| 周诗涵,曾龙欢,徐汉乔,赵东,郑永科.CXCL14在慢性危重症心功能损伤中的作用[J].浙江中西医结合杂志,2024,34(3): |
| CXCL14在慢性危重症心功能损伤中的作用 |
| Role of CXCL14 in cardiac dysfunction of chronic critically ill |
| 投稿时间：2023-11-19 修订日期：2024-02-22 |
| DOI： |
| 中文关键词: 慢性危重症 心功能损害 CXCL14 心肌纤维化 小鼠 |
| 英文关键词:Chronic critical illness Cardiac dysfunction CXCL14 Myocardial fibrosis Mouse |
| 基金项目:杭州市科技发展计划项目(20201203B198) |
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| 中文摘要: |
| 目的 探索CXC趋化因子14(CXCL14)在慢性危重症(CCI)模型小鼠心功能损伤中的作用。方法 采用盲肠结扎穿刺术(CLP)诱导脓毒?症建?慢性危重症小?模型。24只小鼠随机分成假?术组、CCI组、CCI+CXCL14组和CCI+Anti-CXCL14组，每组6只。CLP后12 d，采?M型超声?动图记录各组小?左室射?分数(LVEF)，酶联免疫吸附实验(ELISA)法测定脑钠肽(BNP)?平等评估大鼠心功能。采?苏木精-伊红(HE)染?法观察?肌组织，?较各组???肌细胞排列和纤维化情况。采用ELISA法检测心肌组织CXCL14表达水平。采?蛋白质印迹法(WB)检测???肌组织纤维化蛋?α-平滑肌肌动蛋白(α-SMA)和III型胶原蛋白(Collagen Ⅲ)的表达情况。结果 与假手术组相比，CCI组??LVEF明显降低[(59.17±3.35)%比(74.31±2.16)%，P<0.01]，BNP明显升高(11.27±0.50比6.07±0.45，P<0.01)，心肌组织病理损伤明显，?肌细胞体积增?，心肌纤维排列紊乱，CXCL14明显升高[(0.55±0.02)ng/mg protein比(0.4±0.03)ng/mg protein，P<0.01]，?肌纤维化相关蛋?α-SMA表达增加(0.66±0.02比0.31±0.05，P<0.01)，Collagen Ⅲ表达增加(0.64±0.04比0.40±0.04，P<0.01)。与CCI组比较，CXCL14重组蛋?处理可进?步降低??LVEF[(50.97±3.52)% 比 (59.17±3.35)%，P<0.05]，升高BNP水平(14.73±0.74比11.27±0.50，P<0.01)，加重心肌组织病理损伤，进一步升高CXCL14[(0.75±0.05)ng/mg protein比(0.55±0.02)ng/mg protein，P<0.01]和?肌纤维化相关蛋?α-SMA表达水平(0.79±0.05比0.66±0.02，P<0.05)，对Collagen Ⅲ表达无显著影响(0.75±0.06比0.64±0.04，P>0.05)；而CXCL14抗体处理可抑制CCI模型??LVEF下降[(69.29±2.08)%比(59.17±3.35)%，P<0.01]，降低BNP水平(8.77±0.40比11.27±0.50，P<0.01)，改善心肌组织纤维化，对CXCL14含量无显著影响[(0.54±0.05)ng/mg protein比(0.55±0.02)ng/mg protein，P>0.05]，可抑制CCI模型???肌组织α-SMA(0.61±0.03比0.77±0.04，P<0.01)和Collagen Ⅲ表达(0.57±0.04比0.80±0.05，P<0.01)。结论 CCI模型小鼠心肌CXCL14表达升高，可通过促进心肌纤维化导致心功能损伤。 |
| 英文摘要: |
| Objective To explore the role of CXC chemotactic factor 14(CXCL14) in cardiac dysfunction of chronic critically ill(CCI) model mice. Methods Cecal ligation puncture surgery(CLP) was used to induce sepsis and establish a small CCI model.24 mice were randomly divided into sham surgery group,CCI group,CCI+CXCL14 group and CCI+Anti-CXCL14 group,with 6 mice in each group.At 12 days after CLP, M-mode echocardiography was used to record the left ventricular ejection fraction (LVEF) of each group,and brain natriuretic peptide(BNP) was measured using enzyme linked immunosorbent assay (ELISA) to evaluate the cardiac function of mice.The expression level of CXCL14 in myocardial tissue was detected using ELISA method.Hematoxylin-eosin(HE) staining was used to observe the arrangement and fibrosis of muscle cells in each group.We used Western Blot(WB) to detect expression of fibrotic egg in skeletal muscle tissue,including α-smooth muscle actin(α-SMA) and Type 3 collagen protein(Collagen III). Results Compared with the sham operated group model,the LVEF of the CCI model was significantly reduced[(59.17±3.35)% vs (74.31±2.16)%,P<0.01] and the expression of BNP significantly increased ( 11.27±0.50 vs 6.07±0.45,P<0.001).Myocardial tissue pathological damage was significant, myocardial cell volume increased and myocardial fiber arrangement was disordered.CXCL14 significantly increased [(0.55±0.02)ng/mg protein vs (0.4±0.03)ng/mg protein,P<0.01].And we observed that myocardial fibrosis related eggs increased,including α-SMA (0.66±0.02 vs 0.31±0.05,P<0.01) and Collagen III (0.64±0.04 vs 0.40±0.04，P<0.01).Compared with CCI model,treatment with CXCL14 recombinant egg could further reduce LVEF of the CCI model[(50.97±3.52)% vs (59.17±3.35)%,P<0.05],further increase the expression of BNP(14.73±0.74 vs 11.27±0.50,P<0.01),exacerbate myocardial tissue pathological damage,further increase CXCL14[(0.75±0.05)ng/mg protein vs (0.55±0.02)ng/mg protein,P<0.01] and increase the levels of myofibrosis related eggs ,such as α-SMA (0.79±0.05 vs 0.66±0.02,P<0.05).But it had no significant effect on the expression of Collagen III (0.75±0.06 vs 0.64±0.04,P>0.05);However,CXCL14 antibody treatment could inhibit the decrease of LVEF[(69.29±2.08)% vs (59.17±3.35)%,P<0.01],lower BNP (8.77±0.40 vs 11.27±0.50,P<0.01),improve myocardial fibrosis in the CCI model.However,there was no significant effect on the content of CXCL14 [(0.54±0.05)ng/mg protein vs (0.55±0.02)ng/mg protein,P>0.05].It could inhibit the expression of α-SMA(0.61±0.03 vs 0.77±0.04,P<0.01) and Collagen III(0.57±0.04 vs 0.80±0.05,P<0.01). Conclusion The expression of CXCL14 in the myocardium of CCI model mice increases,which can lead to cardiac function damage by promoting myocardial fibrosis. |
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