This study investigated the potential genes and related pathways in burn-induced myocardial injury. Rat myocardial injury induced by third-degree burn and the histopathological structures, apoptosis, and cardiac injury markers were then identified using hematoxylin & eosin staining, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling staining, and enzyme-linked immunosorbent assay. Next, differentially expressed mRNAs were screened through next-generation sequencing (NGS), followed by functional annotation and key gene validation through quantitative reverse transcription-polymerase chain reaction. Subsequently, CD14 was screened out, and small interfering RNAs against CD14 were transfected to H9C2 cells to further verify the role of CD14 in burn-induced injury. The results showed that third-degree burn could markedly damage the structure of myocardial tissue, induce the apoptosis of myocardial cells, and increase the levels of myocardial injury-related markers, suggesting that burns could induce myocardial injury in rats. Besides, NGS data discovered that third-degree burn could result in 416 differentially upregulated mRNAs and 285 differentially downregulated mRNAs in myocardial tissue. It was also disclosed that differentially expressed mRNAs were mainly enriched in the phosphatidylinositol 3-kinase/Akt, mitogen-activated protein kinase (MAPK), and tumor necrosis factor signaling pathways. Furthermore, cell viability was significantly decreased in H9C2 cells treated with 10% rat burn serum. CD14 was significantly differentially expressed and screened out for further studies. Treatment with burn serum can significantly upregulate the phosphorylation level of extracellular signal-regulated kinase, p38, and c-Jun N-terminal kinase and the expression of cleaved caspase-3 and downregulate the expression of Bcl2 when compared with those in negative control of small interfering RNA transfected H9C2 cells, whereas interfering with CD14 expression reversed the effects of burn serum. The study demonstrated that burn serum treatment could activate the MAPK signaling pathway to promote cell apoptosis, and it can be reversed by interfering with the expression of CD14.

本研究调查了烧伤心肌损伤的潜在基因和相关通路。采用苏木精和伊红染色、末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记染色和酶联免疫吸附试验鉴定三度烧伤诱导的大鼠心肌损伤和组织病理学结构、细胞凋亡和心脏损伤标志物。接下来，通过下一代测序（NGS）筛选差异表达的mRNA，然后通过定量逆转录聚合酶链反应进行功能注释和关键基因验证。随后筛选出CD14，将CD14的小干扰RNA转染到H9C2细胞中，进一步验证CD14在烧伤损伤中的作用。结果表明，三度烧伤可明显损伤心肌组织结构，诱导心肌细胞凋亡，增加心肌损伤相关标志物水平，提示烧伤可诱发大鼠心肌损伤。此外，NGS 数据发现，三度烧伤可导致心肌组织中 416 种差异上调的 mRNA 和 285 种差异下调的 mRNA。还披露了差异表达的 mRNA 主要富集在磷脂酰肌醇 3-激酶/Akt、丝裂原活化蛋白激酶 (MAPK) 和肿瘤坏死因子信号通路中。此外，用 10% 大鼠烧伤血清处理的 H9C2 细胞的细胞活力显着降低。CD14 显着差异表达并被筛选用于进一步研究。烧伤血清治疗可显着上调胞外信号调节激酶、p38、c-Jun N-末端激酶的磷酸化水平和cleaved caspase-3的表达，下调Bcl2的表达。干扰 RNA 转染 H9C2 细胞，而干扰 CD14 表达逆转烧伤血清的作用。研究表明烧伤血清治疗可激活MAPK信号通路促进细胞凋亡，并可通过干扰CD14的表达来逆转。与转染小干扰 RNA 的 H9C2 细胞的阴性对照相比，c-Jun N-末端激酶和 cleaved caspase-3 的表达并下调 Bcl2 的表达，而干扰 CD14 表达逆转了烧伤血清的作用。研究表明烧伤血清治疗可激活MAPK信号通路促进细胞凋亡，并可通过干扰CD14的表达来逆转。与转染小干扰 RNA 的 H9C2 细胞的阴性对照相比，c-Jun N-末端激酶和 cleaved caspase-3 的表达并下调 Bcl2 的表达，而干扰 CD14 表达逆转了烧伤血清的作用。研究表明烧伤血清治疗可激活MAPK信号通路促进细胞凋亡，并可通过干扰CD14的表达来逆转。