantly increased （P<0.01）. The content of AA metabolites， including prostaglandin D₂ （PGD₂）， prostaglandin E₂ （PGE₂）， 11（S）-hydroxy-eicosatetraenoic acid ［11（S）-HETE］， and 5-hydroxy-eicosatetraenoic acid （5-HETE） in serum and lung tissue was significantly increased （P<0.05）， while the content of 11，12-epoxyeicosatrienoic acid （11，12-EET） and 14，15-epoxyeicosatrienoic acid （14，15-EET） in serum was significantly decreased （P<0.01）. Compared with the results in the model group， the content of serum pro-inflammatory cytokines TNF-α， IL-1β， and IL-6 in the dexamethasone group， low-dose Yantiao prescription group， and high-dose Yantiao prescription group was significantly reduced （P<0.05）. Mild thickening of alveolar walls， scattered inflammatory cell infiltration， and relatively intact tissue structure with improved alveolar architecture were observed. The W/D ratio and MPO activity in lung tissue were significantly reduced （P<0.01）. The content of AA metabolites PGD₂， PGE₂， 11（S）-HETE， and 5-HETE in serum from the dexamethasone group was significantly decreased （P<0.05）， while the content of 14，15-EET in serum significantly increased （P<0.01）， and the content of 5-HETE in lung tissue significantly decreased （P<0.01）. In the low-dose and high-dose Yantiao prescription groups， the content of AA metabolites PGD₂， PGE₂， 11（S）-HETE， and 5-HETE in serum and lung tissue was significantly decreased （P<0.05）， while the content of 11，12-EET in both serum and lung tissue was significantly increased （P<0.05）. ConclusionYantiao prescription has significant protective effects against LPS-induced ALI， which are related to its regulation of AA metabolic pathways in vivo.

ObjectiveTo study the mechanism of Huanglian Jiedutang （HLJDT） in treating mice with atherosclerosis （AS） by improving ferroptosis. MethodsA total of 10 SPF C57BL/6J mice were selected as a normal group， and 50 ApoE^-/- mice were randomly divided into five groups： model group， low-dose group of HLJDT， medium-dose group of HLJDT， high-dose group of HLJDT， and atorvastatin （ATV） group. ApoE^-/- mice were fed a high-fat diet for eight weeks to establish the AS model， and at the 9th week， they were given normal saline， low， medium， and high doses of HLJDT （3.9， 7.8， 15.6 g·kg^-1·d^-1）， and atorvastatin calcium tablets （0.01 g·kg^-1·d^-1）， respectively， for a total of eight weeks. The formation of aortic plaque in mice was observed by gross oil red O staining and Masson staining. The levels of total cholesterol （TC）， low-density lipoprotein cholesterol （LDL-C）， triglyceride （TG）， and high-density lipoprotein cholesterol （HDL-C） in blood fat were measured by the automatic biochemical analyzer， and the mitochondrial structure of the aorta was observed by transmission electron microscopy. The content of serum superoxide dismutase （SOD） in serum was detected by enzyme-linked immunosorbent assay （ELISA）. The content of reduced glutathione （GSH） in serum was detected by the microplate method， and that of malondialdehyde （MDA） in serum was detected by the TBA method. The protein expression of nuclear factor E₂-associated factor 2 （Nrf2）/glutathione peroxidase 4 （GPX4） signaling pathway was detected by Western blot. ResultsCompared with those of the normal group， the contents of TC， LDL-C， TG， HDL-C， and MDA in the serum and the aortic vascular plaque deposition of the model group were significantly increased （P<0.01）， while the expression levels of SOD and GSH in serum， as well as Nrf2， solute carrier family 7 member 11 （SLC7A11）， and GPX4 in aorta were significantly decreased （P<0.01）. Mice in the model group appeared mitochondrial fragmentation and vacuolation in the aorta， volume atrophy， mitochondrial crista reduction， or a loose and disorganized form. Compared with those in the model group， the aortic vascular plaque deposition was significantly decreased in the low-dose， medium-dose， and high-dose groups of HLJDT and ATV group， and the contents of serum TC， LDL-C， TG， and MDA in serum were significantly decreased （P<0.05， P<0.01）. The contents of serum SOD and GSH and the expression levels of Nrf2， SLC7A11， and GPX4 in the aorta were increased （P<0.05， P<0.01）， and the symptoms of aortic mitochondrial vacuolation were alleviated. The number of cristae was increased， and they were ordered neatly. ConclusionHLJDT can reduce aortic vascular plaque deposition， decrease blood lipid and MDA expression， increase SOD and GSH expression， and ameliorate the pathological changes of ferroptosis， the mechanism of which is related to the Nrf2/GPX4 signaling pathway.

This study aims to investigate the mechanism by which resveratrol(RES) alleviates cerebral vascular endothelial damage in sepsis-associated encephalopathy(SAE) through network pharmacology and animal experiments. By using network pharmacology, the study identified common targets and genes associated with RES and SAE and constructed a protein-protein interaction( PPI) network. Gene Ontology(GO) analysis and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment analysis were performed to pinpoint key signaling pathways, followed by molecular docking validation. In the animal experiments, a cecum ligation and puncture(CLP) method was employed to induce SAE in mice. The mice were randomly assigned to the sham group, CLP group, and medium-dose and high-dose groups of RES. The sham group underwent open surgery without CLP, and the CLP group received an intraperitoneal injection of 0. 9% sodium chloride solution after surgery. The medium-dose and high-dose groups of RES were injected intraperitoneally with 40 mg·kg-1 and 60 mg·kg~(-1) of RES after modeling, respectively, and samples were collected 12 hours later. Neurological function scores were assessed, and the wet-dry weight ratio of brain tissue was detected. Serum superoxide dismutase(SOD), catalase( CAT) activity, and malondialdehyde( MDA) content were measured by oxidative stress kit. Histopathological changes in brain tissue were examined using hematoxylin-eosin(HE) staining. Transmission electron microscopy was employed to evaluate tight cell junctions and mitochondrial ultrastructure changes in cerebral vascular endothelium. Western blot analysis was performed to detect the expression of zonula occludens1( ZO-1), occludin, claudins-5, optic atrophy 1( OPA1), mitofusin 2(Mfn2), dynamin-related protein 1(Drp1), fission 1(Fis1), and hypoxia-inducible factor-1α(HIF-1α). Network pharmacology identified 76 intersecting targets for RES and SAE, with the top five core targets being EGFR, PTGS2, ESR1, HIF-1α, and APP. GO enrichment analysis showed that RES participated in the SAE mechanism through oxidative stress reaction. KEGG enrichment analysis indicated that RES participated in SAE therapy through HIF-1α, Rap1, and other signaling pathways. Molecular docking results showed favorable docking activity between RES and key targets such as HIF-1α. Animal experiment results demonstrated that compared to the sham group, the CLP group exhibited reduced nervous reflexes, decreased water content in brain tissue, as well as serum SOD and CAT activity, and increased MDA content. In addition, the CLP group exhibited disrupted tight junctions in cerebral vascular endothelium and abnormal mitochondrial morphology. The protein expression levels of Drp1, Fis1, and HIF-1α in brain tissue were increased, while those of ZO-1, occludin, claudin-5, Mfn2, and OPA1 were decreased. In contrast, the medium-dose and high-dose groups of RES showed improved neurological function, increased water content in brain tissue and SOD and CAT activity, and decreased MDA content. Cell morphology in brain tissue, tight junctions between endothelial cells, and mitochondrial structure were improved. The protein expressions of Drp1, Fis1, and HIF-1α were decreased, while those of ZO-1, occludin, claudin-5, Mfn2, and OPA1 were increased. This study suggested that RES could ameliorate cerebrovascular endothelial barrier function and maintain mitochondrial homeostasis by inhibiting oxidative stress after SAE damage, potentially through modulation of the HIF-1α signaling pathway.
Animals ; Mice ; Network Pharmacology ; Resveratrol/administration & dosage* ; Male ; Sepsis-Associated Encephalopathy/genetics* ; Signal Transduction/drug effects* ; Hypoxia-Inducible Factor 1, alpha Subunit/genetics* ; Endothelium, Vascular/metabolism* ; Molecular Docking Simulation ; Protein Interaction Maps/drug effects* ; Humans ; Sepsis/complications* ; Oxidative Stress/drug effects*