目的   探讨肺癌伴癌性疼痛患者心理僵化现状及其影响因素，为临床制定改善患者心理僵化的针对性干预措施以及提升患者生活质量提供参考依据。方法   采用便利抽样法，选取2023年10月—12月期间焦作市某三级甲等医院收治的肺癌伴癌性疼痛患者为研究对象，采用一般资料调查问卷、疼痛心理僵化量表（PIPS）、简易疾病感知问卷（BIPQ）、家庭功能问卷（APGAR）进行调查，采用Pearson相关性分析肺癌伴癌性疼痛患者心理僵化与疾病感知、家庭功能的关系。采用多元线性回归分析肺癌伴癌性疼痛患者心理僵化的影响因素。结果   本次研究共发放问卷152份，回收有效问卷150份，有效回收率为98.68%。150例肺癌伴癌性疼痛患者心理僵化量表总分为（61.66±2.85）分，回避型经验维度得分为（45.52±1.97）分，认知融合维度得分为（19.74±1.59）分。不同文化程度、家庭人均月收入、疼痛程度的肺癌伴癌性疼痛患者心理僵化得分比较，差异有统计学意义（P＜0.05）。Pearson相关性分析结果显示：肺癌伴癌性疼痛患者心理僵化总分、经验性回避维度得分、认知融合维度得分与疾病感知得分均呈正相关关系（P＜0.001），与家庭功能得分均呈负相关关系（P＜0.001）。多元线性回归结果显示：文化程度、家庭人均月收入、疾病感知、家庭功能是肺癌伴癌性疼痛患者心理僵化的影响因素（P＜0.05），可解释肺癌伴癌性疼痛患者心理僵化43.9%的变异度。结论   肺癌伴癌性疼痛患者心理僵化处于较高水平，且受到文化程度、家庭人均月收入、疾病感知和家庭功能的影响，临床医护人员可从疾病感知、家庭支持等角度出发，采用认知干预、同伴支持等方法，加强对患者的健康教育，以缓解其对疾病的负性认知，从而缓解心理僵化，促进身心健康恢复。

       Objective  To explore the status and influencing factors of psychological  rigidity in patients with lung cancer and cancer pain，and to provide reference for clinical development of targeted interventions to improve patients’psychological rigidity andquality of life．Methods  The convenience sampling method was used to select patients with lung cancer and cancer pain who were admitted to a tertiary hospital in Jiaozuo City from October to December 2023 as the research object．The general data questionnaire，Psychological Inflexibility in Pain Scale（PIPS），Brief Illness Perception Questionnaire（BIPQ），and family function questionnaire（APGAR）were used to investigate．Pearson correlation analysis was used to analyze the relationship between psychological rigidity and disease perception and family function in patients with lung cancer and cancer pain．Multivariate linear regression was used to analyze the influencing factors of psychological rigidity in patients with lung cancer and cancer pain．Results  A total of 152 questionnaires were distributed in this study，and 150 valid questionnaires were recovered，with an effective recovery rate of 98.68 %．The total score of PIPS of 150 patients with lung cancer and cancer pain was（61.66±2.85），the score of avoidance experience dimension was（45.52±1.97），and the score of cognitive fusion dimension was（19.74±1.59）．There were statistically significant differences in the scores of psychological rigidity among lung cancer patients with cancer pain with different educational levels，family per capita monthly income，and pain degree（P＜0.05）．The  results of Pearson correlation analysis showed that the total score of PIPS，the score of empirical avoidance dimension and the score of cognitive fusion dimension were positively correlated with the score of disease perception（P＜0.001），and negatively correlated with the score of family function（P＜0.001）．The results of multiple linear regression showed that education level，family per capita monthly income，disease perception and family function were the influencing factors of psychological rigidity in patients with lung cancer and cancer pain（P＜0.05 ），which could explain 43.9 % of the variation of psychological rigidity in patients with lung cancer and cancer pain．Conclusions  The psychological rigidity of lung cancer patients with cancer pain is at a high level，and is affected by education level，family per capita monthly income，disease perception and family function．Clinical medical staff can use cognitive intervention and peer support from the perspective of disease perception and family support to strengthen the health education of patients，so as to alleviate their negative cognition of the disease，to alleviate the psychological rigidity and promote the recovery of physical and mental health．

目的 研究核因子-κB激活剂1（Act1）对高糖诱导肾小管上皮细胞炎症反应及细胞外基质表达的调控作用。方法 培养肾小管上皮细胞MK2,设置对照组和高糖组,处理12 h、24 h、48 h、72 h后检测细胞中Act1的mRNA和蛋白表达水平;设置si-NC组（5.5 mmol/L葡萄糖培养基中转染NC siRNA）、si-NC+高糖组（30 mmol/L葡萄糖培养基中转染NC siRNA）、si-Act1+高糖组（30 mmol/L葡萄糖培养基中转染Act1 siRNA）,48 h后检测细胞中Act1、E-钙黏蛋白（E-cadherin）、N-钙黏蛋白（N-cadherin）、I型胶原（Col-I）、III型胶原（Col-III）的mRNA和蛋白表达水平以及培养基中肿瘤坏死因子-α（TNF-α）、白介素-1β（IL-1β）、干扰素-γ（IFN-γ）的含量。结果 高糖组处理12 h、24 h、48 h、72 h时细胞中Act1的mRNA和蛋白表达水平均高于对照组（P<0.05）;si-NC+高糖组处理48h时细胞中Act1、N-cadherin、Col-I、Col-III的mRNA和蛋白表达水平以及培养基中TNF-α、IL-1β、IFN-γ的含量均高于si-NC组,细胞中E-cadherin的mRNA和蛋白表达水平均低于si-NC组（P<0.05）;si-Act1+高糖组处理48h时细胞中Act1、N-cadherin、Col-I、Col-III的mRNA和蛋白表达水平以及培养基中TNF-α、IL-1β、IFN-γ的含量均低于si-NC+高糖组,细胞中E-cadherin的mRNA和蛋白表达水平均高于si-NC+高糖组（P<0.05）。结论 Act1表达增加对高糖诱导肾小管上皮细胞炎症反应激活和细胞外基质增多具有促进作用。

Objective To study the regulation effect of nuclear factors-κB activator 1（NF-κB activator 1,Act1）on high glucose induced inflammatory response and extracellular matrix expression in renal tubular epithelial cells．Methods Renal tubular epithelial cells MK2 were cultured and control group and high glucose group were set．The mRNA and protein expression of Act1 were detected after treatment for 12,24,48 and 72 hours．MK2 were divided into si-NC group（transfected with NC siRNA in 5.5 mmol/L glucose medium）,si-NC+high glucose group（transfected with NC siRNA in 30 mmol/L glucose medium）and si-Act1+high glucose group（transfected with Act1 siRNA in 30 mmol/L glucose medium）．The mRNA and protein expression of Act1,E-cadherin,N-cadherin,type I collagen（Col-I）,and type III collagen（Col-III）and the contents of tumor necrosis factor-α（TNF-α）,interleukin-1β（IL-1β）,interferon-γ（IFN-γ）in culture medium were detected．Results The mRNA and protein expression levels of Act1 in cells of high glucose group were higher than those of control group at 12 h,24 h,48 h and 72 h（P<0.05）．The mRNA and protein expression levels of Act1,N-cadherin,CoL-I,Col-III in cells and the contents of TNF-α,IL-1β,IFN-γ in culture medium of si-NC+high glucose group were higher than those of si-NC group,the mRNA and protein expression levels of E-cadherin in cells were lower than those of si-NC group at 48 h（P<0.05）．The mRNA and protein expression levels of Act1,N-cadherin,CoL-I,Col-III in cells and the contents of TNF-α,IL-1β,IFN-γ in culture medium of si-Act1+high glucose group were lower than those of si-NC+high glucose group,the mRNA and protein expression levels of E-cadherin in cells were higher than those of si-NC+high glucose group at 48 h（P<0.05）．Conclusions The increased expression of Act1 promotes the activation of inflammatory response and the increase of extracellular matrix in renal tubular epithelial cells induced by high glucose．

目的 研究过表达miR-29a-3p对IL-22诱导的HaCaT细胞增殖的影响。方法 将HaCaT细胞分为Cell组、IL-22组、IL-22+NC组和IL-22+ miR-29a-3p组,荧光定量PCR检测miR-29a-3p的表达水平,CCK8检测细胞的活力,流式细胞仪检测细胞凋亡及周期。结果 与0 μg/L组相比,25 μg/L组、50 μg/L组和100 μg/L组HaCaT细胞的增殖率在24 h、48 h和72 h均出现升高(F值分别为33.27、36.19、52.29,均P<0.000 1)。与0 μg/L组相比,miR-29a-3p在50 μg/L组和100 μg/L组HaCaT中的表达水平降低(F=129,P<0.000 1),分别降低83%和80%。与IL-22+NC组相比,IL-22+ miR-29a-3p组的增殖率在24 h、48 h和72 h均降低(P值分别为0.002 1、0.001 6、0.023 1),细胞总凋亡率增加(6.67±1.06 vs 30.55±1.86,P=0.000 1),G1期细胞比例增加(P=0.000 1),S期细胞比例降低(P=0.000 1)。结论 IL-22可降低HaCaT中miR-29a-3p的表达量,过表达miR-29a-3p通过促进凋亡和引起细胞G1期阻滞抑制IL-22诱发的HaCaT细胞过度增生。

Objective To investigate the effect of miR-29a-3p overexpression on IL-22-induced proliferation of HaCaT cells. Methods HaCaT cells were divided into four groups, Cell group, IL-22 group, IL-22 +NC group and IL-22+miR-29a-3p group. The expression level of miR-29a-3p was detected by fluorescence quantitative PCR. Cell viability was detected by CCK8. Apoptosis and cell cycle were detected by flow cytometry. Results Compared with the 0 g/L group, the proliferation rate of HaCaT cells in the 25 μg/L group, 50 μg/L group and 100 μg/L group was increased at 24 h, 48 h and 72 h (F value was 33.27, 36.19, 52.29,respectively, all P<0.000 1). Compared with the 0 μg/L group, miR-29a-3p expression level in HaCaT in 50 μg/L and 100 μg/L groups was decreased (F=129, P<0.000 1), with a decrease of 83% and 80%, respectively. Compared with the IL-22+NC group, proliferation rate of IL-22+miR-29a-3p group was decreased at 24 h, 48 h and 72 h (P value was 0.002 1, 0.001 6, 0.023 1, respectively), total apoptosis rate was increased (6.67±1.06 vs 30.55±1.86, P=0.000 1), cell proportion in G1 phase was increased (P=0.000 1), and the cell proportion in S phase was decreased (P=0.000 1). Conclusion Il-22 can reduce miR-29a-3p expression level in HaCaT, and miR-29a-3p overexpression can inhibit the excessive proliferation induced by IL-22 in HaCaT cells by promoting apoptosis and inducing G1 phase arrest.