[Objective]To study the expression of Cathepsin B,Caspase-3 and to explore the significance of their expression initially after acute spinal cord injury in rats.[Method]The spinal cord injury of the healthy adult SD rats (78) was induced with Nystrom’s way by the moderate compression at the level of T8 and T9 spinal cord. HE methods were used to detect the pathologic change of spinal cord. The expression of Cathepsin B and Caspase-3 were detected by immunohistochemical study. Besides,using the terminal deoxynucleotidyl transferase mediated DUTP nick and labeling (TUNEL) methods to detect the level of the apoptosis of neural cells.[Result]There were few expressions of Cathepsin B, Caspase-3 and TUNEL positive cells in normal and sham operated spinal cord as detected by immunohistochemical study. The number of positive cells of Cathepsin B increased clearly at 3 days,reached a peak at 5 days,and was constant at 7 days after injury. While the expression of Caspase-3 increased obviously at 8 hours,got to a peak at 3 days,and was lowest at 7 days. And the number of positive cells of TUNEL also increased obviously at 8 hours,got to a peak at 3 days,and was lowest at 7 days. There were significance differences of morphological and position of positive cells between Cathepsin B and Caspase-3 or Tunel. [Conclusion]Caspase-3 protein expressions are enhanced in combination with neuronal apoptosis,while Cathepsin B may involve in the secondary injury by inflammatory cells after acute spinal cord injury.

Objective To study the effects of uhrashortwave and low frequency pulsed electromagnetic fields on the expression of vascular endothelial growth factor(VEGF) in fracture healing. Methods Fifty-six New Zeal-and rabbits with artificial fractures were randomly divided into 4 groups:a control group,an ultrashortwave group,a low frequency pulsed electromagnetic field group and an ultrashortwave combined with low frequency pulsed electro-magnetic field group(combined group),with 14 in each group.Radiographic evaluation of callus formation and frac-ture healing,pathohistological examination and detection of VEGF expression through immunohistochemical staining were performed at the 1 st,2nd,4th and 6th week after the operation. Results Radiographic examination showed that there was significantly greater callus formation in the combined group than in the other groups throughout the healing process. Pathohistological examination also revealed significantly more cartilage islets and callus formation in the combined group.At the 1 st,2nd and 4th week after the operation,VEGF positive indexes in the combined group were significantly higher than in the other groups. Conclusion Uhrashortwave combined with low frequency pulsed electromagnetic field exposure can up-regulate the expression of VEGF and thus can accelerate fracture healing.

Objective To analyze the whole genomic DNA methylation level and estrogen receptor α (ERα) gene promoter methylation status in systemic lupus erythematosus (SLE) with atherosclerosis (AS) in model mouse,and to explore its role in the pathogenesis of SLE with AS.Methods Eleven apoE-/-C57BL/6 mice were randomly divided into the model group (SLE+AS group) and the control group (AS group).Eleven wild C57BL/6 mice were also randomly divided into the model group (SLE group) and the control group (blank group).Single intraperitoneal injection of pristane 0.5 ml for the model group,single intraperitoneal injection of normal saline 0.5 ml for the control group.Eight months after injection,all mice were sacrificed,genomic DNA was extracted from spleen.The total genomic DNA methylation level was detected,and pyrosequencing was performed to determine the methylation status of ERα gene promoter.The differences between groups were compared.ANOVA,LSD-t test,Tamhane's T2 test were used for statistical analysis.Results The total genomic DNA methylation levels were (4.7±1.5)％,(5.1±0.5)％,(6.6±1.6)％,(7.5±1.6)％ respectively in the SLE+AS group,AS group,SLE group,blank group respectively,the average methylation indices of ERα gene promoter were (13.0±3.1)％,(26.7±7.2)％,(15.7±3.8)％ and (21.4±4.2)％ respectively.The total genomic DNA methylation level and the average methylation index of ERα gene promoter in the SLE+AS group and the SLE group was significantly lower than that of the blank group (P＜0.05).Compared with the AS group,the total genomic DNA methylation levels and the average methylation index of ERα gene promoter in the SLE+AS group were significantly decreased (P＜0.05).Conclusion The total genomic DNAs and the ERα gene promoters in SLE with AS model mouse are in low-methylation status.The results of this study suggest that epigenetics may play an important role in the pathogenesis of SLE with AS.

Mitochondria are the main site of energy metabolism within cells,generating a substantial amount of ATP to supply energy to the human body.Research has shown that alterations in mitochondrial structure and function exist in individuals with schizophrenia,suggesting their potential impact on the onset of psychiatric disorders and clinical treatment efficacy.Therefore,understanding the research progress on the genetic mechanisms,pathological processes,image manifestations of schizophrenia and mitochondrial quality control,and summarizing the relevant evidence of mitochondrial-related targets as potential therapeutic targets for schizophrenia,can provide references for further research.

Schizophrenia is a common chronic mental disorder.Cognitive dysfunction is one of its core symptoms,which severely affects the social functioning of patients.Currently,antipsychotic medication treatments have poor efficacy in improving cognitive functions.Recent studies have found that metformin can improve cognitive dysfunction in patients with schizophrenia.However,the mechanism of action remains unclear.This review summarizes the therapeutic effects of metformin on cognitive dysfunction in schizophrenia patients such as improving insulin resistance,repairing neuronal damage,regulating neuroimmunity,and combating oxidative stress,thereby providing new insights for the treatment of cognitive dysfunction in schizophrenia.

ObjectiveIn this study， based on ultra-high performance liquid chromatography-mass spectrometry（UHPLC-MS/MS） and high-throughput transcriptome sequencing technology（RNA-seq）， we investigated the mechanism of Yishen Huashi granules in regulating serum metabolites and renal messenger ribonucleic acid（mRNA） expression to improve diabetic kidney disease（DKD）. MethodSD rats were randomly divided into normal group ， model group and Yishen Huashi granules group， with 8 rats in each group. The rat model of DKD was established by intraperitoneal injection of streptozotocin. Yishen Huashi granules group was given 5.54 g·kg^-1·d^-1 of Yishen Huashi granules by gavage， and the normal group and the model group were given the same amount of normal saline for 6 weeks. During the experiment， the body weight and blood glucose of rats were monitored， and the rats were anesthetized 24 hours after the last administration， blood was collected from the inferior vena cava， serum was separated， and renal function， blood lipid， and inflammatory indicators were detected. Kidney tissue of rats was fixed in neutral paraformaldehyde， and stained with hematoxylin-eosin（HE）， Masson and periodic acid-Schiff（PAS） to observe the renal pathological changes. UHPLC-MS/MS and RNA-seq were used to identify the changes of serum metabolism and the differences of renal mRNA expression， and real time fluorescence quantitative polymerase chain reaction（Real-time PCR） and Western blot were used to detect the differential mRNA and protein expression in renal tissue to explore the common expression mechanism. ResultCompared with the normal group， rats in the model group showed a decrease in body weight， a significant increase in blood glucose， urinary microalbumin to urinary creatinine ratio（UACR）， blood urea nitrogen（BUN）， cystatin-C（Cys-C）， β₂-microglobulin（β₂-MG）， interleukin-6（IL-6）， triglyceride（TG） and total cholesterol（TC）， and a significant decrease in total superoxide dismutase（T-SOD）（P<0.01）. After the intervention of Yishen Huashi granules， all the indexes were improved to different degrees in rats（P<0.05， P<0.01）. Compared with the normal group， the model group showed renal mesangial stromal hyperplasia， fibrous tissue hyperplasia and tubular vacuolar degeneration. Compared with the model group， the renal pathology of rats in Yishen Huashi granules group was improved to a certain extent. A total of 14 target metabolites and 96 target mRNAs were identified， the target metabolites were mainly enriched in 20 metabolic pathways， including sphingolipid metabolism， glycerophospholipid metabolism， and the biosynthesis of phenylalanine， tyrosine and tryptophan. The target mRNAs were enriched to obtain a total of 21 differential mRNAs involved in the TOP20 pathways closely related to glycolipid metabolism. A total of 6 pathways， glycerophospholipid metabolism， arachidonic acid metabolism， purine metabolism， primary bile acid biosynthesis， ascorbic acid and uronic acid metabolism， and galactose metabolism， were enriched by serum differential metabolites and renal differential mRNAs， among them， there were 7 differential metabolites such as phosphatidylethanolamine（PE） and 7 differential mRNAs such as recombinant adenylate cyclase 3（ADCY3）. Seven differential metabolites had high predictive accuracy as verified by receiver operating characteristic（ROC） curve， and the results of Real-time PCR and Western blot were highly consistent with the sequencing results. ConclusionYishen Huashi granules can reduce UACR， BUN and other biochemical indexes， correct the disorder of glucose and lipid metabolism， and improve renal function of DKD rats. And its mechanism may be related to the regulation of the level of PE and other blood metabolites， and expression of Phospho1 and other mRNAs in the kidney， of which six pathways， including glycerophospholipid metabolism， may play an important role.

Renal fibrosis， the final pathological outcome of end-stage chronic kidney diseases， is associated with inflammation， oxidative stress， epithelial-mesenchymal transdifferentiation （EMT）， and extracellular matrix deposition. It belongs to the categories of edema， ischuria， anuria and vomiting， and consumptive disease in traditional Chinese medicine （TCM）， with the key pathogenesis of Qi deficiency and blood stasis and the primary treatment principle of replenishing Qi and activating blood. Astragali Radix-Salviae Miltiorrhizae Radix et Rhizoma mainly contains astragalosides， polysaccharides， calycosin， salvianolic acid， and tanshinone， with the effect of tonifying Qi and activating blood. Studies have shown that this herb pair and its active components can delay the progress of renal fibrosis by regulating multiple signaling pathways. With consideration to the pathogenesis of Qi deficiency and blood stasis， this article reviews the research progress in the mitigation of renal fibrosis by Astragali Radix-Salviae Miltiorrhizae Radix et Rhizoma from the aspects of protecting glomerular filtration barrier， inhibiting EMT and mesangial cell proliferation， improving renal hemodynamics， and protecting renal function. Furthermore， the mechanisms were summarized. Specifically， Astragali Radix-Salviae Miltiorrhizae Radix et Rhizoma and its effective components can improve mitochondrial function and fatty acid metabolism， alleviate endoplasmic reticulum stress and autophagy disorders， and inhibit immune inflammation and oxidative stress by regulating nuclear factor E₂-related factor 2 （Nrf2）/PTEN-induced kinase 1 （Pink1）， Nrf2/antioxidant response element （ARE）， tumor necrosis factor-α （TNF-α）/nuclear transcription factor-κB （NF-κB）， miR-21/Smad7/transforming growth factor beta （TGF-β）， Wnt/β-catenin， long non-coding RNA-taurine up-regulated gene 1 （lncRNA-TUG1）/tumor necrosis factor receptor-associated factor 5 （TRAF5）， Ras-related C3 botulinum toxin substrate 1 （Rac1）/cell division cycle protein 42 （CDC42）， Ras homolog （Rho）/Rho-associated coiled-coil containing protein kinase （ROCK）， phosphatidylinositol-3-kinase （PI3K）/protein kinase B （Akt）， Janus kinase （JAK）/signal transducer and activator of transcription （STAT）， peroxisome proliferator-activated receptor α （PPARα）/peroxisome proliferator-activated receptor γ coactivator l alpha （PGC-1α）， and p38 mitogen-activated protein kinase （p38 MAPK）. This review aims to provide references for the relevant research， give play to the role of Astragali Radix-Salviae Miltiorrhizae Radix et Rhizoma， and provide guidance for the clinical treatment of renal fibrosis.