BACKGROUND:Bone tissue loss caused by tumors and trauma can have an adverse effect on postoperative rehabilitation.Therefore,scaffold materials are usually implanted during treatment.However,the existing implant materials are relatively simple and lack antibacterial properties.Early implantation may lead to iatrogenic autoinfection and have an adverse effect on osteogenesis.OBJECTIVE:To construct a KR-12-a5 polypeptide-nanohydroxyapatite-small intestinal submucosa composite scaffold and evaluate its feasibility as a material for promoting bone defect repair.METHODS:The small intestinal submucosa scaffold and the small intestinal submucosa scaffold containing 25,50,and 100 mg/mL nanohydroxyapatite(referred to as nHA-SIS scaffold)were prepared by 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide hydrochloride/N-hydroxysuccinimide cross-linking method.The appropriate scaffold was screened for subsequent experiments by mechanical property testing.The antibacterial properties of KR-12-a5 polypeptide solution against Staphylococcus aureus,Streptococcus gordonii,and Fusobacterium nucleatum were detected.The nHA-SIS scaffolds were immersed in 250,500,and 1 000 μg/mL KR-12-a5 peptide solutions for 24 hours,and then freeze-dried to obtain peptide-loaded nanohydroxyapatite-porcine small intestinal submucosa composite scaffolds(denoted as P-nHA-SIS scaffolds).The sustained-release properties of the three groups of scaffolds were characterized.The nHA-SIS scaffolds and the three groups of P-nHA-SIS scaffolds were co-cultured with Staphylococcus aureus,Streptococcus gordonii,and Fusobacterium nucleatum for 24 hours or 48 hours.The scaffolds with strong antibacterial ability were screened by live and dead bacteria staining and scanning electron microscopy for subsequent experiments.The degradation properties and water absorption rates of the uncross-linked small intestinal submucosa scaffolds,cross-linked small intestinal submucosa scaffolds,nHA-SIS scaffolds,and P-nHA-SIS scaffolds were characterized.The extracts of cross-linked small intestinal submucosal scaffolds,nHA-SIS scaffolds,and P-nHA-SIS scaffolds were co-cultured with MC3T3-E1 cells.CCK-8 assay and live-dead cell staining were performed.The effects of the extracts of the three scaffolds on the migration of MC3T3-E1 cells were detected by Transwell chamber assay.RESULTS AND CONCLUSION:(1)The elastic modulus and compressive strength of 25,50,and 100 mg/mL nHA-SIS scaffolds were higher than those of small intestinal submucosal scaffolds(P＜0.05),among which the elastic modulus and compressive strength of 25 mg/mL nHA-SIS scaffolds were the highest,and this group of scaffolds were selected for subsequent experiments to load peptides.(2)KR-12-a5 peptide had strong antibacterial activity against common bacteria in bone defects(Staphylococcus aureus,Streptococcus gordonii,and Fusobacterium nucleatum).The three groups of P-nHA-SIS scaffolds all had sustained release properties.With the increase of peptide mass concentration,the antibacterial property of P-nHA-SIS scaffold was enhanced.Among them,the P-nHA-SIS scaffold loaded with 500 μg/mL peptide had achieved a satisfactory antibacterial effect,and this group of scaffolds would be selected in the future.(3)The degradation rate of the three groups of cross-linked scaffolds was lower than that of the uncross-linked scaffolds,and the water absorption rate was greater than that of the uncross-linked scaffolds.P-nHA-SIS scaffolds could promote the proliferation and migration of MC3T3-E1 cells without affecting the activity of MC3T3-E1 cells.(4)The results show that P-nHA-SIS scaffolds have strong antibacterial properties and the ability to promote the proliferation and migration of MC3T3-E1 cells,and are expected to be used in bone defect repair.

BACKGROUND:During diabetic wound healing,the sustained activation of M1 macrophages exacerbates the inflammatory response and hinders wound repair.Auranofin,an anti-inflammatory drug,has not been clearly studied for its effects on M1 macrophages and its potential role in diabetic wound healing.OBJECTIVE:To investigate the effects of different concentrations of auranofin on the biological function of M1 macrophages and evaluate its potential application in diabetic wound healing.METHODS:RAW264.7 and THP-1 cells were used as research models.M1 polarization was induced using different concentrations of interferon-γ and lipopolysaccharide.M1 macrophages were treated with 1 and 2 μmol/L auranofin.Cell counting kit-8 assay was used to evaluate the effect of auranofin on cell viability.Quantitative real-time PCR was performed to detect mRNA expression of interleukin-1β,interleukin-6,and tumor necrosis factor-α.ELISA was employed to measure the levels of interleukin-1β,interleukin-6,and tumor necrosis factor-α in the supernatant.Western blot analysis was used to assess the expression of nuclear factor-κB(p65),phosphorylated mitogen-activated protein kinases(MAPK),and total MAPK proteins.Additionally,6-8-week-old male C57BL/6J and db/db diabetic mice were used for wound healing experiments,with the mice divided into C57 control,db/db control and auranofin treatment groups,each containing six animals.Dorsal skin defect modeling and treatment with intraperitoneal injection of auranofin were performed to observe wound healing in mice.RESULTS AND CONCLUSION:(1)Cell experiments showed that co-treatment with interferon-y(10 ng/mL)and lipopolysaccharide(100 ng/mL)significantly induced M1 polarization in RAW264.7 and THP-1 cells,resulting in increased mRNA expression of interleukin-1β,interleukin-6,and tumor necrosis factor-α.Treatment with auranofin(1 and 2 μmol/L)reduced the mRNA expression of these inflammatory factors in the cells and inhibited the secretion of inflammatory factors in the cell supernatant.(2)Auranofin treatment significantly suppressed the activation of nuclear factor-κB(p65)and phosphorylated MAPK signaling pathways.(3)Animal experiments showed that auranofin promoted wound healing in db/db diabetic mice,suggesting that auranofin has strong anti-inflammatory effects and may facilitate the healing of wounds in diabetic mice.

BACKGROUND:Clinical studies suggest that both bone quality and excessive crown-to-implant ratio are factors that affect the success rate of implant surgery,but there is no consensus on how large the crown-to-implant ratio under each bone quality will affect the prognosis of implant repair.OBJECTIVE:To analyze the stress and strain of bone tissue around implant restorations with different crown-to-implant ratios under different bone types after stress loading using three-dimensional finite element method.Combined with the Frost bone mechanics regulation system theory,the physiological limits of bone strain were observed for each bone type within a certain range of crown to implant ratios.METHODS:Cone beam CT data were selected from a patient to establish solid bone block models with four different bone types(class Ⅰ bone:cortical bone thickness 3 mm+dense cancellous bone,class Ⅱ bone:cortical bone thickness 2 mm+relatively dense cancellous bone,class Ⅲ bone:cortical bone thickness 1 mm+relatively low-density cancellous bone,class Ⅳ bone:cortical bone thickness 1 mm+low-density cancellous bone).Implant restorations with five different crown-to-implant ratios(1,1.5,2,2.5,and 3)were created on each bone block model,for a total of 20 models.Vertical and oblique forces were applied to the dental crown to observe the von Mises stress values,strains,and displacement of the cortical and cancellous bones,as well as the degree of implant displacement.RESULTS AND CONCLUSION:(1)In the class Ⅰ bone model,when the crown-to-implant ratio reached 3 under oblique loading,the cortical bone strain exceeded the physiological limit.In the class Ⅱ bone model,under oblique loading,when the crown-to-implant ratio reached 2.5,the cortical bone strain exceeded the physiological limit.In the class Ⅲ bone model,under oblique loading,cortical bone exceeded the physiological limit when the crown-to-implant ratio reached 2.5,while cancellous bone reached the critical physiological limit at 1.In the class Ⅳ bone model,under oblique loading,when the crown-to-implant ratio reached 1.5,2,2.5,and 3,the cortical bone strain exceeded the physiological limit.In the class Ⅳ bone model,all five crown-to-implant ratios of cancellous bone exceeded physiological limits.(2)Under vertical load,the cancellous bone strain exceeded the physiological limit when the crown-root ratio reached 1,2,2.5,and 3 in the class Ⅲ bone model,and when the cancellous bone strain of the five crown-root ratios in the class Ⅳ bone model exceeded the physiological limit.(3)Under oblique or vertical load,the implant displacement of the 20 groups of models did not exceed 100 μm.(4)From the perspective of biomechanics,when patients with insufficient bone height choose implant restoration,the crown-root ratio that class Ⅰ bone can tolerate is up to 2.5 times,the crown-root ratio that class Ⅱ bone can tolerate is up to 2 times,and the crown-root ratio that class Ⅲ and class Ⅳ bones can tolerate is up to 1 times due to excessive strain of cancellous bone;but the crown-root ratio that cortical bone in class Ⅲ bone can tolerate is up to 2 times.Whether class Ⅲ bone can tolerate implant restoration with a high crown-root ratio and whether cancellous bone can tolerate higher strains needs further study.

BACKGROUND:Oral submucous fibrosis is a chronic progressive disease that is prone to malignant transformation.Traditional treatment methods are not ideal and have limitations.As an emerging discipline,tissue engineering has opened up a new path for the treatment of oral submucous fibrosis.OBJECTIVE:To review the latest progress in the pathogenesis and treatment of oral submucous fibrosis,and to summarize and analyze the role and research progress of mesenchymal stem cells,bioscaffold materials,and tissue-engineered oral mucosa in oral submucous fibrosis,thereby providing ideas for the research and clinical application of tissue engineering in the treatment of oral submucous fibrosis.METHODS:In October 2024,the first author used computers to search for relevant literature from January 1970 to October 2024 in PubMed and CNKI databases.The search terms were"oral submucous fibrosis,tissue engineering,mesenchymal stem cells,bioscaffold materials"in English and Chinese,respectively.A total of 166 articles were finally included for analysis.RESULTS AND CONCLUSION:(1)The pathogenesis of oral submucous fibrosis is complex,and many factors are closely related to oral submucous fibrosis,but ultimately they promote the development of oral submucous fibrosis by promoting collagen deposition and accelerating fibroblast proliferation.(2)Traditional treatment methods for oral submucous fibrosis have problems such as low patient compliance and unsatisfactory results,and new treatment strategies are urgently needed.(3)Mesenchymal stem cells regulate the pathological microenvironment,reduce inflammation and inhibit the process of fibrosis due to their immunomodulatory and antioxidant properties,providing a new idea for the treatment of oral submucous fibrosis.(4)Biomass materials,as drug and cell delivery carriers,regulate the pathological microenvironment and are used in various fibrotic diseases,providing a new solution for the treatment of oral submucous fibrosis.(5)Tissue-engineered oral mucosa can be used as an autologous mucosa substitute to promote tissue repair,and also provides a basis for the establishment of disease models.(6)Tissue engineering treatment strategy has great potential for achieving comprehensive treatment of oral submucous fibrosis,but its role in the treatment of oral submucous fibrosis has not yet been verified.It is of great significance to explore tissue engineering-based treatment strategies for oral submucous fibrosis in the future.

BACKGROUND:Studies have shown that there is a close relationship between pyroptosis,inflammatory factors and osteoporosis.OBJECTIVE:To review the effects of pyroptosis and inflammatory factors on the pathogenesis of osteoporosis from the perspectives of osteogenic differentiation and osteoclastic differentiation,based on an overview of pyroptosis in relation to the interaction of relevant inflammatory factors.METHODS:The first author used the computer to search the literature published by each database until 2024,and searched CNKI,WanFang,VIP and PubMed databases with the search terms of"pyroptosis,inflammatory factors,osteoporosis,osteoblast,osteoclast,bone metabolism,signaling pathway,review"in Chinese and English.A total of 79 papers were finally included according to the inclusion criteria.RESULTS AND CONCLUSION:The progression of osteoporosis is closely related to inflammation,in which pyroptosis plays a key role.Immune cells induce pyroptosis through apoptosis pathway,promote the secretion of inflammatory factors such as interleukin-18,interleukin-1β and NLRP3,build an inflammatory immune microenvironment,and regulate bone metabolism through complex signaling pathways,resulting in enhanced bone absorption and reduced bone formation,thereby leading to osteoporosis.Previous studies have shown that inhibiting pyroptosis is anti-inflammatory and slows the progression of osteoporosis,and it has been shown to improve inflammatory bone loss in vitro and in animal models.At present,research on pyroptosis and osteoporosis is limited.On the one hand,the exact mechanism of osteoporosis and the pathogenesis of pyroptosis are unknown,and the specific pathways and regulatory mechanisms remain to be understood.On the other hand,therapeutic strategies targeting pyroptosis are still theoretical,not clinically proven,and drug side effects are unknown.In the future,the research focus is to further explore the pathogenesis,especially the mechanism of pyroptosis,identify potential therapeutic targets,further study the pyroptosis signaling pathway and Gasdermin protein,and develop new drugs to improve the therapeutic effect in patients with osteoporosis.

OBJECTIVE:Patients with osteoporotic vertebral compression fractures still have residual back pain after vertebral augmentation.The current research is characterized by limited sample size,complex confounding factors,and inconsistent research results.To gain a deeper understanding of this phenomenon,the aim of this study was to identify and evaluate the risk factors for residual back pain after surgery through a systematic review and meta-analysis.METHODS:A comprehensive search was conducted in CNKI,VIP,WanFang,CBMdisc,PubMed,The Cochrane Library,Embase,and Web of Science for case-control studies on residual back pain after vertebral body augmentation for osteoporotic vertebral compression fractures from database inception to July 2024.The search terms were a combination of subject terms and free terms.The basic information,patient characteristics,surgical-related indicators,and risk factors for surgical back pain of the included studies were extracted.After evaluating the bias risk of all included studies,a meta-analysis was conducted using Stata 14.0 software on the relevant indicators.RESULTS:(1)21 case-control studies with a total of 8 043 patients were included.Among them,965 patients developed back pain.The quality score of all 21 studies was ≥7.(2)The meta-analysis results showed that age(WMD=0.98,95％CI:0.40-1.56,P=0.010),bone mineral density(WMD=-0.28,95％CI:-0.34 to-0.21,P=0.000),the number of vertebral fractures(OR=3.50,95％CI:2.65-4.62,P=0.000),thoracolumbar fracture index(OR=3.65,95％CI:2.61-5.11,P=0.000),cement volume(OR=6.89,95％CI:2.62-18.17,P=0.000),and cement distribution(OR=2.38,95％CI:1.93-2.93,P=0.000)were risk factors for the development of back pain after vertebral body augmentation in patients with osteoporotic vertebral compression fractures.CONCLUSION:Current evidence indicates that age,bone mineral density,the number of vertebral fractures,thoracolumbar fracture index,bone cement injection volume,and the distribution of bone cement are risk factors for low back pain.Specifically,bone mineral density,the number of vertebral fractures,thoracolumbar fracture index,and non-uniform distribution of bone cement are identified as independent risk factors for low back pain.Patients exhibiting these high-risk factors require vigilant monitoring and prompt intervention to mitigate the occurrence of clinical low back pain,thereby enhancing patient outcomes and quality of life.

BACKGROUND:Bone tissue loss caused by tumors and trauma can have an adverse effect on postoperative rehabilitation.Therefore,scaffold materials are usually implanted during treatment.However,the existing implant materials are relatively simple and lack antibacterial properties.Early implantation may lead to iatrogenic autoinfection and have an adverse effect on osteogenesis.OBJECTIVE:To construct a KR-12-a5 polypeptide-nanohydroxyapatite-small intestinal submucosa composite scaffold and evaluate its feasibility as a material for promoting bone defect repair.METHODS:The small intestinal submucosa scaffold and the small intestinal submucosa scaffold containing 25,50,and 100 mg/mL nanohydroxyapatite(referred to as nHA-SIS scaffold)were prepared by 1-ethyl-3-(3-dimethylaminopropyl)carbodiimide hydrochloride/N-hydroxysuccinimide cross-linking method.The appropriate scaffold was screened for subsequent experiments by mechanical property testing.The antibacterial properties of KR-12-a5 polypeptide solution against Staphylococcus aureus,Streptococcus gordonii,and Fusobacterium nucleatum were detected.The nHA-SIS scaffolds were immersed in 250,500,and 1 000 μg/mL KR-12-a5 peptide solutions for 24 hours,and then freeze-dried to obtain peptide-loaded nanohydroxyapatite-porcine small intestinal submucosa composite scaffolds(denoted as P-nHA-SIS scaffolds).The sustained-release properties of the three groups of scaffolds were characterized.The nHA-SIS scaffolds and the three groups of P-nHA-SIS scaffolds were co-cultured with Staphylococcus aureus,Streptococcus gordonii,and Fusobacterium nucleatum for 24 hours or 48 hours.The scaffolds with strong antibacterial ability were screened by live and dead bacteria staining and scanning electron microscopy for subsequent experiments.The degradation properties and water absorption rates of the uncross-linked small intestinal submucosa scaffolds,cross-linked small intestinal submucosa scaffolds,nHA-SIS scaffolds,and P-nHA-SIS scaffolds were characterized.The extracts of cross-linked small intestinal submucosal scaffolds,nHA-SIS scaffolds,and P-nHA-SIS scaffolds were co-cultured with MC3T3-E1 cells.CCK-8 assay and live-dead cell staining were performed.The effects of the extracts of the three scaffolds on the migration of MC3T3-E1 cells were detected by Transwell chamber assay.RESULTS AND CONCLUSION:(1)The elastic modulus and compressive strength of 25,50,and 100 mg/mL nHA-SIS scaffolds were higher than those of small intestinal submucosal scaffolds(P＜0.05),among which the elastic modulus and compressive strength of 25 mg/mL nHA-SIS scaffolds were the highest,and this group of scaffolds were selected for subsequent experiments to load peptides.(2)KR-12-a5 peptide had strong antibacterial activity against common bacteria in bone defects(Staphylococcus aureus,Streptococcus gordonii,and Fusobacterium nucleatum).The three groups of P-nHA-SIS scaffolds all had sustained release properties.With the increase of peptide mass concentration,the antibacterial property of P-nHA-SIS scaffold was enhanced.Among them,the P-nHA-SIS scaffold loaded with 500 μg/mL peptide had achieved a satisfactory antibacterial effect,and this group of scaffolds would be selected in the future.(3)The degradation rate of the three groups of cross-linked scaffolds was lower than that of the uncross-linked scaffolds,and the water absorption rate was greater than that of the uncross-linked scaffolds.P-nHA-SIS scaffolds could promote the proliferation and migration of MC3T3-E1 cells without affecting the activity of MC3T3-E1 cells.(4)The results show that P-nHA-SIS scaffolds have strong antibacterial properties and the ability to promote the proliferation and migration of MC3T3-E1 cells,and are expected to be used in bone defect repair.

BACKGROUND:During diabetic wound healing,the sustained activation of M1 macrophages exacerbates the inflammatory response and hinders wound repair.Auranofin,an anti-inflammatory drug,has not been clearly studied for its effects on M1 macrophages and its potential role in diabetic wound healing.OBJECTIVE:To investigate the effects of different concentrations of auranofin on the biological function of M1 macrophages and evaluate its potential application in diabetic wound healing.METHODS:RAW264.7 and THP-1 cells were used as research models.M1 polarization was induced using different concentrations of interferon-γ and lipopolysaccharide.M1 macrophages were treated with 1 and 2 μmol/L auranofin.Cell counting kit-8 assay was used to evaluate the effect of auranofin on cell viability.Quantitative real-time PCR was performed to detect mRNA expression of interleukin-1β,interleukin-6,and tumor necrosis factor-α.ELISA was employed to measure the levels of interleukin-1β,interleukin-6,and tumor necrosis factor-α in the supernatant.Western blot analysis was used to assess the expression of nuclear factor-κB(p65),phosphorylated mitogen-activated protein kinases(MAPK),and total MAPK proteins.Additionally,6-8-week-old male C57BL/6J and db/db diabetic mice were used for wound healing experiments,with the mice divided into C57 control,db/db control and auranofin treatment groups,each containing six animals.Dorsal skin defect modeling and treatment with intraperitoneal injection of auranofin were performed to observe wound healing in mice.RESULTS AND CONCLUSION:(1)Cell experiments showed that co-treatment with interferon-y(10 ng/mL)and lipopolysaccharide(100 ng/mL)significantly induced M1 polarization in RAW264.7 and THP-1 cells,resulting in increased mRNA expression of interleukin-1β,interleukin-6,and tumor necrosis factor-α.Treatment with auranofin(1 and 2 μmol/L)reduced the mRNA expression of these inflammatory factors in the cells and inhibited the secretion of inflammatory factors in the cell supernatant.(2)Auranofin treatment significantly suppressed the activation of nuclear factor-κB(p65)and phosphorylated MAPK signaling pathways.(3)Animal experiments showed that auranofin promoted wound healing in db/db diabetic mice,suggesting that auranofin has strong anti-inflammatory effects and may facilitate the healing of wounds in diabetic mice.

Objective:To investigate the survival outcomes and prognostic factors in patients undergoing radical resection for pancreatic body and tail cancer.Methods:A retrospective case series study was conducted on 992 patients who underwent radical resection for pancreatic body and tail cancer at the Pancreatic Center of the First Affiliated Hospital of Nanjing Medical University from January 2016 to June 2024. In this study, 577 (58.2%) were male and 415 (41.8%) were female,with an age of (65±9) years (range: 26 to 86 years). Follow-up continued until June 2024. Survival rates were estimated using the Kaplan-Meier method,and prognostic factors were identified using univariate and multivariate Cox proportional hazards models.Results:Among 992 patients,open surgery was the predominant approach (89.1%, 884/992), and radical antegrade modular pancreatosplenectomy (RAMPS) was performed in 317 patients (32.0%). Combined organ resection,venous resection,and arterial resection were performed in 23.5%, 9.3%,and 11.2% of patients,respectively. The rates of R0, R1-1 mm, and R1-direct resections were 49.8% (494/992),41.5% (412/992), and 8.7% (86/992),respectively. Stage ⅡB was the most common TNM stage (32.2%,319/992). A total of 801 patients (80.8%) received adjuvant chemotherapy. The median follow-up period was 32.0(8.8) months(range:3.2 to 105.3 months),during which 508 patients (51.2%) died. The overall median survival (OS) was 26.4 months,with 1-,3-, and 5-year survival rates of 79.0%,40.0%, and 29.0%, respectively. In the recent five years (from 2020 to 2024), the median OS improved significantly to 34.1 months compared to 20.0 months from 2016 to 2019 ( P<0.01). Histological subtype analysis showed that the median OS time was 26.7 months for pancreatic ductal adenocarcinoma (PDAC, n=855),58.9 months for invasive intraductal papillary mucinous carcinoma (IPMC, n=32),and 15.7 months for adenosquamous carcinoma of pancreas (ASCP, n=73) ( P=0.001). Among PDAC patients, adjuvant chemotherapy significantly improved survival (29.1 months vs. 14.4 months, P<0.01);in IPMC patients, adjuvant chemotherapy also extended survival (65.7 months vs. 58.9 months, P=0.047). Although ASCP patients receiving chemotherapy had a longer median OS time than those without (18.8 months vs. 8.9 months),the difference was not statistically significant ( P=0.151). Multivariate Cox regression analysis in PDAC patients indicated that adjuvant chemotherapy, R0 resection, T stage,N stage,and tumor differentiation were independent prognostic factors ( P<0.01). The median OS time by TNM stage was:not reached for stage ⅠA, 51.6 months for ⅠB, 25.5 months for ⅡA, 23.7 months for ⅡB, 23.0 months for Ⅲ, and 14.4 months for Ⅳ. The median OS time for R0,R1-1 mm,and R1-direct resections was 34.1,24.7,and 15.7 months,respectively ( P<0.01). Conclusion:Adjuvant chemotherapy,R0 resection,tumor stage,and differentiation are independent prognostic factors for pancreatic body and tail cancer.

ObjectiveTo investigate the mechanism by which Xiebai San regulates respiratory tract and intestinal mucosal immunity in rats with allergic asthma. MethodsForty male SD rats were randomly divided into four groups based on body weight: control group, model group, positive control group, and Xiebai San group. The model group, positive control group, and Xiebai San group were sensitized with ovalbumin to establish a rat model of allergic asthma. From day 21 (the aerosol challenge phase), each group received daily gavage interventions simultaneously: the positive control group was administered dexamethasone (0.068 mg/kg), the Xiebai San group received Xiebai San solution (2 g/mL, 11.3 mL/kg), while the control and model groups were given an equal volume of normal saline, once daily for 14 consecutive days. After euthanasia, lung and intestinal tissues were collected. Hematoxylin and eosin staining was used to observe histopathological changes. Transmission electron microscopy was employed to examine tissue ultrastructure. Immunohistochemistry was applied to detect the positive reaction areas of phosphatidyl-inositol 3-kinase (PI3K) and protein kinase B (Akt) proteins. Total protein and total RNA were extracted from lung and intestinal tissues, then the protein and mRNA expression levels of PI3K and Akt genes were detected by Western blotting and real-time quantitative PCR, respectively. ResultsHistopathological results showed alveolar emphysema accompanied by inflammatory cell infiltration, and intestinal mucosal injury with inflammatory cell infiltration in the model group as compared with the control group; the cellular structure of lung tissues was disrupted in the model group, with reduced organelles, while the ultrastructural lesions in the intestine were relatively mild. Compared with the model group, Xiebai San group exhibited milder pathological changes in lung tissues, with occasional alveolar wall damage and a small amount of inflammatory cell infiltration; the intestinal mucosal structure was improved, glands were arranged regularly, and pathological changes such as tissue loosening and inflammatory infiltration were alleviated; the cellular structure of lung tissues was relatively intact with reduced severity of lesions, and no ultrastructural pathological changes were observed in intestinal tissues. Immunohistochemistry and Western blotting results showed that compared with the control group, the specific positive reaction areas of PI3K and Akt in lung and intestinal tissues were significantly increased in the model group (all P<0.001); meanwhile, the protein expression levels of PI3K and Akt were significantly upregulated (all P<0.05). Compared with the model group, the positive area of Akt protein in lung tissue was significantly reduced in the Xiebai San group (P<0.001), and the positive area of PI3K in intestinal tissue was also significantly decreased (P<0.000 1). Additionally, the protein expression levels of PI3K and Akt in lung and intestinal tissues were significantly downregulated (all P<0.01). Real-time quantitative PCR results showed that compared with the control group, the mRNA expression levels of PI3K and Akt genes in lung and intestinal tissues were significantly elevated in the model group (all P<0.05). Compared with the model group, the mRNA expression levels of PI3K and Akt genes in lung and intestinal tissues were significantly reduced in the Xiebai San group (all P<0.05). ConclusionXiebai San exerts protective effects on rats with allergic asthma by inhibiting the expression of key nucleic acids and proteins in the PI3K-Akt signaling pathway in lung and intestinal tissues, improving the morphological structure of lung tissue, and maintaining intestinal mucosal integrity, and regulating intestinal mucosal immune function.