目的 探讨血浆细胞周期依赖性激酶9（CDK9）水平与大动脉粥样硬化（LAA）型脑梗死病情进展及预后的相关性，评估其作为疾病风险分层及预后评估生物标志物的临床价值。方法 选取2020年1月—2024年12月期间于本院就诊的400例急性LAA型脑梗死患者作为观察组，并同期纳入100名健康体检者作为对照组。发病90 d后，采用改良Rankin量表（mRS）对所有患者进行预后评估。根据评估结果，将观察组进一步划分为预后不良组（152例）与预后良好组（248例）。检测患者血浆CDK9水平并收集临床资料。分析CDK9水平与美国国立卫生研究院卒中量表（NIHSS）评分、梗死灶体积的相关性；分析预后不良的影响因素。结果 观察组CDK9水平高于对照组［（185.6±42.3） pg/mL vs （62.4±18.5） pg/mL，P＜0.001］，且与梗死体积（r=0.586）、NIHSS评分（r=0.628）、高敏C反应蛋白（r=0.452）及白介素6（r=0.418）呈正相关（均P＜0.001）。多因素Logistic回归分析显示，CDK9升高是90天预后不良的独立危险因素。受试者工作特征曲线（ROC）曲线分析显示，CDK9预测预后不良的曲线下面积（AUC）为0.854（最佳截断值为198.6 pg/mL，灵敏度为78.3%，特异度为82.5%），联合NIHSS评分及梗死体积后AUC提升至0.912（P＜0.001）。结论 血浆CDK9水平可作为急性LAA型脑梗死病情进展及预后的独立预测标志物，联合传统指标可提高预后评估效能。

      Objective To investigate the correlation between plasma cyclin-dependent kinase 9（CDK9）level and disease progression and prognosis in patients with acute large artery atherosclerosis（LAA）cerebral infarction，and to evaluate its clinical value as a biomarker for disease risk stratification and prognostic assessment．Methods This study enrolled 400 patients with acute LAA-type cerebral infarction who visited our hospital between January 2020 and December 2024 as the observation group，along with 100 healthy individuals as the control group during the same period．After 90 days of symptom onset，all patients were assessed using the modified Rankin Scale（mRS）for prognostic evaluation．Based on the assessment results，the observation group was further divided into two subgroups：the poor prognosis group（152 cases）and the good prognosis group（248 cases）．Plasma CDK9 levels were measured，and clinical data were collected．The correlation between CDK9 level and National Institutes of Health Stroke Scale（NIHSS）score and infarct volume，and the factors affecting poor prognosis were analyzed．Results Plasma CDK9 levels in the observation group were higher than those in the control group（［185.6±42.3］ pg/mL vs ［62.4±18.5］ pg/mL，P＜0.001），and were positively correlated with infarct volume（r=0.586），NIHSS score（r=0.628），high-sensitivity C-reactive protein（r=0.452），and interleukin-6（r=0.418）（all P＜0.001）．Multivariate Logistic regression analysis showed that elevated CDK9 level was an independent risk factor for poor prognosis at 90 d．Receiver Operating Characteristic（ROC）curve analysis revealed that the area under the curve（AUC）of CDK9 for predicting poor prognosis was 0.854（optimal cut-off value：198.6 pg/mL，sensitivity：78.3%，specificity：82.5%），and the AUC increased to 0.912 when combined with NIHSS score and infarct volume（P＜0.001）．Conclusions Plasma CDK9 level may serve as an independent predictive biomarker for disease progression and prognosis in acute LAA cerebral infarction，and combining it with traditional indicators can improve the efficacy of prognostic assessment．

目的 探讨不同浓度的青藤碱对肾癌细胞增殖、细胞周期及凋亡的影响。方法 以不同浓度的青藤碱处理肾癌细胞786-O,采用四氮唑蓝盐法检测细胞增殖能力,流式细胞术检测细胞周期分布,Annexin-v FITC/PI双染流式细胞分析仪检测细胞凋亡率;采用实时荧光定量PCR及蛋白免疫印迹(WB)检测c-myc、Bax、Caspase-3等细胞周期、凋亡相关基因表达情况。结果 青藤碱显著抑制786-O细胞的增殖能力,诱导细胞周期G1/S期阻滞及细胞凋亡;且随着青藤碱浓度的增加,其抑制率也逐渐增加;青藤碱显著下调c-myc蛋白表达,而诱导凋亡蛋白Bax、Caspase-3表达上调。结论 青藤碱可以显著抑制786-O细胞中c-myc表达,使其增殖能力减弱,诱导细胞周期阻滞及凋亡。青藤碱可能具有潜在的抑制肾癌生长作用。

Objective To investigate the effects of different concentrations of sinomenine on proliferation, cell cycle and apoptosis of renal carcinoma cells. Methods The renal carcinoma cells were treated with different concentrations of sinomenine. MTS was used to analyze the effects of sinomenine on proliferation in 786-O renal carcinoma cells, the cell cycle changes were determined using flow cytometry, while the changes of apoptosis were detected by Annexin V-FITC / PI double staining. The expression of apoptosis-related proteins such as c-myc, Bax and Caspase-3 were detected by Western blot. Results Sinomenine significantly inhibited the proliferation of 786-O cells and induced cell cycle arrest and apoptosis in G1/S phase. With the increase of sinomenine concentration, the inhibition rate increased gradually. Sinomenine significantly down-regulated the expression of c-myc protein, while the expressions of the apoptotic protein Bax, Caspase-3 were up-regulated. Conclusions Sinomenine can significantly inhibit the expression of c-myc in 786-O cells, reduce proliferation ability, and induce cell cycle arrest and apoptosis. Sinomenine may have a potential therapeutic effect on renal cancer.

目的 体外细胞实验检测吴茱萸碱对骨肉瘤HOS细胞株细胞周期及体外增殖能力的影响。方法 通过利用浓度为0、3、6、12 μmol/L吴茱萸碱处理骨肉瘤HOS细胞48 h后,Hoechst-33258荧光染色观察不同浓度吴茱萸碱处理后HOS细胞核的形态学变化。利用流式细胞术检测3 μmol/L的吴茱萸碱处理后骨肉瘤HOS细胞的细胞周期分布变化。结果 3、6、12 μmol/L的骨肉瘤吴茱萸碱处理细胞,细胞呈现凋亡核碎裂等典型变化,而且随药物剂量增加而更趋明显。呈剂量依赖性抑制其体外增殖能力。3 μmol/L吴茱萸碱处理骨肉瘤HOS细胞0、24、48、72 h,各组细胞周期变化如下:G0/G1期:对照组(51.12±2.13)%、24 h(19.17±1.02)%、48 h(16.94±1.67)%、72 h(11.05±1.25)%;S期:对照组(32.92±0.73)%、24 h(31.00±1.42)%、48 h(32.38±3.03)%、72 h(29.18±2.87)%;G2/M期:对照组(16.01±2.26)%、24 h(49.82±0.62)%、48 h(50.6767±2.80)%、72 h(59.56±1.97)%。结论 吴茱萸碱可诱导人骨肉瘤HOS细胞发生G2/M期阻滞,而S期变化不明显。说明吴茱萸碱可以抑制骨肉瘤细胞的增殖能力,并阻滞细胞周期于G2/M期。

Objective Using transcriptome sequencing and in vitro cell assay to detect the effect of evodiamine on cell cycle and proliferation in osteosarcoma HOS cell line. Methods HOS cells were treated with evodiamine at 0, 3, 6, and 12 μmol/L for 48 hours, Hoechst-33258 fluorescence staining was used to observe the morphological changes of HOS nuclei after treatment with different concentrations of evodiamine.The cell cycle distribution of HOS cells treated with 3 μmol/L evodiamine was detected by flow cytometry. Results 3,6,12 μmol/L osteosarcoma treated with evodiamine, the cells showed typical changes such as apoptotic nuclear fragmentation, and it became more obvious with the increase of drug dosage. Inhibition of proliferation in vitro in a dose-dependent manner.HOS cells were treated with 3 μmol/L evodiamine for 0, 24, 48, 72 h. The cell cycle changes of each group were as follows: G0/G1 phase: control group(51.12±2.13)%, 24 h(19.17±1.02)%, 48 h(16.94±1.67) %, 72 h(11.05±1.25)%;S phase: control group(32.92±0.73)%, 24 h(31.00±1.42)%, 48 h(32.38±3.03)%, 72 h(29.18±2.87)%;G2/M period: control group(16.01±2.26)%, 24 h(49.82±0.62)%, 48 h(50.6767±2.80)%, 72 h(59.56±1.97)%. Conclusion Analysis of the above results revealed that evodiamine can induce G2/M phase arrest in human osteosarcoma HOS cells, but the S phase changes are not obvious. It indicated that evodiamine would inhibit the proliferation of osteosarcoma cells and block the cell cycle in G2/M phase.