冠心病是临床高发的心血管疾病，其病理核心为动脉粥样硬化，而炎症反应异常激活是推动病变进展的关键驱动力。PI3K/Akt通路通过调控炎症反应等，在CHD进程中发挥双向调节作用。现代研究表明，该通路保护性激活不足可加剧血管内皮损伤与斑块不稳定性，而炎症反应的持续又可进一步抑制PI3K/Akt通路活性，形成恶性循环。当动脉粥样斑块破裂，AMI发生后炎症级联反应放大，该通路异常激活，诱发MIRI。“荣泣卫除”出自《黄帝内经》，指营气耗损（荣泣）、卫气失守（卫除），荣卫失和则气血运行不畅、脉络瘀阻。本团队结合该理论与现代研究，认为CHD中PI3K/Akt通路介导的异常炎症反应的病理机制，与“荣泣卫除”理论内涵存在对应关系。研究发现，通过调控PI3K/Akt通路活性，抑制炎症因子激活与炎症蛋白表达，可抑制CHD发生发展进程。故本文基于“荣泣卫除”理论，系统梳理了PI3K/Akt通路介导的炎症反应在CHD中的作用及与中医病机的内在关联，总结中医药防治的研究进展，为中西医结合防治CHD提供参考依据。

Coronary heart disease is a clinically prevalent cardiovascular disease, with atherosclerosis as its core pathology. Abnormal activation of the inflammatory response is a key driving force for disease progression. The PI3K/Akt pathway exerts bidirectional regulatory effects on the progression of CHD by modulating inflammatory responses, among other functions. Modern studies indicate that insufficient protective activation of this pathway can exacerbate vascular endothelial injury and plaque instability, while persistent inflammation further suppresses PI3K/Akt pathway activity, forming a vicious cycle. Following atherosclerotic plaque rupture and the onset of AMI, the inflammatory cascade is amplified, leading to aberrant activation of this pathway and triggering MIRI. The theory of "depletion of nutritive level and exhaustion of defensive level" originates from the?Yellow Emperor's Inner Classic, referring to the depletion of nutritive level (Rong Qi) and the exhaustion of defensive level (Wei Qi), resulting in disharmony between nutritive and defensive levels, which impedes the smooth flow of Qi and blood and causes stasis in the collaterals. By integrating this theory with modern research, our team proposes a correspondence between the pathological mechanism of abnormal PI3K/Akt pathway-mediated inflammatory response in CHD and the theoretical connotation of "depletion of nutritive level and exhaustion of defensive level". Studies have found that modulating PI3K/Akt pathway activity to inhibit the activation of inflammatory factors and expression of inflammatory proteins can suppress the occurrence and progression of CHD. Therefore, based on the theory of "depletion of nutritive level and exhaustion of defensive level", this paper systematically reviews the role of the PI3K/Akt pathway-mediated inflammatory response in CHD and its intrinsic relationship with traditional Chinese medicine pathogenesis, summarizes research progress in TCM prevention and treatment, and provides a reference for the integrated traditional Chinese and Western medicine management of CHD.

目的 研究甲泼尼龙琥珀酸钠对重症支原体肺炎（SMPP）患儿的治疗效果及安全性。方法 采用随机数表法将南华大学附属长沙中心医院2021年1月—2022年12月收治的108例SMPP患儿分为两组,对照组（54例）采用常规治疗,研究组（54例）采用常规治疗联合甲泼尼龙琥珀酸钠治疗,比较2组临床疗效。结果 治疗后研究组炎症因子水平低于对照组,肺功能指标、健康状况评分均高于对照组,发热、咳嗽、肺啰音及肺阴影消失时间均短于对照组（P<0.05）;两组不良反应发生率比较差异无统计学意义（P>0.05）。结论 应用甲泼尼龙琥珀酸钠治疗可加快患儿症状缓解,改善机体炎症反应及肺功能,且安全性较高。

Objective To study the therapeutic effect and safety of methylprednisolone sodium succinate on children with severe Mycoplasma pneumoniae pneumonia（SMPP）．Methods A total of 108 children with SMPP admitted to Changsha Central Hospital from January 2021 to December 2022 were divided into two groups by random number table method．The control group（54 cases）was treated with conventional therapy,and the study group（54 cases）was treated with conventional therapy combined with methylprednisolone sodium succinate．The clinical effects of the two groups were compared．Results After treatment,the levels of inflammatory factors in the study group were lower than those in the control group,and lung function indicators and health status scores were higher than those in the control group．The disappearance time of fever,cough,lung rales and lung shadows was shorter than that in the control group（P<0.05）．There was no statistically significant difference in the incidence of adverse reactions between the two groups（P>0.05）．Conclusions The application of methylprednisolone sodium succinate treatment can accelerate the relief of symptoms in children,improve the body's inflammatory response and lung function,and has high safety．

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．

严重烧伤后患者免疫功能的失调,易导致创面感染、全身炎症反应综合征、脓毒症、感染性休克等并发症,增加患者病死率。免疫细胞功能适度的活化将有助于烧伤患者抵御外界病原体的侵袭、促进创面的愈合,但功能过度激活或者功能低下,则会引发一系列严重的后果。本文旨在归纳严重烧伤后中性粒细胞、单核/巨噬细胞、肥大细胞、NK细胞及T淋巴细胞等免疫细胞的功能变化与炎症反应之间的关系,为完善烧伤患者诊疗、减少并发症、改善预后提供新的思路。

The imbalance of immune function in severely burned patients can easily lead to wound infection,systemic inflammatory response syndrome,sepsis,septic shock and other complications,which increase the mortality of patients. Moderate activation of immune cell function will help burned patients to resist the invasion of external pathogens and promote wound healing,but excessive activation or low function can lead to a series of serious consequences. The purpose of this paper is to summarize the relationship between the functional changes of immune cells such as neutrophils,monocytes/macrophages,mast cells,NK cells,T lymphocytes and inflammatory reaction after severe burns,and to provide new ideas for improving the diagnosis and treatment of burned patients,reducing complications and improving the prognosis.

目的 探究连续性静脉-静脉血液滤过（CVVH）联合HA330血液灌流在改善创伤脓毒症急性肾损伤患者肾功能及炎症反应中的应用效果。方法 选择我院2021年1月—2023年1月期间接诊的98例创伤脓毒症急性肾损伤患者开展研究,随机抽签法分为观察组（联合CVVH、HA330血液灌流治疗）、对照组（予以CVVH治疗）,各49例,对比临床疗效,包括肾功能、炎症反应、不良反应、预后情况。结果 治疗5 d后,观察组临床总有效率为93.84%,高于对照组73.47%（P<0.05）;观察组血清肌酐、尿素氮较对照组明显改善（P<0.05）;观察组IL-6、hs-CRP水平低于对照组（P<0.05）;观察组不良反应总发生率低于对照组（P<0.05）;观察组序贯器官衰竭估计评分、急性生理与慢性健康评分系统评分较对照组低（P<0.05）。结论 CVVH联合HA330血液灌流在改善创伤脓毒症急性肾损伤患者肾功能及炎症反应中的疗效良好,且安全性高,有利于减轻患者炎症反应,控制病情进展,从而改善肾功能及预后。

目的 探讨吸烟对稳定期COPD患者炎症反应和肺功能的影响。方法 选取2013年8月—2016年9月我院门诊收治的稳定期COPD患者70例为研究对象,其中吸烟35例(X1组)、不吸烟35例(X2组),另选取同期入院的不吸烟健康志愿者35例纳入健康组,采用酶联免疫吸附试验(ELISA)测定血清白介素-6(IL-6)、白细胞介素-8(IL-8)及肿瘤坏死因子-α(TNF-α)水平,以肺功能检测仪测定三组一秒用力呼气容积(FEV1)、一秒用力呼气容积/用力肺活量比值(FEV1/FVC)、FEV1占预计值百分比(FEV1％),并采用自拟症状评分表及简明健康调查简表(SF-36)评价呼吸困难程度及生活质量。结果 X1组IL-6、IL-8及TNF-α依次为(135.27±1.24)pg/mL、(189.45±1.14)pg/mL、(39.39±1.14)pg/mL,明显高于X2组、健康组(P均<0.05);X1组FEV1(0.75±0.14)L、FEV1/FVC(3.65±1.87)％、FEV1％(3.45±0.12)％低于X2组、健康组(P均<0.05);X1组症状积分(10.17±1.02)分较X2组、健康对照组高(P<0.05),而其SF-36评分(54.27±1.46)分明显低于X2及健康组(P<0.05);X2组上述指标与健康组比较亦有统计学意义(P均<0.05)。结论 吸烟可明显增加稳定期COPD患者IL-6、IL-8、TNF-α等炎症因子水平,同时降低肺功能,临床应采取措施进行有效干预,防止患者病情恶化。