Department of Orthopaedics, Wuxi No. 9 People's Hospital Affiliated to Soochow University, Wuxi 214000 Jiangsu, China.
Oxid Med Cell Longev. 2022 Oct 17;2022:1175078. doi: 10.1155/2022/1175078. eCollection 2022.
This research is aimed at exploring the influences of the Bax gene in the p38 mitogen-activated protein kinase (MAPK) pathway and its protective mechanism against ischemia-reperfusion injury (IRI) of skin flap. Forty male Sprague-Dawley (SD) rats were equally divided into the experimental group (Bax gene knockout rats) and control group. The dorsal flap model was prepared, and the survival rate of flap was observed after surgery. The rat flap tissue was cut and stained with hematoxylin-eosin (HE) and in situ terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL). The distribution characteristics of p38MAPK and Bax were detected to evaluate the protective mechanism of Bax gene knockout on IRI of skin flap. After surgery, the survival rate of flaps in the experimental group (82.32%, 70.28%) was significantly higher than that in the control group (57.64%, 46.14%) ( < 0.05). The results of HE staining showed that on the 1 day after surgery, compared with those in the control group, the skin flaps of the rats in the experimental group were arranged more neatly. The results of TUNEL staining showed that compared with that of the control group, the tissue structure of the skin flap of the experimental group was normal and only a few apoptotic cells appeared. In addition, compared with that in the control group (7.14, 4.25, 3.48, 2.18/6.46, 7.12, 4.86, and 2.44), the expression of Bax and p38 MAPK in the experimental group (0.96, 0.81, 0.76, 0.55/1.63, 1.33, 1.01, and 0.56) significantly decreased ( < 0.05). In short, after the Bax gene was knocked out, injury of the flap after ischemia-reperfusion was considerably improved, which may play a protective role on the IRI of the flap by affecting the p38MAPK pathway.
本研究旨在探讨 Bax 基因在 p38 丝裂原活化蛋白激酶（MAPK）通路中的影响及其对皮瓣缺血再灌注损伤（IRI）的保护机制。将 40 只雄性 Sprague-Dawley（SD）大鼠等分为实验组（Bax 基因敲除大鼠）和对照组。制备背部皮瓣模型，术后观察皮瓣存活率。切取大鼠皮瓣组织，行苏木精-伊红（HE）染色和原位末端脱氧核苷酸转移酶介导的 dUTP 缺口末端标记（TUNEL）染色。检测 p38MAPK 和 Bax 的分布特征，评估 Bax 基因敲除对皮瓣 IRI 的保护机制。术后实验组（82.32%、70.28%）皮瓣存活率明显高于对照组（57.64%、46.14%）（<0.05）。HE 染色结果显示，术后 1 天实验组大鼠皮瓣排列较整齐，与对照组相比，组织结构更为清晰。TUNEL 染色结果显示，实验组皮瓣组织结构正常，仅出现少量凋亡细胞，与对照组相比差异有统计学意义（<0.05）。此外，与对照组（7.14、4.25、3.48、2.18/6.46、7.12、4.86、2.44）相比，实验组 Bax 和 p38MAPK 的表达（0.96、0.81、0.76、0.55/1.63、1.33、1.01、0.56）明显降低（<0.05）。综上所述，Bax 基因敲除后，皮瓣缺血再灌注损伤明显改善，可能通过影响 p38MAPK 通路对皮瓣 IRI 发挥保护作用。
