目的探讨HPV16(Human Papillomavirus Type 16)E6-295T/G和E6-350T/G变异位点对IFNκ、MHC-Ⅰ、STAT1和IRF9蛋白质表达的影响。方法在宫颈癌细胞C33A(HPV阴性)中分别转染真核表达载体295G/350G-GV230、295T/350G-GV230和295T/350T-GV23...
详细信息
目的探讨HPV16(Human Papillomavirus Type 16)E6-295T/G和E6-350T/G变异位点对IFNκ、MHC-Ⅰ、STAT1和IRF9蛋白质表达的影响。方法在宫颈癌细胞C33A(HPV阴性)中分别转染真核表达载体295G/350G-GV230、295T/350G-GV230和295T/350T-GV230作为实验组,以NC-GV230作为对照组。通过免疫组织化学法、Western blot方法检测HPV16 E6295T/G、350T/G不同变异位点对IFNκ、MHC-Ⅰ、STAT1和IRF9蛋白质表达的影响。通过IBM SPSS Statistics 26软件对实验结果进行统计学分析,P<0.05为差异具有统计学意义,免疫组织化学法定量采用image J软件进行阳性细胞计数。结果Western blot结果显示,免疫分子干扰素κ(Interferon Kappa,IFNκ)的表达,HPV16 E6-295G/350G变异组较HPV16 E6-295T/350T原型组和HPV16 E6-295T/350G组降低(P<0.01,P<0.05)。HPV16 E6-295G/350G变异组的免疫分子主要组织相容性复合体I类(Major Histocompatibility Complex Class I,MHC-I)的表达显著低于HPV16 E6-295T/350T原型组和HPV16 E6-295T/350G组(P<0.05)。HPV16 E6-295G/350G变异组的信号转导子和转录激活子1(Signal Transducer and Activator of Transcription 1,STAT1)表达显著低于HPV16 E6-295T/350T原型组和HPV16 E6-295T/350G组(P<0.05,P<0.01)。变异组HPV16 E6-295G/350G与HPV16 E6-295T/350T原型组和HPV16 E6-295T/350G变异组相比,干扰素调节因子9(Interferon Regulatory Factor 9,IRF9)表达显著降低(P<0.05,P<0.01)。结论HPV16病毒E6蛋白质可以降低IFNκ、MHC-Ⅰ、STAT1和IRF9的蛋白质表达水平,E6基因T295G/T350G变异降低这些分子的表达作用最强。
系统性红斑狼疮(SLE)是一种慢性自身免疫性疾病,可引起多器官系统损伤,心脏受累率超过50%,冠状动脉粥样硬化性心脏病(CHD)是其常见并发症,患病风险显著高于普通人群。本文报道了一例42岁女性SLE合并不稳定性心绞痛患者。冠状动脉造影显示左前降支及右冠状动脉重度狭窄,术中植入多枚支架并行高压球囊扩张,术后血管通畅,患者恢复良好,随访未发生急性心血管事件。SLE相关CHD的发病机制涉及慢性炎症、免疫异常和传统心血管危险因素协同作用,患者常表现非典型症状,诊断需结合病史、影像学和实验室评估。治疗以控制SLE炎症、预防血栓和管理心血管风险为核心,严重狭窄者可选择经皮冠状动脉介入治疗(PCI)。本研究结合病例与文献,强调早期识别、综合评估和多学科协作对改善SLE合并CHD患者预后的重要性。Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that can cause multi-organ system damage, with cardiac involvement reported in over 50% of cases. Coronary heart disease (CHD) is a common complication of SLE, with a significantly higher prevalence compared to the general population. This article reports a case of a 42-year-old female patient with SLE complicated by unstable angina. Coronary angiography revealed severe stenosis in the left anterior descending artery and the right coronary artery. Multiple stents were implanted during the procedure, followed by high-pressure balloon dilation. Postoperatively, the blood vessels remained unblocked, the patient recovered well, and no acute cardiovascular events occurred during follow-up. The pathogenesis of SLE-associated CHD involves the interplay of chronic inflammation, immune dysfunction, and traditional cardiovascular risk factors. Patients often present with atypical symptoms, and diagnosis requires a combination of medical history, imaging, and laboratory evaluations. Treatment focuses on controlling SLE-related inflammation, preventing thrombosis, and managing cardiovascular risks. For severe stenosis, percutaneous coronary intervention (PCI) is a viable option. This study integrates case findings with a literature review, highlighting the importance of early recognition, comprehensive evaluation, and multidisciplinary collaboration in improving outcomes for patients with SLE and CHD.
暂无评论