Objective The objective of this study was to explore the effect of knocking down CXCL8 on the efficacy of pacli-taxel chemotherapy in cervical squamous cell carcinoma and to investigate its potential mechanism of action.Methods The Hela cell model was used to specifically inhibit CXCL8 gene expression through lentivirus-mediated RNA interference(RNAi)technology.The optimal transfection conditions were HitransG P and a multiplicity of infection(MOI)of 100.The CCK-8 assay was used to screen the optimal intervention concentration of puromycin as 1.5μg/mL.The LV-CXCL8-RNAi(3 targets)and negative control lentivirus were transfected into cells under optimal transfection conditions and set up a blank control group.The qRT-PCR assay was used to select the sh-CXCL8-13 group lentivirus as the intervention sequence and virus for subsequent experiments.The experiments were divided into the blank control group,negative control group,sh-CXCL8 group,paclitaxel group,and sh-CXCL8+paclitaxel group.The prolifer-ative activity and invasive ability of cervical cancer cells were assessed by CCK-8 and cell invasion assays.The expression of CXCL8,Bcl2,Bax,and β-actin were detected by qRT-PCR and Western blot.Results Compared with the other four groups,the proliferative and invasive ability of Hela cells was significantly reduced in the sh-CXCL8+paclitaxel group,and the difference was statistically sig-nificant(P<0.01).The qRT-PCR results showed that the expression of CXCL8,Bcl2,PIK3CB,and Akt1 genes was significantly re-duced,and the expression of Bax gene was significantly increased in the sh-CXCL8+paclitaxel group.The difference between the groups was statistically significant(P<0.001).The results of Western blot showed that the expression of CXCL8,PIK3CB,and p-Akt1 proteins was reduced in the sh-CXCL8+paclitaxel group(P<0.05).Conclusion Knocking down CXCL8 can reduce the prolif-erative and invasive capacity of Hela cells,possibly by affecting the PI3K/Akt pathway to affect the drug sensitivity of Hela cells to paclitaxel.

BACKGROUND:Osteoarthritis is a degenerative disease characterized by cartilage degeneration and abnormal bone remodeling of subchondral bone.In recent years,many studies have shown that stromal cell diffracting factor-1 plays a key role in the pathological progression of osteoarthritis.Targeted regulation of stromal cell-derived factor-1 and its CXC chemokine receptor 4 and CXC chemokine receptor 7 signaling pathways is a new method for prevention and treatment of osteoarthritis.OBJECTIVE:To review the role of stromal derived factor-1 in regulating the proliferation,differentiation,and apoptosis of chondrocytes,bone marrow mesenchymal stem cells,osteoblasts,and osteoclasts,as well as explore the mechanism by which the interaction of these cells leads to cartilage degeneration and abnormal bone remodeling of subchondral bone and accelerates the pathological progression of osteoarthritis,in order to provide new ideas for the prevention and treatment of osteoarthritis.METHODS:CNKI,WanFang Data,and VIP,were searched with Chinese search terms"stromal cell-derived factor 1,cartilage,chondrocytes,subchondral bone,bone marrow mesenchymal stem cells,osteoblasts,osteoclasts,CXC chemokine receptor 4,CXC chemokine receptor 7."PubMed,Medline,and Embase databases were searched with English search terms"stromal cell-derived factor 1,SDF-1,CXCL12,cartilage,chondrocyte,subchondral bone,mesenchymal stem cells,osteoblasts,osteoclasts,CXCR4,CXCR7."Literature retrieval time was from inception to January 2024.A total of 77 articles were included and summarized in accordance with the inclusion and exclusion criteria.RESULTS AND CONCLUSION:(1)Stromal cell-derived factor-1 regulates the migration,proliferation,differentiation,and death of chondrocytes,bone marrow mesenchymal stem cells,osteoblasts,and osteoclasts,which plays an important role in maintaining cartilage and subchondral bone homeostasis,promoting or inhibiting cartilage degeneration and abnormal bone remodeling in osteoarthritis.Targeted regulation of stromal cell-derived factor-1/CXC chemokine receptor type 4/CXC chemokine receptor type 7 signaling pathway is expected to become the focus of future research on the prevention and treatment of osteoarthritis.(2)Because of the difference in the expression of stromal cell-derived factor-1 subtypes in tissues,stromal cell-derived factor-1 α is the most widely studied at present.The related studies of stromal cell-derived factor-1β and stromal cell-derived factor-1y are mainly focused on exploring the effects on the biological behavior of stem cells,the role in the regulation of cartilage and subchondral bone homeostasis,and the correlation with osteoarthritis.(3)Stromal cell-derived factor-1 can effectively promote stem cells homing to cartilage injury sites,and induce their proliferation,survival,and cartilage differentiation.The application of stromal cell-derived factor-1-loaded biological scaffolds to improve the quality of cartilage repair has become the focus of cartilage tissue engineering research.However,previous studies have shown that stromal cell-derived factor-1 can promote the differentiation of bone marrow mesenchymal stem cells into hypertrophic chondrocytes,while the hypertrophic phenotype of newborn chondrocytes can lead to endochondral bone formation and chondrocyte apoptosis.The whole tissue is vascularized and ossified,which affects the quality of cartilage repair.In addition,when different scaffolds combined with stromal cell-derived factor-1 can repair partial cartilage injury and full-thickness cartilage injury,the regenerated tissue is not all ideal hyaline cartilage tissue.Therefore,in the future,in-depth exploration of the potential mechanism of stromal cell-derived factor-1 in stem cell biological effects and the best combination of stromal cell-derived factor-1 and scaffold in repairing different cartilage defects will help to improve the quality of cartilage repair.(4)The studies on CXC chemokine receptor 4 antagonists are mainly focused on AMD3100,T140 and TN14003,and most of them are in the basic experimental stage and need to be transformed into clinical practice.The safety and effectiveness of the therapeutic drugs developed for stromal cell-derived factor-1/CXC chemokine receptor 4/CXC chemokine receptor 7 signaling pathway still need a large number of biological and clinical trials to support.

Objective To assess the expression of CXCL8 in cervical cancer and its association with clinicopathological features and therapeutic efficacy of patients.Methods Bioinformatic analysis was performed using The Cancer Genome Atlas and Genotype-Tissue Expression databases to compare CXCL8 expression between cervical cancer and normal tissues.R software(version 4.4.0)was used for data analysis,with the timeROC package applied to construct time-dependent receiver operating characteristic(ROC)curves for evalua-ting the prognostic predictive efficacy of CXCL8.The survival package with the survfit function was used to compare survival differences between CXCL8 high-and low-expression groups.Clinical data and tissue specimens were collected from 94 patients with cervical squa-mous cell cancer treated at The First Affiliated Hospital of Xinjiang Medical University between January 2017 and December 2021.Immu-nohistochemical staining was used to detect CXCL8 expression levels and analyze its correlation with clinicopathological characteristics,therapeutic efficacy,and prognosis.Results Bioinformatic analysis showed that CXCL8 was highly expressed in cervical cancer tissues than in normal tissues(P＜0.05).Time-dependent ROC curves and survival analyses showed that patients with high CXCL8 expression had significantly shorter overall survival than those with low CXCL8 expression(P＜0.001).Immunohistochemical results showed that CXCL8 expression in cervical cancer tissues was significantly higher than that in adjacent tissues(P＜0.000 1).Clinical correlation analy-sis revealed that CXCL8 expression levels were associated with treatment regimen(P＜0.001)and short-term therapeutic efficacy(P=0.017).Compared to the low-expression group,the high-expression group showed a significantly lower therapeutic efficacy and shorter overall survival(P＜0.05).Conclusion CXCL8 is highly expressed in cervical cancer tissues,and patients with high CXCL8 expression have poor prognosis.Thus,CXCL8 may be an effective target for assessing the prognosis and clinical treatment of cervical cancer.

Objective To assess the expression of CXCL8 in cervical cancer and its association with clinicopathological features and therapeutic efficacy of patients.Methods Bioinformatic analysis was performed using The Cancer Genome Atlas and Genotype-Tissue Expression databases to compare CXCL8 expression between cervical cancer and normal tissues.R software(version 4.4.0)was used for data analysis,with the timeROC package applied to construct time-dependent receiver operating characteristic(ROC)curves for evalua-ting the prognostic predictive efficacy of CXCL8.The survival package with the survfit function was used to compare survival differences between CXCL8 high-and low-expression groups.Clinical data and tissue specimens were collected from 94 patients with cervical squa-mous cell cancer treated at The First Affiliated Hospital of Xinjiang Medical University between January 2017 and December 2021.Immu-nohistochemical staining was used to detect CXCL8 expression levels and analyze its correlation with clinicopathological characteristics,therapeutic efficacy,and prognosis.Results Bioinformatic analysis showed that CXCL8 was highly expressed in cervical cancer tissues than in normal tissues(P＜0.05).Time-dependent ROC curves and survival analyses showed that patients with high CXCL8 expression had significantly shorter overall survival than those with low CXCL8 expression(P＜0.001).Immunohistochemical results showed that CXCL8 expression in cervical cancer tissues was significantly higher than that in adjacent tissues(P＜0.000 1).Clinical correlation analy-sis revealed that CXCL8 expression levels were associated with treatment regimen(P＜0.001)and short-term therapeutic efficacy(P=0.017).Compared to the low-expression group,the high-expression group showed a significantly lower therapeutic efficacy and shorter overall survival(P＜0.05).Conclusion CXCL8 is highly expressed in cervical cancer tissues,and patients with high CXCL8 expression have poor prognosis.Thus,CXCL8 may be an effective target for assessing the prognosis and clinical treatment of cervical cancer.

BACKGROUND:Osteoarthritis is a degenerative disease characterized by cartilage degeneration and abnormal bone remodeling of subchondral bone.In recent years,many studies have shown that stromal cell diffracting factor-1 plays a key role in the pathological progression of osteoarthritis.Targeted regulation of stromal cell-derived factor-1 and its CXC chemokine receptor 4 and CXC chemokine receptor 7 signaling pathways is a new method for prevention and treatment of osteoarthritis.OBJECTIVE:To review the role of stromal derived factor-1 in regulating the proliferation,differentiation,and apoptosis of chondrocytes,bone marrow mesenchymal stem cells,osteoblasts,and osteoclasts,as well as explore the mechanism by which the interaction of these cells leads to cartilage degeneration and abnormal bone remodeling of subchondral bone and accelerates the pathological progression of osteoarthritis,in order to provide new ideas for the prevention and treatment of osteoarthritis.METHODS:CNKI,WanFang Data,and VIP,were searched with Chinese search terms"stromal cell-derived factor 1,cartilage,chondrocytes,subchondral bone,bone marrow mesenchymal stem cells,osteoblasts,osteoclasts,CXC chemokine receptor 4,CXC chemokine receptor 7."PubMed,Medline,and Embase databases were searched with English search terms"stromal cell-derived factor 1,SDF-1,CXCL12,cartilage,chondrocyte,subchondral bone,mesenchymal stem cells,osteoblasts,osteoclasts,CXCR4,CXCR7."Literature retrieval time was from inception to January 2024.A total of 77 articles were included and summarized in accordance with the inclusion and exclusion criteria.RESULTS AND CONCLUSION:(1)Stromal cell-derived factor-1 regulates the migration,proliferation,differentiation,and death of chondrocytes,bone marrow mesenchymal stem cells,osteoblasts,and osteoclasts,which plays an important role in maintaining cartilage and subchondral bone homeostasis,promoting or inhibiting cartilage degeneration and abnormal bone remodeling in osteoarthritis.Targeted regulation of stromal cell-derived factor-1/CXC chemokine receptor type 4/CXC chemokine receptor type 7 signaling pathway is expected to become the focus of future research on the prevention and treatment of osteoarthritis.(2)Because of the difference in the expression of stromal cell-derived factor-1 subtypes in tissues,stromal cell-derived factor-1 α is the most widely studied at present.The related studies of stromal cell-derived factor-1β and stromal cell-derived factor-1y are mainly focused on exploring the effects on the biological behavior of stem cells,the role in the regulation of cartilage and subchondral bone homeostasis,and the correlation with osteoarthritis.(3)Stromal cell-derived factor-1 can effectively promote stem cells homing to cartilage injury sites,and induce their proliferation,survival,and cartilage differentiation.The application of stromal cell-derived factor-1-loaded biological scaffolds to improve the quality of cartilage repair has become the focus of cartilage tissue engineering research.However,previous studies have shown that stromal cell-derived factor-1 can promote the differentiation of bone marrow mesenchymal stem cells into hypertrophic chondrocytes,while the hypertrophic phenotype of newborn chondrocytes can lead to endochondral bone formation and chondrocyte apoptosis.The whole tissue is vascularized and ossified,which affects the quality of cartilage repair.In addition,when different scaffolds combined with stromal cell-derived factor-1 can repair partial cartilage injury and full-thickness cartilage injury,the regenerated tissue is not all ideal hyaline cartilage tissue.Therefore,in the future,in-depth exploration of the potential mechanism of stromal cell-derived factor-1 in stem cell biological effects and the best combination of stromal cell-derived factor-1 and scaffold in repairing different cartilage defects will help to improve the quality of cartilage repair.(4)The studies on CXC chemokine receptor 4 antagonists are mainly focused on AMD3100,T140 and TN14003,and most of them are in the basic experimental stage and need to be transformed into clinical practice.The safety and effectiveness of the therapeutic drugs developed for stromal cell-derived factor-1/CXC chemokine receptor 4/CXC chemokine receptor 7 signaling pathway still need a large number of biological and clinical trials to support.

Objective The objective of this study was to explore the effect of knocking down CXCL8 on the efficacy of pacli-taxel chemotherapy in cervical squamous cell carcinoma and to investigate its potential mechanism of action.Methods The Hela cell model was used to specifically inhibit CXCL8 gene expression through lentivirus-mediated RNA interference(RNAi)technology.The optimal transfection conditions were HitransG P and a multiplicity of infection(MOI)of 100.The CCK-8 assay was used to screen the optimal intervention concentration of puromycin as 1.5μg/mL.The LV-CXCL8-RNAi(3 targets)and negative control lentivirus were transfected into cells under optimal transfection conditions and set up a blank control group.The qRT-PCR assay was used to select the sh-CXCL8-13 group lentivirus as the intervention sequence and virus for subsequent experiments.The experiments were divided into the blank control group,negative control group,sh-CXCL8 group,paclitaxel group,and sh-CXCL8+paclitaxel group.The prolifer-ative activity and invasive ability of cervical cancer cells were assessed by CCK-8 and cell invasion assays.The expression of CXCL8,Bcl2,Bax,and β-actin were detected by qRT-PCR and Western blot.Results Compared with the other four groups,the proliferative and invasive ability of Hela cells was significantly reduced in the sh-CXCL8+paclitaxel group,and the difference was statistically sig-nificant(P<0.01).The qRT-PCR results showed that the expression of CXCL8,Bcl2,PIK3CB,and Akt1 genes was significantly re-duced,and the expression of Bax gene was significantly increased in the sh-CXCL8+paclitaxel group.The difference between the groups was statistically significant(P<0.001).The results of Western blot showed that the expression of CXCL8,PIK3CB,and p-Akt1 proteins was reduced in the sh-CXCL8+paclitaxel group(P<0.05).Conclusion Knocking down CXCL8 can reduce the prolif-erative and invasive capacity of Hela cells,possibly by affecting the PI3K/Akt pathway to affect the drug sensitivity of Hela cells to paclitaxel.

Objective To explore the clinical features of critical cases of coronavirus disease 2019 (COVID-19). Methods The clinical data of nine patients who were diagnosed with critical COVID-19 in Hainan General Hospital from January 21, 2020 to February 6, 2020 were retrospectively analyzed. RT-PCR testing for 2019 novel coronavirus (2019-nCoV) was performed with multi-sites synchronize specimens including pharyngeal swab, blood, excrement, and urine. The serum levels of leucocyte, C-reactive protein, procalcitonin and lactic acid between the improved group (five cases) and the deteriorated group (four cases) were compared. The t test was used for comparison of normally distributed continuous data between groups. Results There were eight males (88.9%) and 1 female enrolled. The patients aged 28-77 years old, with an age of (52.9±18.0) years. By March 4, 2020, all five cases in improved group were cured and discharged, three cases in deteriorated group died and 1case remained in critical condition. All multi-sites specimens of patients in improved group turned negative in 2-4 weeks of illness onset, while those of cases in deteriorated group showed sustained viral nucleic acid positive (up to 48th day of illness onset). The white blood cell counts ((13.52±8.24)×10 9 /L vs (10.49±4.46) ×10 9 /L), C-reactive protein ((139.71±87.46) mg/L vs (78.60±55.40) mg/L) and procalcitonin ((2.32±4.03) ng/mL vs (0.28±0.58) ng/mL) , lactic acid ((3.70±4.14) mmol/L vs (2.33±0.53) mmol/L) in deteriorated group were all significantly higher than those in improved group ( t =2.908, 5.009, 4.391 and 2.942, respectively, all P <0.01). A rapid rise of serum IL-6 level up to 8 500 pg/mL was observed in one patient three days prior to death. Conclusion Among the patients with critical COVID-19, serum levels of inflammatory cytokines of the death cases are higher than those of improved and discharged cases.

Objective To investigate the effect ofmiR-27a-3p on proliferation,apoptosis and cell cycle of hepatoma cells.Methods A quantitative real-time polymerase chain reaction (qPCR) was used to detect differential expression of miR-27a-3p in normal hepatic epithelial cells (L02) and hepatoma cells (HepG2 and PLC).Cell experiment was divided into four groups:HepG2 overexpression cells,Mi-27a-3p overexpression group (Mi-27a) and negative control group (Mi-Con);PLC knockdown cells,Mi-27a-3p knockdown group (Miinhibitor-27a) and negative control group (Mi-inhibitor-Con).The expression of microRNA-27a-3p in each group after transfection was detected by qPCR analysis.MTT assay was used to detect the cell proliferation.Flow cytometry was used to detect the apoptosis and cell cycle.One-way ANOVA was used for multiple comparisons,and t-test was used to compare two groups.Results qPCR results showed that the expression levels of miR27a-3p in L02,HepG2 and PLC increased sequentially,and the relative expression levels were 1.07 ± 0.04,4.81 ± 0.64 and 11.31 ± 0.92,respectively (P ＜ 0.05).MTT assay showed that the cell viability of HepG2 cells transfected with miR-27a-3p overexpression plasrnid was significantly deereased compared with the negative control group (P ＜ 0.05).The apoptosis assay showed that the apoptosis rate of miR-27a-3p overexpression group was higher than the negative control group (P ＜ 0.05).The cell cycle results showed that the proportion of S phase cells in the miR-27a-3p overexpression cell group was significantly lower than the negative control group (P ＜ 0.05).Furthermore,microRNA-27a-3p knockdown validation in PLC cells showed that MTT,apoptosis and cell cycle tests results were opposite to the results of HepG2 overexpression cells,and the differences were statistically significant (P ＜ 0.05).Conclusion miR-27a-3p can significantly inhibit the proliferation of hepatoma cells,promote cell apoptosis,alter the cell cycle distribution,and may become a potential target in hepatocellular carcinoma therapy.

Objective To observe the effects of Coix seed injection on the cell viability and radiosensitivity of human hepatoma cell line Bel-7402.Methods Bel-7402 cells were irradiated by X-rays,or treated with Coix seed injection,or treated with both of them.The cells proliferation and apoptosis were detected by MTT and by flow cytometry respectively.Cell cloning was used to observe the number of viable cells and to draw the cell survival curve.The mRNA and protein level of Bax,Bcl-2 were detected by RT-PCR and Western blot respectively.Results It was found that the Coix seed injection group (12 μmol/L) and X-ray group (8 Gy) had a significant inhibitory effect on the growth of hepatocellular carcinoma cells (t =17.03,11.26,P ＜ 0.05).And compared with Coix group and irradiation group,the combined treatment group showed higher inhibition rate (t =24.80,20.19,P ＜0.05).The mRNA and protein levels of Bax were gradually elevated (F =437.92,67.91,P ＜ 0.05),while the expressions of Bcl-2 reflected a decreased trend (F =31.18,48.50,P ＜ 0.05).The D0 values of pure irradiation group and combined treatment group were 4.27 and 3.34,respectively,and the sensitization enhancement ratio was 1.27.Conclusions The Coix seed injection inhibit cell growth and induce apoptosis,as well as increase radiative sensitization may via the apoptosis related factors Bax and Bcl-2 in hepatocellular carcinoma.

Objective To study the effect of corrected TIMI frame count (CTFC) of infarction related artery on systolic function of infarct area of myocardium after primary percutaneous coronary intervention (PCI) in patients with acute myocardial infarction (AMI). Methods One hundred and six patients with AMI having undergone successful PCI in Cangzhou Central Hospital were selected, and they were divided into two groups (each, 53 cases). The standard of fast or slow flow was in accord to the CTFC of infarction related artery (IRA) measured soon after successful PCI. The patients with greater value of CTFC were enrolled in the slow flow group, while the patients with smaller such value were assigned in the fast flow group. At 6, 12, 24 and 48 hours after PCI, the venous plasma MB isoenzyme of creatine kinase (CK-MB) level was measured. And at 1 week, 1 month and 3 months after PCI, the left ventricular ejection fraction (LVEF) was measured by cardiac ultrasound, and the levels of radial strain (RS) and longitudinal strain (LS) of the infarct area were measured via speckle tracking imaging (STI). The differences in CTFC, CK-MB, RS and LS between the two groups were analyzed, and the correlations between the strains and CTFC, CK-MB were analyzed by Pearson linear correlation method. Results After successful PCI, the CK-MB of fast flow group was higher than that of the slow flow group at 6 hours. However, the CK-MB of slow flow group was higher than that of the fast flow group after 12 hours, appearing separate phenomenon, and the statistical significance occurred beginning from 24 hours after PCI (U/L, 24 hours:98.43±11.65 vs. 86.43±18.97, 48 hours:51.09±8.94 vs. 49.80±6.92, both P<0.05). CTFC in fast flow group was significantly lower than that of slow flow group (frame: 22.69±4.83 vs. 26.14±5.67, P < 0.01). After 3 months of follow-up, LVEF in fast flow group was higher than that of the slow flow group, but the difference had no significance (P > 0.05). RS and LS in fast flow group were higher than those in slow flow group, and the statistically significant difference appeared from 1 month after PCI (1 month RS:29.74±6.66 vs. 26.86±5.61, LS:-16.37±3.91 vs. -15.27±3.22, 3 months RS: 30.03±6.31 vs. 27.63±5.67, LS: -17.74±3.96 vs. -15.75±4.17, all P < 0.05). Pearson linear correlation showed:the strains (both RS and LS) and CK-MB had no significant relation (both P>0.05). Both RS and LS at 1 week, 1 month and 3 months were of significantly positive correlation with CTFC of each group (fast flow group:r value of CTFC and RS was respectively-0.526,-0.515,-0.532, r value of CTFC and LS was respectively-0.532,-0.541,-0.572;slow flow group:r value of CTFC and RS was respectively-0.691,-0.685,-0.702, r value of CTFC and LS was respectively-0.621,-0.584,-0.605, all P<0.01). Conclusion CTFC has some relationship with the recovery of the systolic function in area of infarct myocardium after PCI, and can be regarded as an important index to predict the long-term prognosis in patients with AMI.