本研究旨在探讨Bax基因对p38丝裂原活化蛋白激酶(MAPK)通路的影响及其对皮瓣缺血再灌注损伤(IRI)的保护机制。40只雄性SD大鼠随机分为实验组(Bax基因敲除大鼠)和对照组。制备背侧皮瓣模型,术后观察皮瓣的成活率。切割大鼠皮瓣组织并用苏木精-伊红(HE)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。通过检测p38MAPK和Bax的分布特点,评价Bax基因敲除对皮瓣IRI的保护机制。手术后,实验组皮瓣成活率(82.32%,70.28%)显著高于对照组(57.64%,46.14%)(P<0.05)。HE染色结果显示,手术后第1天,与对照组相比,实验组大鼠的皮瓣排列更整齐。TUNEL染色结果显示,与对照组相比,实验组皮瓣组织结构正常,仅有少数凋亡细胞出现。此外,与对照组相比(7.14、4.25、3.48、2.18/6.46、7.12、4.86和2.44),实验组Bax和p38MAPK的表达(0.96、0.81、0.76、0.55/1.63、1.33、1.01和0.56)显著降低(P<0.05)。总之,Bax基因被敲除后,缺血再灌注后皮瓣的损伤明显改善,可能通过影响p38MAPK通路对皮瓣的IRI起到保护作用。
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%) (P < 0.05). The results of HE staining showed that on the 1st 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 (P < 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.