Spine fracture and dislocation are common traumatic spinal conditions that often require surgical intervention due to compromised spinal stability. Surgical approaches include anterior, posterior, and combined anterior-posterior spinal procedures. According to the specific surgical requirements, patients may be placed in the prone position or repositioned between prone and supine positions during surgery. Intraoperative repositioning has become an essential step in patient positioning. However, during repositioning, patients with spinal fracture and dislocation are at increased risk for complications such as hemodynamic instability, nerve injury, and pressure injuries to the skin and soft tissue. Notably, due to the instability of the spinal cord, even minor manipulations can further exacerbate the damage, potentially leading to severe outcomes like paraplegia. Although the current clinical guidelines provide instructive recommendations for standard position, there remains no specific protocols for intraoperative repositioning in patients with spine fracture and dislocation. With a concern for the lack of clinical studies on positioning techniques, risk prevention, and operational norms for special patients, no applicable guidelines or standards are available. A consensus was required to provide clinical reference, meet the requirements of surgical treatment, and minimize the safety risks of patients caused by improper placement of positions. Professional Committee of Operating Room Nursing of Shaanxi Nursing Association organized experts in nursing management and operating room nursing from major hospitals across China to formulate Expert consensus on intraoperative repositioning for patients with spinal fracture and dislocation ( version 2025). The consensus provides 11 recommendations covering pre-repositioning preparation, intraoperative maneuvers, and post-repositioning observation, aiming to provide references for clinical standardization of the intraoperative repositioning process and protection of patients′ safety.

Spine fracture and dislocation are common traumatic spinal conditions that often require surgical intervention due to compromised spinal stability. Surgical approaches include anterior, posterior, and combined anterior-posterior spinal procedures. According to the specific surgical requirements, patients may be placed in the prone position or repositioned between prone and supine positions during surgery. Intraoperative repositioning has become an essential step in patient positioning. However, during repositioning, patients with spinal fracture and dislocation are at increased risk for complications such as hemodynamic instability, nerve injury, and pressure injuries to the skin and soft tissue. Notably, due to the instability of the spinal cord, even minor manipulations can further exacerbate the damage, potentially leading to severe outcomes like paraplegia. Although the current clinical guidelines provide instructive recommendations for standard position, there remains no specific protocols for intraoperative repositioning in patients with spine fracture and dislocation. With a concern for the lack of clinical studies on positioning techniques, risk prevention, and operational norms for special patients, no applicable guidelines or standards are available. A consensus was required to provide clinical reference, meet the requirements of surgical treatment, and minimize the safety risks of patients caused by improper placement of positions. Professional Committee of Operating Room Nursing of Shaanxi Nursing Association organized experts in nursing management and operating room nursing from major hospitals across China to formulate Expert consensus on intraoperative repositioning for patients with spinal fracture and dislocation ( version 2025). The consensus provides 11 recommendations covering pre-repositioning preparation, intraoperative maneuvers, and post-repositioning observation, aiming to provide references for clinical standardization of the intraoperative repositioning process and protection of patients′ safety.

ObjectiveTo induce the rat model of ulcerative colitis （UC） with spleen-kidney Yang deficiency and liver depression， and explore the efficacy and mechanism of Sishenwan combined with Tongxie Yaofang （SSW&TXYF） based on the therapeutic principles of tonifying spleen， soothing liver， warming kidney， and astringing intestine. MethodSixty male SD rats were randomized into normal， model， mesalazine， and high-， medium-， and low-dose SSW&TXYF groups. The rats in other groups except the normal group were administrated with Sennae Folium decoction and hydrocortisone and received tail clamping for 14 days. On day 14， rats received enema with TNBS-ethanol solution to induce UC. The rats were administrated with corresponding drugs from day 15 of modeling， and the body weight and mental state were observed and recorded. The sucrose preference test was performed from day 25. On day 28， the rectal temperature was measured， and the rats were administrated with 3% D-xylose solution at a dose of 10 mL·kg^-1 by gavage. Blood was sampled 1 h later， from which the serum was collected for measurement of the D-xylose content. The serum， hippocampus， and colorectum samples of rats were collected on day 29. The levels of gastrin （GAS）， adrenocorticotropic hormone （ACTH）， corticosterone （CORT）， cyclic adenosine monophosphate （cAMP）， cyclic guanosine monophosphate （cGMP）， interleukin （IL）-4， tumor necrosis factor （TNF）-α， and interferon （IFN）-γ in the serum and 5-hydroxytryptamine （5-HT） in the hippocampus were determined by enzyme-linked immunosorbent assay. Hematoxylin-eosin staining was employed to reveal the colonic lesions. The mRNA and protein levels of p38 mitogen-activated protein kinase （MAPK）， extracellular signal-regulated kinase （ERK）， and c-Jun N-terminal kinase （JNK） in the colon tissue were determined by Real-time PCR and Western blot， respectively. ResultCompared with the normal group， the model group showed decreased body weight， anal temperature， and D-xylose content in the serum and increased GAS content （P<0.01）. The modeling led to cAMP/cGMP unbalance and decreased the ACTH and CORT content in the serum （P<0.01）， the preference for sucrose water， and the 5-HT content in the hippocampus （P<0.01）. Moreover， it shortened the colorectal length and caused massive infiltration of inflammatory cells and severe structural damage in the colon tissue. High， medium， and low doses of SSW&TXYF improved above indicators （P<0.05， P<0.01）， reduced inflammatory infiltration， and repaired the pathological damage of the tissue. Compared with the normal group， the model group showed lowered IL-4 level （P<0.01） and elevated TNF-α and IFN-γ levels （P<0.05， P<0.01） in the serum， as well as up-regulated expression of p38 MAPK， ERK， and JNK （P<0.05， P<0.01）. Compared with the model group， SSW&TXYF elevated the IL-4 level （P<0.01）， lowered the TNF-α and IFN-γ levels （P<0.05， P<0.01）， and down-regulated the mRNA and protein levels of p38 MAPK， ERK， and JNK （P<0.05， P<0.01）. ConclusionA rat model of UC with spleen-kidney Yang deficiency and liver depression was successfully established. SSW&TXYF can significantly mitigate this syndrome by reducing the inflammatory response in the colon and inhibiting the MAPK pathway.

Objective To optimize the method of combining azomethane oxide(AOM)and dextran sodium sulfate(DSS)to create a colitis-associated colon cancer(CAC)model,and to explore the pathogenesis of the intestinal flora in CAC.Methods Model groups A and B were established by one and two injections of AOM,respectively,combined with free drinking of DSS,and a normal control group was injected intraperitoneally with normal saline combined with purified water(n=10 mice per group).The better modeling scheme was selected by comprehensive evaluation of the disease activity index score,colon length,tumor rate,and mortality.Serum levels of interleukin-6(IL-6),tumor necrosis factor-α(TNF-α),and tumor markers CA199,CEA,and CA724 were detected by enzyme-linked immunosorbent assay.Colon lesions were evaluated by hematoxylin and eosin(HE)staining.Changes in the intestinal microbiota in CAC mice were detected by 16S rDNA high-throughput gene sequencing analysis of mouse feces.Results Both single and enhanced AOM injections combined with DSS induced CAC mice;however,colon growths were larger,more closely arranged,and their morphological size was more consistent in group B compared with group A,with a tumor-formation rate of 100％.IL-6 levels were increased in the model group compared with the normal group(P＜0.05).TNF-α levels were increased in the model group compared with the normal group(P＞0.05).The CA199 and CEA levels were also significantly increased(P＜0.05),but CA724 levels were not.Infiltration of inflammatory cells in the colon detected by HE pathology was accompanied by high-grade intraepithelial tumor-like changes on the surface of the lumen.The diversity and abundance of intestinal bacteria were decreased in CAC mice compared with normal mice:phyla Verrucomicrobiota and Actinobacteriota were significantly increased(P＜0.05),Bacteroidota and Campilobacterota were significantly decreased(P＜0.05).Akkermansia,Prevotellaceae,Ruminococcus,and Bifidobacterium were significantly increased(P＜0.05),and Roseburia,Rikenellaceae_RC9_gut_group,Anaeroplasma,and Muribaculaceae were significantly decreased(P＜0.05).Conclusions Two injections of AOM combined with 1.5％(1.5 g/100 mL)DSS induced CAC model mice with a high colon-tumorigenesis rate,uniform tumor morphology,and low mortality,and may thus be the preferred modeling scheme for pharmacodynamic experiments.Disorders or dysfunction of the intestinal flora may lead to increased permeability,loss of intestinal mucosal barrier function,and the release of enterogenic endotoxins,Resultsing in a sustained inflammatory response,as an indirect or direct cause of CAC pathogenesis.

ObjectiveTo construct a mouse model of inflammation-associated colorectal cancer （CAC） by using azoxymethane （AOM）/dextran sulfate sodium （DSS） and investigate the effect of Huangqintang on the gut microbiota structure of mice during the occurrence and development of CAC by 16S rRNA gene high-throughput sequencing. MethodA total of 225 C57BL/6J mice were randomized into 5 groups （n=45）： Normal， model， positive drug （mesalazine）， and high （18 g·kg^-1） and low （9 g·kg^-1）-dose Huangqintang. Except those in the normal group， each mouse was injected with 10 mg·kg^-1 AOM on day 1 and day 5 within 1 week and then given 1.5% DSS solution for 7 days， which was then changed to sterile water for 14 days. This process referred to as one cycle， and mice were treated for a total of 3 cycles. On the first day of DSS treatment， mice were administrated with corresponding drugs by gavage， and the normal group and the model group were administrated with pure water by gavage， once a day until the end of the third cycle. The progression of CAC was divided into inflammation， proliferation， and tumorigenesis stages. At the end of each cycle， the body weight and colon length were measured for mice in each group， and the number of colon tumors in mice was recorded. Meanwhile， the disease activity index （DAI） was determined. The serum levels of interleukin-6 （IL-6）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and carbohydrate antigen-199 （CA199）， a tumor marker in the gastrointestinal tract of mice， were measured by ELISA. Hematoxylin-eosin staining was employed to observe colon lesions. At the same time， 3-5 pellets of fresh feces of mice in the normal group， model group， and high-dose Huangqintang group were collected， from which the fecal DNA of mice was extracted for 16S rRNA gene high-throughput sequencing. ResultCompared with the normal group， the model group showed decreased body weight （P<0.01）， increased DAI， and shortened colon length （P<0.05） at the three stages. Compared with the normal group， the model group showed elevated levels of IL-1β， IL-6， and TNF-α （P<0.05） at the proliferation stage and elevated levels of CA199 at the inflammation， proliferation， and tumorigenesis （P<0.01） stages. Compared with the normal group， the model group presented obvious infiltration of inflammatory cells at the inflammation stage， thickening of the muscle layer and abnormal proliferation of mucosal layer cells at the proliferation and tumorigenesis stages， and final formation of advanced intraepithelial tumor lesions. Compared with the model group， the Huangqintang groups showed no significant improvement in the body weight， decreased DAI score， and increased colon length at the three stages， and the increase of colon length in the tumorigenesis stage was significant （P<0.01）. At the tumorigenesis stage， the administration of Huangqintang inhibited tumor formation and growth， reduced the number of tumors （P<0.01）， lowered the levels of IL-6 （P<0.05， P<0.01）， TNF-α （P<0.05， P<0.01）， and IL-1β at the three stages， and decreased CA199 at the inflammation stage as well as at the proliferation and tumorigenesis stages （P<0.01， P<0.05）. Compared with the model group， the administration of Huangqintang reduced inflammation and abnormal cell proliferation， delaying the occurrence of tumors. Compared with the normal group， the model group showcased decreased alpha and beta diversity and altered structure of gut microbiota at the inflammation， proliferation， and tumorigenesis stages. The administration of Huangqintang adjusted the abundance and diversity of gut microbiota to the normal levels. At the inflammation stage， Huangqintang positively regulated two differential phyla （Firmicutes and Bacteroidetes） and three differential genera （Muribaculaceae， Rikenellaceae_RC9_gut_group， and Flavonifractor） in mice. At the proliferation stage， Huangqintang positively regulated two differential phyla （Bacteroidetes and Patescibacteria） and five differential genera （Muribaculaceae， Rikenellaceae_RC9_gut_group， Candidatus_Saccharimonas， norank_f__UCG-010， and Allobaculum）. At the tumorigenesis stage， Huangqintang positively regulated two differential phyla （Proteobacteria and Patescibacteria） and eight differential genera （Muribaculaceae， Candidatus_Saccharimonas， norank_f_UCG-010， Lachnospiraceae_UCG-006， Allobaculum， Bacteroides， Lachnospiraceae_NK4A136_group， and Flavonifractor） in mice. ConclusionHuangqintang can intervene in the AOM/DSS-induced transformation of inflammation to CAC in mice by correcting inflammation and short-chain fatty acid-related microbiota disorders.

Background: Ulcerative colitis (UC) is a diffuse nonspecific intestinal inflammation. Spleen-kidney Yang deficiency combined with liver stagnation is the most common symptom. Sishen Pills-Tongxie Yaofang (SSP-TXYF) is a traditional Chinese medicine (TCM) that is widely used in the treatment of this symptom. However, its pharmacological mechanism and active components remain unclear. Objective: This study elucidated the potential mechanism and active components of SSP-TXYF in the treatment of UC from the perspective of TCM syndrome. Methods: Metascape, STRING, and Cytoscape were used to explore the SSP-TXYF-compound-target-UC network and biological enrichment pathways, so as to screen the active compounds, key targets, and pathways of SSP-TXYF. Through the construction of a rat model with UC, the key targets and active components were verified after SSP-TXYF administration. Results: A total of 77 effective active chemical components, 208 potential targets, and 5 core target genes were screened out. Gene Ontology biological process items and Kyoto Encyclopedia of Genes and Genomes signaling pathways showed that SSP-TXYF played a role in regulating nerve-endocrine, cell proliferation and apoptosis, and immune-related pathways. The main compounds and the target protein exhibited a good binding ability in molecular docking. The results of animal experiments showed that SSP-TXYF could improve UC through IL-6, AKT1, PTGS2, CASP3, and JUN, and nobiletin and wogonin were identified as the main active components. Conclusions: This study suggests that nobiletin and wogonin are the main components of SSP-TXYF in the treatment of UC, which provides effective therapeutic targets and drugs for future clinical treatment of UC.

At present， major depressive disorder （MDD） is highly prevalent with advanced neurological disorders as the main pathological manifestations. As the physiological function bearer of higher neural activity， gray matter has become the focus of MDD treatment. However， recent research has shown that white matter and gray matter are independent of each other in the central nervous system （CNS）， and their functions are integrated and linked. In addition to gray matter damage， white matter damage is also the core driving event of disease progression and determines the outcome of MDD. At the treatment level， the current drug treatment of MDD mainly focuses on gray matter repair， while ignoring the importance of white matter integrity for the treatment of the disease， which has become the weakness of the current treatment of MDD. Traditional Chinese medicine （TCM） has good application potential in white matter repair. This paper elaborated on the following three aspects. ① The roles of white matter damage in the occurrence and development of MDD were summarized. ② The key link of white matter repair in MDD was elaborated with microglia microenvironment regulation as the entry point. ③ The application value of TCM in white matter repair in MDD was analyzed. This review aims to highlight the importance of white matter integrity in the treatment of MDD and is expected to expand the understanding dimension of the activity of related Chinese medicines in MDD from the perspective of white matter repair and analyze its potential application value.

Ulcerative colitis （UC） is a chronic intestinal disease with unknown etiology， with main symptoms of abdominal pain， diarrhea， mucus， pus， and blood in the stool. It can be accompanied by various complications and has a high risk of developing to colon cancer. In recent years， the incidence of UC and related colon cancer has been increasing， which seriously affects human health and quality of life. The operation， immunosuppressant， etc. are the main approaches in the modern clinical treatment of UC and related colon cancer， but these methods all have different toxic and side effects， and the therapeutic effect is not ideal. For many years， traditional Chinese medicine （TCM） has attracted much attention in the treatment of UC and related colon cancer due to its slightly toxic side effects and remarkable curative efficacy. Huangqintang， derived from the Shang Han Lun （伤寒论）， is composed of Scutellariae Radix， Paeoniae Radix Alba， Glycyrrhizae Radix et Rhizoma， and Jujubae Fructus with the functions of clearing heat， checking diarrhea， harmonizing the middle， and relieving pain， and has a significant effect on the treatment of UC. Huangqintang has complex compositions and plays roles with multiple targets and pathways. According to the literature and the research results of this research group for many years， it was found that the mechanism of Huangqintang in the treatment of UC and related colon cancer was presumably related to the protection of the intestinal mucosal barrier， inhibition of inflammatory response， promotion of mitophagy， inhibition of oxidative stress， regulation of intestinal flora， cell cycle， and gene expression， suppression of cell proliferation， and promotion of apoptosis. To provide theoretical references for an in-depth study of the mechanism and clinical use of Huangqintang， this paper reviewed the research advances in recent years.

ObjectiveTo evaluate the pharmacodynamic effect of Huangqintang （HQT） on ulcerative colitis （UC） model mice and investigate its protective effect against UC by regulating intestinal flora. MethodMale Balb/c mice were randomly divided into control group，model group， high-， medium-， and low-dose HQT groups （20， 10， 5 g·kg^-1）， flora interference group， flora interference model group， and flora interference-drug treatment group （HQT， 20 g·kg^-1）. The flora interference model was constructed through intragastric administration of antibiotics （200 mg·kg^-1 bacitracin and 200 mg·kg^-1 vancomycin） for 8 d， and the UC model was constructed by allowing mice with free access to 3% dextran sulfate sodium （DSS） solution for 7 d. HQT was administered for 7 d. After the experiments， the mice were sacrificed， and blood， colon， and feces were collected. Hematoxylin-eosin （HE） staining was performed to observe the colonic lesions. The serum levels of interleukin （IL）-4， IL-6， IL-10， and tumor necrosis factor （TNF）-α were detected by enzyme-linked immunosorbent assay （ELISA）. The mRNA and protein expression of Claudin1， MUC1， Occludin， and zonula occludens-1（ZO-1） in colon tissues was detected by Real-time fluorescence quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively. The fecal DNA of mice was extracted and analyzed by high-throughput sequencing. ResultCompared with the normal group， the model group showed increased serum content of IL-4， IL-6， and TNF-α （P<0.05， P<0.01） and decreased IL-10 （P<0.05）. Compared with the model group， the HQT groups displayed decreased serum levels of IL-4， IL-6， and TNF-α （P<0.05， P<0.01）， increased IL-10 content （P<0.01）， increased mRNA and protein expression levels of Claudin1， MUC1， Occludin， and ZO-1 （P<0.05， P<0.01）. After flora interference， the diversity and abundance of intestinal bacteria decreased. To be specific， Proteobacteria increased （P<0.01）， and Firmicutes and Bacteroidetes decreased （P<0.01）. After UC induction by DSS， Bacteroidetes and Tenericutes decreased （P<0.05）. The high-， medium-， and low-dose HQT groups showed increased Bacteroidetes and Tenericutes （P<0.05， P<0.01） and decreased Firmicutes （P<0.05）. Additionally， the abundance of Lactobacillus， Lachnospiraceae NK4A136 group， Escherichia-Shigella， and Helicobacteris was positively proportional to the dose of HQT. ConclusionHQT can inhibit the inflammatory response of UC mice， restore the imbalance of intestinal flora， and repair the damaged intestinal mucosal barrier.

ObjectiveTo explore the anti-inflammatory mechanism of Huangqintang based on the inflammation model in RAW264.7 cells. MethodHuangqintang was prepared and the safe dose to RAW264.7 cells was screened out. The RAW264.7 cells were seeded in 24-well plates and incubated with Huangqintang and lipopolysaccharide （LPS）， successively. The concentrations of nitric oxide （NO）， interleukin （IL）-6， tumor necrosis factor （TNF）-α， and prostaglandin E₂ （PGE₂） were measured by Griess assay and enzyme-linked immunosorbent assay （ELISA）， respectively. Meanwhile， RAW264.7 cells were inoculated in 6-well plates， and normal group， LPS group， LPS+Huangqintang group， nuclear factor-κB （NF-κB） p65 inhibitor PDTC group， p38 mitogen-activated protein kinase （MAPK） inhibitor SB203580 group， extracellular signal-regulated kinase （ERK） inhibitor PD98059 group， c-Jun N-terminal kinase （JNK） inhibitor SP600125 group， and Janus kinase （JAK） inhibitor AG490 group were set up. After the cells were incubated with corresponding inhibitors and Huangqintang and stimulated by LPS， RNA and protein were extracted. The mRNA and protein expression levels of NF-κB p65， p38 MAPK， ERK， JNK， and JAK were detected by Real-time fluorescence-based quantitative polymerase chain reaction （Real-time PCR） and Western blot， respectively， to explore the anti-inflammatory mechanism of Huangqintang by regulating the NF-κB， MAPK， and JAK/signal transducer and activator of transcription protein （STAT） signaling pathways. ResultAfter stimulation with LPS， the concentrations of NO， IL-6， TNF-α， and PGE₂ in the cells of the model group increased significantly（P<0.05，P<0.01）. Compare with the model group， after incubation with Huangqintang， the secretion of NO， IL-6， TNF-α， and PGE₂ showed a downward trend （P<0.05，P<0.01）. Compared with the normal group， the model group showed increased mRNA expression of p38 MAPK， ERK， JNK， JAK， and NF-κB p65 and total protein expression in cells after stimulation with LPS （P<0.05，P<0.01）. Compare with the model group，after incubation with Huangqintang， the total protein and mRNA expression of p38 MAPK， ERK， JNK， JAK， and NF-κB p65 in inflammatory cells decreased （P<0.05，P<0.01）. Meanwhile， the expression of NF-κB p65 total protein and mRNA in each inhibitor group showed a downward trend （P<0.05，P<0.01）. ConclusionHuangqintang can inhibit the inflammatory response through the NF-κB， MAPK， and JAK-STAT signaling pathways.