Objective: To explore the efficacy of a novel injectable hydrogel (GelMA/P11/IL4@LIP) loaded with P11 bacteriophages and interleukin-4 (IL-4) liposomes (LIP) in preventing relapse after maxillary expansion in mice, providing experimental evidence for its clinical application. Methods: This study was approved by the experimental animal ethics committee of our hospital. First, 15 7-week-old C57BL/6 mice were used to establish a maxillary expansion model and divided into 5 groups (3 mice in each group): a control group, post expansion day 3 group (PED3 group), post expansion day 7 group (PED7 group), retention for 14 days group (RET group), and relapse for 7 days group (REL group). The mice in each group were sacrificed at their designated time points (day 0, 3, 7, 21, 28), and their maxilla and anterior cranial regions were collected. Bone parameters and the inter-crestal distance (ICD) of maxillary incisor mesial alveolar ridge were measured using micro-computed tomography (micro-CT). Histological staining was performed to evaluate bone formation and resorption, while immunohistochemistry (IHC) was performed for macrophage markers (CD86 and CD206), mesenchymal stem cell markers (glioma-associated oncogene homolog 1 [Gli1]), and osteogenic markers (Runt-related transcription factor 2 [Runx2] and Osterix [OSX]). Next, GelMA/P11/IL4@LIP was synthesized and administered to mouse models of maxillary expansion. A total of 24 7-week-old C57BL/6 mice were divided into 4 groups (6 mice in each group): a blank control group, GelMA group, GelMA/P11 group, and GelMA/P11/IL4@LIP group. All mice underwent palatal expansion. On PED7, the expanders of all 24 mice were cemented with resin to initiate the 14-day retention period. On day 1 of the retention phase, the mice in each group received injections of saline, GelMA, GelMA/P11, or GelMA/P11/IL4@LIP at the midpalatal suture. After the 14-day retention period, three mice in each group were randomly selected and sacrificed, while the other three had their expanders removed and underwent a 7-day relapse before being sacrificed on day 28 (REL). Micro-CT, histological staining, and IHC were performed to evaluate the preventive effect of GelMA/P11/IL4@LIP on post-expansion relapse. Results: The mice maxillary expansion model exhibited a decreased ICD at REL compared to RET in micro-CT analysis (P = 0.008). IHC analysis demonstrated prolonged M1 macrophage infiltration, scarce Gli1+ mesenchymal stem cells, and insufficient expression of osteogenic markers (RUNX2 and OSX) (P < 0.001). Compared to the blank control and GelMA groups, GelMA/P11/IL4@LIP hydrogel injection in the midpalatal suture led to increased ICD at REL, promoted the timely M2 polarization of macrophages, recruited Gli1+ mesenchymal stem cells, and upregulated the expression of RUNX2 and OSX (P < 0.05). Conclusion The mechanism of relapse after maxillary expansion involves the persistent infiltration of M1 macrophages, as well as the inadequate recruitment and insufficient osteogenic differentiation of MSCs in the midpalatal suture. The GelMA/P11/IL4@LIP composite enhanced orofacial mesenchymal stem cell recruitment and promoted the M2 polarization of macrophages, thereby enhancing osteogenesis in the midpalatal suture and preventing post-expansion relapse.

Objective Exploring the therapeutic mechanism of Yishen Jiangzhuo Granules(YSJZG)on chronic kidney disease(CKD)based on mitochondrial dynamics and apoptosis of renal tubular epithelial cells.Methods The CKD model of rats with 5/6 nephrectomy was adopted and divided into 6 groups according to random number table:sham operation control group,model group,emodin group(500 mg/kg/d),Yishen Jiangzhuo granule low,middle and high dose groups.After 8 weeks of treatment with YSJZG,serum creatinine(SCR)and urea nitrogen(BUN),pathological changes of renal cortex,mitochondrial morphology and ultrastructure were detected,and mitochondrial kinetic protein in renal tubular epithelial cells was detected by immunohistochemistry(Drp1,Fis1)and fusion proteins(Opa1,Mfn1)were detected by Western blot,and apoptotic proteins(CytC,Bax)in cytoplasm and mitochondria were detected by real-time PCR.Results Renal injury:Compared with the model group,YSJZG groups significantly reduced the levels of SCR and BUN,renal tubular degeneration and necrosis,and mitochondrial structural damage in rats.Renal tubule mitochondrial dynamic protein:Compared with the model group,the expression of division proteins Drp1 and Fis1 was downregulated,the expression of fusion proteins Opa1 and Mfn1 was upregulated,and transmission electron microscopy observed that the mitochondrial fragmentation changes were relatively mild.Apoptosis related indicators and mtDNA copy number of renal tubular cells:Compared with the model group,the content of Bax protein in renal tubular epithelial cells of YSJZG groups increased significantly in cytoplasm(P<0.05)and decreased significantly in mitochondria(P<0.05).The content of CytC protein decreased significantly in cytoplasm(P<0.05)and increased significantly in mitochondria(P<0.05).The copy number of mtDNA increased significantly(P<0.05),and the total levels of SMAC,CytC and Bax mRNA decreased significantly(P<0.05).Correlation between mitochondrial dynamic protein and apoptosis in renal tubular cells:Pearson correlation analysis showed that the expression of Drp1 and Fis1 was negatively correlated with the expression of CytC in mitochondria,and positively correlated with the expression of CytC in cytoplasm.The expression levels of fusion proteins Opa1 and Mfn1 showed a significant positive correlation with CytC expression in mitochondria,and a significant negative correlation with CytC expression in cytoplasm.Conclusion YSJZG can significantly delay the progression of CKD,and its mechanism may be achieved by regulating mitochondrial dynamics of renal tubular epithelial cells,thereby inhibiting endogenous cell apoptosis pathway.

Objective Exploring the therapeutic mechanism of Yishen Jiangzhuo Granules(YSJZG)on chronic kidney disease(CKD)based on mitochondrial dynamics and apoptosis of renal tubular epithelial cells.Methods The CKD model of rats with 5/6 nephrectomy was adopted and divided into 6 groups according to random number table:sham operation control group,model group,emodin group(500 mg/kg/d),Yishen Jiangzhuo granule low,middle and high dose groups.After 8 weeks of treatment with YSJZG,serum creatinine(SCR)and urea nitrogen(BUN),pathological changes of renal cortex,mitochondrial morphology and ultrastructure were detected,and mitochondrial kinetic protein in renal tubular epithelial cells was detected by immunohistochemistry(Drp1,Fis1)and fusion proteins(Opa1,Mfn1)were detected by Western blot,and apoptotic proteins(CytC,Bax)in cytoplasm and mitochondria were detected by real-time PCR.Results Renal injury:Compared with the model group,YSJZG groups significantly reduced the levels of SCR and BUN,renal tubular degeneration and necrosis,and mitochondrial structural damage in rats.Renal tubule mitochondrial dynamic protein:Compared with the model group,the expression of division proteins Drp1 and Fis1 was downregulated,the expression of fusion proteins Opa1 and Mfn1 was upregulated,and transmission electron microscopy observed that the mitochondrial fragmentation changes were relatively mild.Apoptosis related indicators and mtDNA copy number of renal tubular cells:Compared with the model group,the content of Bax protein in renal tubular epithelial cells of YSJZG groups increased significantly in cytoplasm(P<0.05)and decreased significantly in mitochondria(P<0.05).The content of CytC protein decreased significantly in cytoplasm(P<0.05)and increased significantly in mitochondria(P<0.05).The copy number of mtDNA increased significantly(P<0.05),and the total levels of SMAC,CytC and Bax mRNA decreased significantly(P<0.05).Correlation between mitochondrial dynamic protein and apoptosis in renal tubular cells:Pearson correlation analysis showed that the expression of Drp1 and Fis1 was negatively correlated with the expression of CytC in mitochondria,and positively correlated with the expression of CytC in cytoplasm.The expression levels of fusion proteins Opa1 and Mfn1 showed a significant positive correlation with CytC expression in mitochondria,and a significant negative correlation with CytC expression in cytoplasm.Conclusion YSJZG can significantly delay the progression of CKD,and its mechanism may be achieved by regulating mitochondrial dynamics of renal tubular epithelial cells,thereby inhibiting endogenous cell apoptosis pathway.

ObjectiveTo observe the clinical efficacy and safety of Guben Quyu Jiedu prescription in treating nocturnal hypoxemia of chronic obstructive pulmonary disease （COPD） combined with Obstructive sleep apnea hypopnea syndrome （ OSAHS ） （deficiency of lung， spleen and kidney with blood stasis and toxicity）. MethodsThe paper used a forward-looking， random double-blind， placebo-controlled design method to select 96 patients with COPD combined with OSAHS， and their traditional Chinese medicines （TCM） syndrome differentiation was deficiency of lung， spleen and kidney with blood stasis and toxicity. These patients were randomly divided into the observation group and the control group， with 48 cases in each group. Based on conventional Western medicine treatment， the observation group was treated with Guben Quyu Jiedu prescription and the control group was treated with traditional Chinese medicine placebo. Both courses of treatment were 90 days. Then the paper compared the changes in minimum pulse oxygen saturation （SpO₂） during the night， apnea index （AHI）， OSAHS efficacy evaluation， TCM syndrome efficacy evaluation， and TCM symptom score before and after treatment between the two groups. ResultsThere were 5 withdrawals in the observation group and 8 withdrawals in the control group， so 43 cases in the observation group and 40 cases in the control group completed the trial. Compared with the condition before treatment， the minimum SpO₂ during the night and AHI in the observation group were significantly improved at night （P<0.01） and were better than those in the control group （P<0.01）. OSAHS efficacy in the observation group was better than in the control group （χ²=7.085， P<0.05）. In terms of TCM syndrome efficacy， the total effective rate was 81.40% （35/43） in the observation group， significantly higher than that in the control group， which was 15.00% （6/40） （χ²=36.78， P<0.01）. The TCM symptom scores of the two groups were improved compared with the condition before treatment， and the effect of the two groups was similar in the four main symptoms of snoring， choking， lethargy， and cough. However， the observation group was better than the control group in 10 details such as dizziness， headache， chest tightness， chest pain， wheezing， dry mouth， and thirst （P<0.05）. ConclusionUsing Guben Quyu Jiedu prescription combined with conventional Western medicine can treat COPD combined with OSAHS hypoxemia at night （deficiency of lung， spleen and kidney with blood stasis and toxicity）. In this way， the minimum pulse oxygen saturation （SpO₂） of patients， the level of disease control， and the quality of life of patients can be improved， and the clinical symptoms can be relieved.

Objective To investigate the correlation between the change of muscle tissues and bone mineral density(BMD)in elderly women with hip fracture,with consideration of the impact of muscle mechanics on bone mass changes.Methods A total of 79 elderly patients with hip fracture were selected as the fracture group,and 45 physical examination personnel as the control group.The differences in total muscle mass,total body fat,trunk muscle mass,trunk fat mass,arm muscle mass,arm fat mass,leg muscle mass,leg fat mass,as well as BMD at the lumbar spine(L1-4),femoral neck,hip joint,and whole body were analyzed.Results Muscle content and fat content of the whole body,upper limb and lower limb,fat content of the trunk,relative skeletal muscle index(SMI)and BMD of the whole body in fracture group were significantly lower than those in control group(P＜0.05).The incidence rate of sarcopenia for elderly women in fracture group was higher than that in control group.BMD of femoral neck of the affected side was significantly lower than that of the intact side in women with intertrochanteric fractures.Logistic regression analysis found that SMI in elderly women with hip fracture was negatively correlated with age,and positively correlated with body mass index(BMI),BMD of the femoral neck and whole body.Conclusions The rate of sarcopenia was significantly higher in elderly patients with hip fracture,and SMI was closely related to BMD of the femoral neck and whole body.Therefore,sarcopenia should be highly emphasized in the prevention and treatment of osteoporotic fracture in elderly people.

Objective To investigate the correlation between the change of muscle tissues and bone mineral density(BMD)in elderly women with hip fracture,with consideration of the impact of muscle mechanics on bone mass changes.Methods A total of 79 elderly patients with hip fracture were selected as the fracture group,and 45 physical examination personnel as the control group.The differences in total muscle mass,total body fat,trunk muscle mass,trunk fat mass,arm muscle mass,arm fat mass,leg muscle mass,leg fat mass,as well as BMD at the lumbar spine(L1-4),femoral neck,hip joint,and whole body were analyzed.Results Muscle content and fat content of the whole body,upper limb and lower limb,fat content of the trunk,relative skeletal muscle index(SMI)and BMD of the whole body in fracture group were significantly lower than those in control group(P＜0.05).The incidence rate of sarcopenia for elderly women in fracture group was higher than that in control group.BMD of femoral neck of the affected side was significantly lower than that of the intact side in women with intertrochanteric fractures.Logistic regression analysis found that SMI in elderly women with hip fracture was negatively correlated with age,and positively correlated with body mass index(BMI),BMD of the femoral neck and whole body.Conclusions The rate of sarcopenia was significantly higher in elderly patients with hip fracture,and SMI was closely related to BMD of the femoral neck and whole body.Therefore,sarcopenia should be highly emphasized in the prevention and treatment of osteoporotic fracture in elderly people.

Objective To investigate the role of sphingosine kinase-1(SPHK1)in regulating migration and invasion of gastric cancer(GC)cells.Methods TIMER2.0,GEPIA and HPA databases were used to investigate SPHK1 expression in GC,and its association with prognosis of the patients was analyzed using Kaplan-Meier Plotter database.In 40 clinical GC and adjacent tissue samples,SPHK1 and MKI67 expressions were detected with immunohistochemistry,Western blotting,and RT-qPCR.Gene enrichment pathway analysis was conducted to explore the biological functions of SPHK1.In HGC-27 and MGC-803 cells,the effects of lentivirus-mediated SPHK1 knockdown or overexpression on cell migration and invasion and expressions of key proteins in the nuclear factor-κB(NF-κB)signaling were evaluated using cell scratch test,Transwell assays and Western blotting.The changes in tumorigenic capacity of the transfected GC cells were evaluated in nude mice.Results SPHK1 was highly expressed in GC tissues in negative correlation with overall survival,overall survival after progression,and relapse-free survival of the patients(all P<0.001).In clinical GC samples,SPHK1 and MKI67 expressions showed a positive correlation(P=0.00049)and were both significantly up-regulated(P<0.001).Gene enrichment pathway analysis suggested the involvement of SPHK1 in cell adhesion,migration,angiogenesis and the NF-κB pathway(P<0.05).In the cell experiment,SPHK1 knockdown significantly decreased while SPHK1 overexpression enhanced migration and invasion abilities of the GC cells.SPHK1 positively regulated the expressions of phosphorylated P65(P-P65),VEGFA and IL-17,and blocking the NF-κB pathway by PDTC significantly lowered migration and invasion ability of the cells.In nude mice,the GC cells with SPHK1 knockdown resulted in significantly reduced tumor size and mass,while the SPHK1-overexpressing cells showed enhanced tumorigenicity.Conclusion SPHK1 regulates migration and invasion of GC cells via the NF-κB signaling pathway and may serve as a potential diagnostic marker for GC progression.

Hyperbaric oxygen therapy characterized by fewer side effects and simple operation has been explored as a potential therapy for depression. This article provides a review of researches relevant to current clinical application and mechanism of hyperbaric oxygen therapy for depression， aiming to provide valuable references for the formulation of new strategies for the treatment of depression. Hyperbaric oxygen therapy has been demonstrated to be useful as an adjunctive therapy for depression， which can effectively alleviate depression by regulating the homeostasis of hypothalamus-pituitary-adrenal axis， inhibiting inflammation and enhancing synaptic plasticity. And hyperbaric oxygen therapy as adjuvant to antidepressants for depression can contribute to increasing the treatment effectiveness to some extent.

Objective To investigate the role of sphingosine kinase-1(SPHK1)in regulating migration and invasion of gastric cancer(GC)cells.Methods TIMER2.0,GEPIA and HPA databases were used to investigate SPHK1 expression in GC,and its association with prognosis of the patients was analyzed using Kaplan-Meier Plotter database.In 40 clinical GC and adjacent tissue samples,SPHK1 and MKI67 expressions were detected with immunohistochemistry,Western blotting,and RT-qPCR.Gene enrichment pathway analysis was conducted to explore the biological functions of SPHK1.In HGC-27 and MGC-803 cells,the effects of lentivirus-mediated SPHK1 knockdown or overexpression on cell migration and invasion and expressions of key proteins in the nuclear factor-κB(NF-κB)signaling were evaluated using cell scratch test,Transwell assays and Western blotting.The changes in tumorigenic capacity of the transfected GC cells were evaluated in nude mice.Results SPHK1 was highly expressed in GC tissues in negative correlation with overall survival,overall survival after progression,and relapse-free survival of the patients(all P<0.001).In clinical GC samples,SPHK1 and MKI67 expressions showed a positive correlation(P=0.00049)and were both significantly up-regulated(P<0.001).Gene enrichment pathway analysis suggested the involvement of SPHK1 in cell adhesion,migration,angiogenesis and the NF-κB pathway(P<0.05).In the cell experiment,SPHK1 knockdown significantly decreased while SPHK1 overexpression enhanced migration and invasion abilities of the GC cells.SPHK1 positively regulated the expressions of phosphorylated P65(P-P65),VEGFA and IL-17,and blocking the NF-κB pathway by PDTC significantly lowered migration and invasion ability of the cells.In nude mice,the GC cells with SPHK1 knockdown resulted in significantly reduced tumor size and mass,while the SPHK1-overexpressing cells showed enhanced tumorigenicity.Conclusion SPHK1 regulates migration and invasion of GC cells via the NF-κB signaling pathway and may serve as a potential diagnostic marker for GC progression.

Objective To evaluated the efficacy of Supplemented Buyang Huanwu Decoction in preventing and treating postoperative abdominal adhesions.Methods One hundred and eight male SD rats were randomly divided into ordinary group,mold group,Sodium hyaluronate group and Supplemented Buyang Huanwu Decoction group.The animals were sacrificed 7,14 and 28 days after the operation,Visual scoring was performed,and samples were taken from the injury site for hematoxylin-eosin staining and Masson staining,and scanning electron microscope to observe the morphology of peritoneal mesothelial cells in the modeling site.Immunohistochemical method was used to observe the expression of epithelial mesenchymal transition(EMT)related cell marker proteins E-cadherin and α-SMA in the adhesive site.Results ①Efficacy of Supplemented Buyang Huanwu Decoction in the prevention and treatment of postoperative abdominal adhesions:The Supplemented Buyang Huanwu Decoction group can reduce the Diamod visual adhesion score(P<0.05),as well as the adhesion levels of HE staining and Masson staining(P<0.05).②Degree of damage to peritoneal mesothelial cells:Scanning electron microscopy showed that in the field of view of the Supplemented Buyang Huanwu Decoction group,paving like peritoneal mesothelial cells could be seen,indicating that the Supplemented Buyang Huanwu Decoction can improve the damage of peritoneal mesothelial cells on the serosal side of the cecum in PAA.③Expression of Epithelial mesenchymal transition-related indicators:The expression of E-Cadherin protein in the Supplemented BuyangHuanwu Decoction group increased(P<0.05).The expression of α-SMA protein in the Supplemented Buyang Huanwu Decoction group decreased(P<0.05).Conclusion The effect of Supplemented Buyang Huanwu Decoction in the prevention and treatment of postoperative abdominal adhesions is exact,which mechanism may be by reducing Epithelial mesenchymal transition of peritoneal mesothelial cells,reducing the deposition of extracellular matrix,thereby reducing peritoneal adhesion.