OBJECTIVE To investigate the effects of jaceosidin on osteoarthritis （OA） of rats by regulating adenosine monophosphate-activated protein kinase （AMPK）/NOD-like receptor protein 3 （NLRP3） pathway. METHODS Rats were randomly separated into OA group， jaceosidin group （33.33 mg/kg）， AMPK inhibitor （Compound C， 20 mg/kg） group， jaceosidin （33.33 mg/kg）+Compound C （20 mg/kg） group， and sham operation group， with 12 rats in each group. Except for the sham operation group， the OA model was induced with modified Hulth method in all other groups. After successful modeling， they were given a relevant dose of jaceosidin or normal saline intragastrically， and Compound C or normal saline intraperitoneally， once a day， for consecutive 8 weeks. Twenty-four h after the last medication， the degree of knee joint swelling in rats from each group was measured. The pathological changes of the articular cartilage tissue in the knee joints， and the Mankin score were assessed. The levels of tumor necrosis factor-α （TNF-α）， interleukin-18 （IL-18）， and IL-6， as well as the protein expressions of collagen Ⅱ， aggrecan （ACAN）， and a disintegrin and metalloproteinase with thrombospondin 5 （ADAMTS5）， phosphorylated AMPK （p-AMPK）， AMPK， NLRP3， cleaved-caspase-1， and cleaved-IL-1β were detected in the articular cartilage tissue of rats’ knees. RESULTS Compared with OA group， the cartilage tissue defect of jaceosidin group was relieved， the cartilage matrix staining was deepened， and the number of chondrocytes was increased. Knee swelling， Mankin score， the levels of TNF- α， IL-18 and IL-6， and protein expressions of ADAMTS5， NLRP3， cleaved-caspase-1 and cleaved-IL-1β in knee cartilage were significantly decreased or down-regulated. Protein expressions of collagen Ⅱ， ACAN and phosphorylation level of AMPK were significantly increased or up-regulated （P＜0.05）. Compound C significantly reversed the improvement effects of jaceosidin on the above indexes of OA rats （P＜0.05）. CONCLUSIONS Jaceosidin may inhibit inflammation and extracellular matrix degradation in OA rats by regulating the AMPK/NLRP3 signaling pathway.

With the rapid development of social economy and the continuous improvement of human living standard, the incidence, fatality and recurrence rates of cardiovascular disease (CVD) are increasing year by year, which seriously affects people's life and health. Conventional therapeutic drugs have limited improvement on the disability rate, so the search for new therapeutic drugs and action targets has become one of the hotspots of current research. In recent years, the therapeutic role of the natural compound rosmarinic acid (RA) in CVD has attracted much attention, which is capable of preventing CVD by modulating multiple signalling pathways and exerting physiological activities such as antioxidant, anti-apoptotic, anti-inflammatory, anti-platelet aggregation, as well as anti-coagulation and endothelial function protection. In this paper, the role of RA in the prevention of CVD is systematically sorted out, and its mechanism of action is summarised and analysed, with a view to providing a scientific basis and important support for the in-depth exploration of the prevention value of RA in CVD and its further development as a prevention drug.

Osteoarthritis (OA) is one of the most prevalent joint disorders, with aging considered a primary, irreversible factor contributing to its progression. Telomere-related cellular senescence may be a crucial factor influencing the OA process, yet biomarkers for OA based on telomere-related genes have not been clearly identified. The datasets GSE51588, GSE12021, and GSE55457 were retrieved from the Gene Expression Omnibus database. Initially, R software was utilized to identify differentially expressed genes between OA and normal samples. Subsequently, differentially expressed telomere-related genes (DETMRGs) were obtained, and their functional enrichment was analyzed. Feature genes for OA diagnosis were selected from DETMRGs using a combination of least absolute shrinkage and selection operator, support vector machine-recursive feature elimination, and Random Forest algorithms. The diagnostic value of these feature genes was then validated through receiver operating characteristic (ROC) curves and decision curve analysis. Additionally, CIBERSORT and xCell were employed to assess the infiltration of immune cells in OA tissues.Finally, potential drugs targeting candidate genes were predicted. Three telomererelated genes, PGD, SLC7A5, and TKT, have been identified as biomarkers for OA diagnosis and were confirmed through ROC diagnostic tests. The immune infiltration of mast cells, neutrophils, common lymphoid precursors, and eosinophils associated with PGD, SLC7A5, and TKT was reduced. Recognizing telomere-related genes PGD, SLC7A5, and TKT as potential diagnostic biomarkers for OA is significant, as it offers valuable insights into the role of telomere-related genes in OA. This discovery also provides valuable information for the diagnosis and treatment of OA.

Osteoarthritis (OA) is one of the most prevalent joint disorders, with aging considered a primary, irreversible factor contributing to its progression. Telomere-related cellular senescence may be a crucial factor influencing the OA process, yet biomarkers for OA based on telomere-related genes have not been clearly identified. The datasets GSE51588, GSE12021, and GSE55457 were retrieved from the Gene Expression Omnibus database. Initially, R software was utilized to identify differentially expressed genes between OA and normal samples. Subsequently, differentially expressed telomere-related genes (DETMRGs) were obtained, and their functional enrichment was analyzed. Feature genes for OA diagnosis were selected from DETMRGs using a combination of least absolute shrinkage and selection operator, support vector machine-recursive feature elimination, and Random Forest algorithms. The diagnostic value of these feature genes was then validated through receiver operating characteristic (ROC) curves and decision curve analysis. Additionally, CIBERSORT and xCell were employed to assess the infiltration of immune cells in OA tissues.Finally, potential drugs targeting candidate genes were predicted. Three telomererelated genes, PGD, SLC7A5, and TKT, have been identified as biomarkers for OA diagnosis and were confirmed through ROC diagnostic tests. The immune infiltration of mast cells, neutrophils, common lymphoid precursors, and eosinophils associated with PGD, SLC7A5, and TKT was reduced. Recognizing telomere-related genes PGD, SLC7A5, and TKT as potential diagnostic biomarkers for OA is significant, as it offers valuable insights into the role of telomere-related genes in OA. This discovery also provides valuable information for the diagnosis and treatment of OA.

Osteoarthritis (OA) is one of the most prevalent joint disorders, with aging considered a primary, irreversible factor contributing to its progression. Telomere-related cellular senescence may be a crucial factor influencing the OA process, yet biomarkers for OA based on telomere-related genes have not been clearly identified. The datasets GSE51588, GSE12021, and GSE55457 were retrieved from the Gene Expression Omnibus database. Initially, R software was utilized to identify differentially expressed genes between OA and normal samples. Subsequently, differentially expressed telomere-related genes (DETMRGs) were obtained, and their functional enrichment was analyzed. Feature genes for OA diagnosis were selected from DETMRGs using a combination of least absolute shrinkage and selection operator, support vector machine-recursive feature elimination, and Random Forest algorithms. The diagnostic value of these feature genes was then validated through receiver operating characteristic (ROC) curves and decision curve analysis. Additionally, CIBERSORT and xCell were employed to assess the infiltration of immune cells in OA tissues.Finally, potential drugs targeting candidate genes were predicted. Three telomererelated genes, PGD, SLC7A5, and TKT, have been identified as biomarkers for OA diagnosis and were confirmed through ROC diagnostic tests. The immune infiltration of mast cells, neutrophils, common lymphoid precursors, and eosinophils associated with PGD, SLC7A5, and TKT was reduced. Recognizing telomere-related genes PGD, SLC7A5, and TKT as potential diagnostic biomarkers for OA is significant, as it offers valuable insights into the role of telomere-related genes in OA. This discovery also provides valuable information for the diagnosis and treatment of OA.

Osteoarthritis (OA) is one of the most prevalent joint disorders, with aging considered a primary, irreversible factor contributing to its progression. Telomere-related cellular senescence may be a crucial factor influencing the OA process, yet biomarkers for OA based on telomere-related genes have not been clearly identified. The datasets GSE51588, GSE12021, and GSE55457 were retrieved from the Gene Expression Omnibus database. Initially, R software was utilized to identify differentially expressed genes between OA and normal samples. Subsequently, differentially expressed telomere-related genes (DETMRGs) were obtained, and their functional enrichment was analyzed. Feature genes for OA diagnosis were selected from DETMRGs using a combination of least absolute shrinkage and selection operator, support vector machine-recursive feature elimination, and Random Forest algorithms. The diagnostic value of these feature genes was then validated through receiver operating characteristic (ROC) curves and decision curve analysis. Additionally, CIBERSORT and xCell were employed to assess the infiltration of immune cells in OA tissues.Finally, potential drugs targeting candidate genes were predicted. Three telomererelated genes, PGD, SLC7A5, and TKT, have been identified as biomarkers for OA diagnosis and were confirmed through ROC diagnostic tests. The immune infiltration of mast cells, neutrophils, common lymphoid precursors, and eosinophils associated with PGD, SLC7A5, and TKT was reduced. Recognizing telomere-related genes PGD, SLC7A5, and TKT as potential diagnostic biomarkers for OA is significant, as it offers valuable insights into the role of telomere-related genes in OA. This discovery also provides valuable information for the diagnosis and treatment of OA.

Osteoarthritis (OA) is one of the most prevalent joint disorders, with aging considered a primary, irreversible factor contributing to its progression. Telomere-related cellular senescence may be a crucial factor influencing the OA process, yet biomarkers for OA based on telomere-related genes have not been clearly identified. The datasets GSE51588, GSE12021, and GSE55457 were retrieved from the Gene Expression Omnibus database. Initially, R software was utilized to identify differentially expressed genes between OA and normal samples. Subsequently, differentially expressed telomere-related genes (DETMRGs) were obtained, and their functional enrichment was analyzed. Feature genes for OA diagnosis were selected from DETMRGs using a combination of least absolute shrinkage and selection operator, support vector machine-recursive feature elimination, and Random Forest algorithms. The diagnostic value of these feature genes was then validated through receiver operating characteristic (ROC) curves and decision curve analysis. Additionally, CIBERSORT and xCell were employed to assess the infiltration of immune cells in OA tissues.Finally, potential drugs targeting candidate genes were predicted. Three telomererelated genes, PGD, SLC7A5, and TKT, have been identified as biomarkers for OA diagnosis and were confirmed through ROC diagnostic tests. The immune infiltration of mast cells, neutrophils, common lymphoid precursors, and eosinophils associated with PGD, SLC7A5, and TKT was reduced. Recognizing telomere-related genes PGD, SLC7A5, and TKT as potential diagnostic biomarkers for OA is significant, as it offers valuable insights into the role of telomere-related genes in OA. This discovery also provides valuable information for the diagnosis and treatment of OA.

Ulcerative colitis （UC） is a chronic inflammatory bowel disease with complex etiology. The pathogenesis of this disease， due to a combination of factors， is complex and has not yet been elucidated. Among them， intestinal mucosal barrier damage is the basic pathological change of UC. As a non-destructive response of cells， autophagy regulates intestinal mucosal immunity， inflammation， oxidative stress， and bacterial homeostasis through degradation and reabsorption to actively repair damaged intestinal mucosal barrier， exerting a key role in the occurrence and development of UC. The disease is mainly treated clinically with aminosalicylic acid preparations， glucocorticoids， and immunosuppressants. Western medicine treatment of the disease has a fast onset of effect， and the short-term efficacy is definite， but the long-term application is easy to be accompanied by more adverse reactions. Moreover， some drugs are expensive， bringing great physical and mental pain and economic burden to patients. Therefore， it is urgent to explore new therapies with stable efficacy and mild adverse effects. In recent years， a large number of studies have shown that Chinese medicine can regulate autophagy of the intestinal mucosa with multiple targets and effects and repair the intestinal mucosal barrier function， thereby inhibiting the development of UC. Many experiments have shown that the active ingredient or monomers and compound formulas of Chinese medicine can improve the immunity of the intestinal mucosa， inflammation， oxidative stress， and flora by regulating the level of autophagy to maintain the normal function of the intestinal mucosal barrier to effectively intervene in UC， providing a new measure for the prevention and treatment of UC. However， there is a lack of systematic review of Chinese medicine in regulating the level of autophagy in the intestinal mucosa for the prevention and treatment of UC. Therefore， based on the current research on UC， autophagy process， and Chinese medicine treatment， this article reviewed the relationship of autophagy and its key target proteins with UC to clarify the key role of autophagy in UC production and systematically summarized Chinese medicines targeting the regulation of autophagy to treat UC in recent years to provide new ideas for the treatment and drug development of UC.

Objective To explore the effect and mechanism of microRNA-133a-3p(miR-133a-3p)on invasion and apoptosis of breast cancer cells through targeted regulation of cullin-associated NEDD8-dissociated 1(CAND1).Methods MCF-7 cells were divided into overexpression group(mimics miR-133 a-3p transfection),NC group(mimics control transfection),co-transfection group(mimics miR-133a-3p transfection with pcDNA-CAND1 co-transfection)and control group(only adding the same amount of transfection reagents).Flow cytometry was used to detect cell apoptosis,Transwell assay was used to detect cell invasion,and real-time fluorescence quantitative polymerase chain reaction was used to detect miR-133a-3p and CAND1 expression.Results After transfection,the expression levels of miR-133a-3p in control group,NC group,overexpression group and co-transfection group were 0.50±0.08,0.51±0.09,1.06±0.10 and 1.05±0.15,respectively;the expression of CAND1 mRNA were 0.91±0.09,0.91±0.07,0.80±0.10 and 1.21±0.10,respectively.There were statistically significant differences in the above indexes between the co-transfection group and the control group,the NC group(all P＜0.05),and there were statistically significant differences between the overexpression group and the control group,the NC group(all P＜0.05).The apoptosis rates in control group,NC group,overexpression group and co-transfection group were(7.88±1.62)％,(8.87±2.01)％,(53.41±5.46)％,(29.54±3.78)％,respectively.The number of invasive cells in control group,NC group,overexpression group and co-transfection group were 161.02±10.31,155.87±12.30,85.21±9.11 and 118.37±10.84,respectively.There were statistically significant differences in the above indexes between transfection group and overexpression group,control group and NC group(all P＜0.05),and there were statistically significant differences between overexpression group and control group and NC group(all P＜0.05).Conclusion Overexpression of miR-133a-3p in human breast cancer cells MCF-7 can inhibit CAND1 and promote apoptosis and invasion of MCF-7 cells.

Objective To study the effect of Hedysarum polysaccharides(HPS)on the farnisol X receptor(FXR)-small heterodimer chaperone(SHP)-sterol regulatory element-binding protein 1 c(SREBP-1c)signaling pathway in the non-alcoholic fatty liver disease cell model.Methods The cells were cultured with 1.2 mmol·L-1 fatty acids to construct the non-alcoholic fatty liver disease cell model.The cell were divided into normal group(complete medium),model group(1.2 mmol·L-1 fatty acid solution),positive control group(1.2 mmol·L-1 fatty acid solution+50 μmol·L-1 alpha-lipoic acid)and experimental group(1.2 mmol·L-1 fatty acid solution+80 mg·L-1 HPS),culture for 24 h.The content of triglyceride(TG)and total cholesterol(TC),the activity of glutamate transaminase(GOT)and glutamate transaminasewas(GPT)detected by GPO-PAP enzyme method;the apoptosis rate was detected by flow cytometry;the expressions of FXR,SHP,SREBP-1c protein and mRNA in hepatocytes were detected by Western blot and reverse transcription-polymerase chain reaction(RT-PCR).Results The contents of TG in hepatocytes of normal group,model group,positve control group and experimental group were(2.91±1.13),(6.81±1.32),(3.72±0.52)and(4.67±0.62)mmol·gprot-1;the contents of TC in these four groups were(23.66±4.92),(67.96±5.56),(29.41±4.22)and(54.34±3.96)mmol·gprot-1;the activity of GOT in these four groups were(249.10±11.59),(322.63±28.81),(288.89±19.14)and(266.91±8.77)U·gprot-1;the activity of GPT in these four groups were(58.83±16.88),(134.55±22.96),(89.63±15.81)and(77.37±7.25)U·gprot-1,respectively;FXR mRNA expression levels were 1.01±0.16,2.09±0.12,1.83±0.17 and 1.45±0.15,respectively;SHP mRNA expression levels were 1.00±0.11,0.51±0.15,0.64±0.14 and 0.70±0.14,respectively;SREBP-1c mRNA were 1.00±0.08,1.57±0.19,1.37±0.13 and 1.21±0.15;the expression levels of FXR protein were 1.00±0.02,1.63±0.03,1.42±0.02 and 1.25±0.03,respectively;the expression levels of SHP protein were 1.00±0.02,0.23±0.01,0.54±0.21 and 0.62±0.02;the expression levels of SREBP-1c protein were 1.00±0.03,4.08±0.05,1.99±0.02 and 1.48±0.01,respectively.Compared with the normal group,there were significant differences in the above indexes of model group(all P＜0.05);compared with the model group,there were significant differences in the above indexes of experimental group(all P＜0.05).Conclusion HPS may protect liver cells by regulating the FXR-SHP-SREBP-1 c signaling pathway,reducing lipid synthesis in liver cells.