OBJECTIVE To explore the potential mechanism by which drug-containing serum of Dianxianqing granules （DXQ） inhibits microglial ferroptosis. METHODS Male SD rats were given normal saline and Dianxianqing granules solution via intragastric administration to prepare normal serum and DXQ， respectively. Mice microglia BV2 cells were collected and successfully transfected with a negative control small interfering RNA （si-NC）， and then they were included in the si-NC group and cultured under normal conditions. Cells successfully transfected with small interfering RNA targeting glutathione peroxidase 4 （GPX4） （si-GPX4） were divided into the si-GPX4 group， the CsA group （treated with 1 μmol/L cyclosporine A）， and the DXQ- L， DXQ-M and DXQ-H groups （treated with 5%， 7% and 10% DXQ， respectively）. These groups were subsequently treated with their corresponding drug solutions and ferroptosis inducer Erastin （10 μmol/L）. The intracellular levels of total iron ions， glutathione （GSH）， reactive oxygen species （ROS）， and the expression of mitochondrial superoxide were determined in each group after 48 h of treatment. Additionally， mitochondrial membrane potential， the opening degree of mitochondrial permeability transition pore （MPTP）， and mRNA expressions of GPX4 and cyclophilin D （CypD） were detected. Furthermore， the expressions of ferroptosis-related proteins[GPX4， transferrin receptor 1 （TfR1） and ferritin heavy chain 1 （FTH1）]， as well as MPTP-related proteins [adenine nucleotide translocator （ANT）， cytochrome C （CytC）， mitochondrial calcium uniporter （MCU） and CypD] were assessed. RESULTS Compared with si-NC group， the levels of total iron ions and ROS， the expression level of mitochondrial superoxide， the opening degree of MPTP， protein and its mRNA expressions of CypD as well as protein expressions of TfR1 and MCU were increased or up-regulated significantly （P＜0.01）； however， GSH content， mitochondrial membrane potential， protein and mRNA expressions of GPX4， and protein expressions of FTH1， ANT and CytC were decreased or down-regulated significantly （P＜0.01）. Compared with the si-GPX4 group， the cells in the DXQ-M， DXQ-H groups showed a general improvement in the above quantitative indicators （P＜0.01 or P＜0.05）. CONCLUSIONS DXQ can enhance antioxidant capacity by activating the GSH/GPX4 pathway， regulate the expressions of TfR1 and FTH1 protein to correct iron ion homeostasis， inhibit excessive opening of MPTP to improve mitochondrial function， and ultimately suppress microglial ferroptosis.

ObjectiveTo investigate the feasibility， safety， and efficacy of surgery-assisted transjugular intrahepatic portosystemic shunt （SA-TIPS） in the treatment of portal hypertension comorbid with complex portal vein thrombosis， including cavernous transformation of the portal vein （CTPV）. MethodsAn analysis was performed for the data of 36 patients with portal hypertension and complex portal vein thrombosis who underwent SA-TIPS in Beijing Shijitan Hospital， Capital Medical University， from November 2023 to January 2025， including general status， technical data of the surgical process （surgical success rate， puncture times， time of operation， the number of stents used， and the length of shunt）， perioperative complications， and surgical recovery. The change in portal pressure gradient （PPG） after shunt was compared， and the rate of reaching the standard for PPG reduction was calculated， as well as stent patency rate within 1 week after surgery. The paired samples t-test was used for comparison of continuous data between two groups. ResultsAmong the 36 patients， 34 （94.4%） underwent SA-TIPS successfully. The incidence rate of perioperative complications was 16.7% （6/36）， including 3 cases of thoraco-abdominal hemorrhage， 2 cases of intraoperative arrhythmia， and 1 case of incision infection. There was a significant reduction in PPG after SA-TIPS （t=19.85， P<0.01）， and the patients achieving a ≥50% reduction in PPG accounted for 76.5% （26/34）. Imaging reexamination within 1 week showed a shunt patency rate of 100%. ConclusionSA-TIPS has a high technical success rate， a favorable safety profile， and good efficacy in the treatment of portal hypertension comorbid with complex portal vein thrombosis （including CTPV）， and therefore， it holds promise for clinical application.

ObjectiveTo establish and evaluate a hyperuricemia （HUA） mouse model with the damp-turbidity internal accumulation syndrome. MethodsThirty-six C57BL/6J mice were randomly divided into control group， chemically induced model group （Model）， and model combined with high-fat and fatigue group （Model+HF）. Twenty-four uricase gene knockout （UOX^-/-） mice were randomly divided into UOX^-/- group and UOX^-/-+HF group， with 12 mice in each group. The Model group and the Model+HF group established the HUA model by intragastric administration of potassium oxyazinate combined with adenine. The Model+HF group and the UOX^-/-+HF group adopted a high-fat diet combined with weight-bearing exhaustive swimming to establish the HUA model with the damp-turbidity internal accumulation syndrome. On day 1， 7， 14， 21， and 28 after modeling， the damp-turbidity internal accumulation syndrome score of each group was evaluated. On day 1 and day 28， a weight-bearing swimming exhaustion test was performed， and the exhaustive swimming time was recorded. On day 28， liver and kidney indexes were calculated， and hematoxylin-eosin （HE） staining was used to observe histopathological changes in liver and kidney tissues. Serum levels of uric acid （UA）， xanthine dehydrogenase （XDH）， xanthine oxidase （XOD） and urea nitrogen （BUN） were detected through biochemical assays. ELISA was used to detect serum levels of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β）. Immunohistochemistry was used to detect the protein expression of organic anion transporter 1 （OAT1） and glucose transporter 9 （GLUT9） in renal tissues. Quantitative real-time PCR （qRT-PCR） was used to detect the mRNA expressions of adenosine triphosphate binding transporter G2 （ABCG2）， hypoxia-inducible factor-1α （HIF-1α）， urate anion transporter 1 （URAT1）， and GLUT9 in renal tissues. ResultsOn day 14 of modeling， the damp-turbidity internal accumulation syndrome scores of mice in the Model+HF group and the UOX^-/-+HF group were elevated compared with the control group（P＜0.05）； on day 28， the scores significantly increased， and the exhaustive swimming time was shortened （P＜0.01）， indicating successful establishment of the damp-turbidity internal accumulation syndrome model. Compared with the control group， all other groups exhibited increased kidney index， serum levels of UA， XDH， XOD， BUN， TNF-α， and IL-1β， elevated renal mRNA expression of HIF-1α， URAT1， OAT1， and GLUT9， and decreased renal ABCG2 mRNA expression （P＜0.01 or P＜0.05）. Significant pathological damage in the kidney was observed in the Model+HF group and the UOX^-/-+HF group compared to the Model group and the UOX^-/- group， with decreased serum UA and increased BUN and TNF-α levels （P＜0.05 or P＜0.01）， as well as increased expression of OAT1 and GLUT9 in the renal tissue. ConclusionBoth chemical induction and gene knockout， combined with a high-fat diet and weight-bearing exhaustive swimming， can successfully establish mouse models of HUA with damp-turbidity internal accumulation syndrome. Chemical induction is simple to operate and cost-effective， suitable for short-term drug screening， while UOX gene knockout induces spontaneous elevation of serum uric acid levels without drug administration， which may better mimick human metabolic characteristics.

ObjectiveTo establish and evaluate a hyperuricemia （HUA） mouse model with the damp-turbidity internal accumulation syndrome. MethodsThirty-six C57BL/6J mice were randomly divided into control group， chemically induced model group （Model）， and model combined with high-fat and fatigue group （Model+HF）. Twenty-four uricase gene knockout （UOX^-/-） mice were randomly divided into UOX^-/- group and UOX^-/-+HF group， with 12 mice in each group. The Model group and the Model+HF group established the HUA model by intragastric administration of potassium oxyazinate combined with adenine. The Model+HF group and the UOX^-/-+HF group adopted a high-fat diet combined with weight-bearing exhaustive swimming to establish the HUA model with the damp-turbidity internal accumulation syndrome. On day 1， 7， 14， 21， and 28 after modeling， the damp-turbidity internal accumulation syndrome score of each group was evaluated. On day 1 and day 28， a weight-bearing swimming exhaustion test was performed， and the exhaustive swimming time was recorded. On day 28， liver and kidney indexes were calculated， and hematoxylin-eosin （HE） staining was used to observe histopathological changes in liver and kidney tissues. Serum levels of uric acid （UA）， xanthine dehydrogenase （XDH）， xanthine oxidase （XOD） and urea nitrogen （BUN） were detected through biochemical assays. ELISA was used to detect serum levels of tumor necrosis factor-α （TNF-α） and interleukin-1β （IL-1β）. Immunohistochemistry was used to detect the protein expression of organic anion transporter 1 （OAT1） and glucose transporter 9 （GLUT9） in renal tissues. Quantitative real-time PCR （qRT-PCR） was used to detect the mRNA expressions of adenosine triphosphate binding transporter G2 （ABCG2）， hypoxia-inducible factor-1α （HIF-1α）， urate anion transporter 1 （URAT1）， and GLUT9 in renal tissues. ResultsOn day 14 of modeling， the damp-turbidity internal accumulation syndrome scores of mice in the Model+HF group and the UOX^-/-+HF group were elevated compared with the control group（P＜0.05）； on day 28， the scores significantly increased， and the exhaustive swimming time was shortened （P＜0.01）， indicating successful establishment of the damp-turbidity internal accumulation syndrome model. Compared with the control group， all other groups exhibited increased kidney index， serum levels of UA， XDH， XOD， BUN， TNF-α， and IL-1β， elevated renal mRNA expression of HIF-1α， URAT1， OAT1， and GLUT9， and decreased renal ABCG2 mRNA expression （P＜0.01 or P＜0.05）. Significant pathological damage in the kidney was observed in the Model+HF group and the UOX^-/-+HF group compared to the Model group and the UOX^-/- group， with decreased serum UA and increased BUN and TNF-α levels （P＜0.05 or P＜0.01）， as well as increased expression of OAT1 and GLUT9 in the renal tissue. ConclusionBoth chemical induction and gene knockout， combined with a high-fat diet and weight-bearing exhaustive swimming， can successfully establish mouse models of HUA with damp-turbidity internal accumulation syndrome. Chemical induction is simple to operate and cost-effective， suitable for short-term drug screening， while UOX gene knockout induces spontaneous elevation of serum uric acid levels without drug administration， which may better mimick human metabolic characteristics.

OBJECTIVE To investigate the mechanism of Yangfei tongluo formula in delaying airway remodeling in post-infectious bronchiolitis obliterans （PIBO） model rats.METHODS Forty-eight 2-week-old SPF male SD rats were randomly divided into control group （Control group）， PIBO model group （Model group）， Prednisone Acetate tablets+Azithromycin tablets group [positive control group， Prednisone Acetate tablets 0.006 3 g/（kg·d）+Azithromycin tablets 0.031 5 g/（kg·d）]， and high-， medium-， and low-dose Yangfei tongluo formula groups [42.42， 21.21， 10.60 g/（kg·d）]. The PIBO rat model was established by intratracheal instillation of diacetyl. After modeling， rats in each group were administered corresponding drug solution or distilled water by gavage once daily for 21 consecutive days. Hematoxylin-eosin staining was used to evaluate the pathological changes of lung tissue， and Masson staining was used to assess the degree of pulmonary fibrosis. Western blot and real-time quantitative PCR were performed to detect the protein and mRNA expression levels of epithelial-mesenchymal transition （EMT）-related markers [E-cadherin， N-cadherin， α -smooth muscle actin （ α -SMA）， Vimentin] and transcription factors [snail homolog 1（Drosophila）-like 1 protein （Snail1）， zinc finger E-box-binding homeobox protein 1 （ZEB1）， Twist-related protein 1 （Twist1）] in lung tissue. ELISA was used to detect the levels of transforming growth factor-β 1 （TGF-β 1 ） and vascular endothelial growth factor （VEGF） in blood and bronchoalveolar lavage fluid.RESULTS Compared with the Control group， the lung tissues of rats in the Model group showed extensive destruction of alveolar structure and massive inflammatory cell infiltration in the interstitium. The protein and mRNA expression levels of E-cadherin were significantly decreased， while the protein and mRNA expression levels of N-cadherin， Vimentin， α -SMA， Snail1， ZEB1， and Twist1， as well as the collagen-positive area and the levels of TGF-β 1 and VEGF， were significantly increased （ P ＜0.05）. Compared with the Model group， the pathological injury of lung tissue in each administration group was significantly improved， and the above indicators （except collagen-positive area） were significantly reversed （ P ＜0.05）.CONCLUSIONS Yangfei tongluo formula may delay airway remodeling in PIBO by regulating the TGF-β 1 /VEGF-mediated signaling network and inhibiting the activation of EMT-related transcription factors， thereby blocking the EMT process.

OBJECTIVE To provide guidance for pharmaceutical care in patients with severe Cryptococcus gattii infections.METHODS Clinical pharmacists participated in the diagnosis and treatment of a male patient with disseminated Cryptococcus gattii infection （involving the lungs and central nervous system）. Given the patient’s poor response to initial therapy， the clinical pharmacists， based on antimicrobial susceptibility test results， recommended voriconazole as an alternative azole. In response to refractory hypokalemia caused by liposomal amphotericin B， the clinical pharmacists assisted the physician in developing an intensive potassium replacement regimen. Regarding the interaction between voriconazole and nifedipine， the clinical pharmacists proactively identified the risk and intensified monitoring of the patient’s blood pressure. In response to the onset of hepatitis C during treatment， the clinical pharmacists thoroughly weighed the priority of infection treatment and recommended temporarily postponing antiviral therapy for hepatitis C. For the individualized use of voriconazole， the clinical pharmacists repeatedly performed therapeutic drug monitoring （TDM）. Regarding the patient’s poor lesion resolution， the clinical pharmacists participated in multidisciplinary team discussions to clarify the indications for surgery.RESULTS The physician adopted the clinical pharmacists’ recommendations. Following pharmacological treatment and surgical intervention， the patient’s condition stabilized， and he was discharged while still on medication.CONCLUSIONS For severe Cryptococcus gattii infections， clinical pharmacists should focus on pathogen characteristics， strengthen adverse reaction management， pay close attention to drug interactions， conduct TDM， and actively participate in multidisciplinary team collaboration to ensure the safety and efficacy of patient treatment.

This study aims to explore the mechanism of Huanglian Jiedu Decoction(HJD) in treating acute liver injury(ALI) in the mouse model of sepsis induced by lipopolysaccharide(LPS). Fifty-four male C57BL/6 mice were randomized into six groups: blank group, model group, low-, medium-, and high-dose group HJD, and dexamethasone group. The mouse model of sepsis was established by intraperitoneal injection of LPS after 7 days of gavage with HJD, and dexamethasone(0.2 mL) was injected intraperitoneally 1.5 h after modeling. The murine sepsis score(MSS) was recorded 12 h after modeling. The levels of alanine aminotransferase(ALT) and aspartate aminotransferase(AST) in the liver tissue and tumor necrosis factor-α(TNF-α) and interleukin-6(IL-6) in the serum were measured by ELISA. Hematoxylin-eosin(HE) staining was used to observe the pathological changes of the mouse liver. The content of light chain 3 of microtubule-associated protein 1(LC3) was detected by immunofluorescence, and that of sirtuin 1(SIRT1) was detected by immunohistochemistry. The mRNA levels of adenosine 5'-monophosphate-activated protein kinase(AMPK), LC3, and P62 were detected by RT-PCR. Western blot was employed to determine the protein levels of AMPK, p-AMPK, and SIRT1 in the liver tissue. The results showed that compared with model group, drug interventions decreased the MSS and liver injury indicators, lowered the levels of inflammatory cytokines, improved the liver tissue structure, upregulated the protein levels of of p-AMPK/AMPK and SIRT1 and the mRNA levels of AMPK and LC3, and downregulated the mRNA level of P62. To sum up, HJD can regulate the autophagy level and reduce inflammation to ameliorate acute liver injury in septic mice by activating the AMPK/SIRT1 autophagy pathway.
Animals ; Drugs, Chinese Herbal/administration & dosage* ; Sirtuin 1/genetics* ; Male ; Mice ; Sepsis/metabolism* ; Mice, Inbred C57BL ; Autophagy/drug effects* ; AMP-Activated Protein Kinases/genetics* ; Liver/metabolism* ; Humans ; Signal Transduction/drug effects* ; Disease Models, Animal ; Tumor Necrosis Factor-alpha/genetics*

Medical institutions, with their clinical practice foundation and abundant human use experience data, have become important carriers for the inheritance and innovation of traditional Chinese medicine(TCM) and the "cradles" of the preparation of new TCM. To effectively promote the transformation of new TCM originating from the TCM clinical practice in medical institutions and establish an effective evaluation index system for the transformation of new TCM conforming to the characteristics of TCM, consensus experts adopted the literature research, questionnaire survey, Delphi method, etc. By focusing on the policy and technical evaluation of new TCM originating from the TCM clinical practice in medical institutions, a comprehensive evaluation from the dimensions of drug safety, efficacy, feasibility, and characteristic advantages was conducted, thus forming a comprehensive evaluation system with four primary indicators and 37 secondary indicators. The expert consensus reached aims to encourage medical institutions at all levels to continuously improve the high-quality research and development and transformation of new TCM originating from the TCM clinical practice in medical institutions and targeted at clinical needs, so as to provide a decision-making basis for the preparation, selection, cultivation, and transformation of new TCM for medical institutions, improve the development efficiency of new TCM, and precisely respond to the public medication needs.
Medicine, Chinese Traditional/standards* ; Humans ; Consensus ; Drugs, Chinese Herbal/therapeutic use* ; Surveys and Questionnaires

OBJECTIVE: To elucidate the effect of Huanglian-Renshen-Decoction (HRD) on ameliorating type 2 diabetes mellitus by maintaining islet β -cell identity through regulating paracrine and endocrine glucagon-like peptide-1 (GLP-1)/GLP-1 receptor (GLP-1R) in both islet and intestine. METHODS: The db/db mice were divided into the model (distilled water), low-dose HRD (LHRD, 3 g/kg), high-dose HRD (HHRD, 6 g/kg), and liraglutide (400 µ g/kg) groups using a random number table, 8 mice in each group. The db/m mice were used as the control group (n=8, distilled water). The entire treatment of mice lasted for 6 weeks. Blood insulin, glucose, and GLP-1 levels were quantified using enzyme-linked immunosorbent assay kits. The proliferation and apoptosis factors of islet cells were determined by immunohistochemistry (IHC) and immunofluorescence (IF) staining. Then, GLP-1, GLP-1R, prohormone convertase 1/3 (PC1/3), PC2, v-maf musculoaponeurotic fibrosarcoma oncogene homologue A (MafA), and pancreatic and duodenal homeobox 1 (PDX1) were detected by Western blot, IHC, IF, and real-time quantitative polymerase chain reaction, respectively. RESULTS: HRD reduced the weight and blood glucose of the db/db mice, and improved insulin sensitivity at the same time (P<0.05 or P<0.01). HRD also promoted mice to secrete more insulin and less glucagon (P<0.05 or P<0.01). Moreover, it also increased the number of islet β cell and decreased islet α cell mass (P<0.01). After HRD treatment, the levels of GLP-1, GLP-1R, PC1/3, PC2, MafA, and PDX1 in the pancreas and intestine significantly increased (P<0.05 or P<0.01). CONCLUSION HRD can maintain the normal function and identity of islet β cell, and the underlying mechanism is related to promoting the paracrine and endocrine activation of GLP-1 in pancreas and intestine.
Animals ; Glucagon-Like Peptide 1/metabolism* ; Diabetes Mellitus, Type 2/metabolism* ; Glucagon-Like Peptide-1 Receptor/metabolism* ; Insulin-Secreting Cells/pathology* ; Drugs, Chinese Herbal/pharmacology* ; Male ; Blood Glucose/metabolism* ; Insulin/blood* ; Mice ; Intestinal Mucosa/pathology* ; Apoptosis/drug effects* ; Cell Proliferation/drug effects* ; Islets of Langerhans/pathology*

Objective To analyze the effect of graded exercise rehabilitation in patients with acute exacerbation of chronic obstructive pulmonary disease,and to provide references for clinical nursing practice.Methods A total of 70 patients with acute exacerbation of chronic obstructive pulmonary disease who met the criteria in the Department of Respiratory Medicine of a tertiary hospital in Zunyi City from September to December 2023 were randomly divided into an experimental group and a control group(with 35 cases in each group).The experimental group implemented graded exercise rehabilitation based on the Global Chronic Obstructive Pulmonary Initiative guidelines,and the control group implemented routine exercise rehabilitation.After intervention,the lung function,blood gas analysis,oxygenation index,6 min walking test and the incidence of complications related to non-invasive mechanical ventilation were compared between the 2 groups.Results Finally,34 cases were included in the experimental group and 35 cases in the control group.After intervention,the forced expiratory volume in the first second of the experimental group was improved compared with the control group(P＜0.05).The 6-minute walking test of the experimental group was higher than that of the control group(P＜0.05).The total incidence of non-invasive mechanical ventilation-related complications in the experimental group was lower than that in the control group(P＜0.05).There was no significant difference in blood gas analysis and oxygenation index between the 2 groups(P＜0.05).Conclusion The implementation of graded exercise rehabilitation based on the Global Chronic Obstructive Pulmonary Initiative guidelines can help patients with acute exacerbation of chronic obstructive pulmonary disease improve their respiratory function,improve their exercise endurance,and reduce non-invasive mechanical ventilation-related complications.