Du Ming-Hua, Luo Hong-Min, Tian Yi-Jun, Zhang Li-Jian, Zhao Zeng-Kai, Lv Yi, Xu Rui-Jiang, Hu Sen
Research Laboratory of Shock and Multiple Organ Dysfunction, Burns Institute, First Hospital Affiliated to the PLA General Hospital, Beijing, China; Department of Pediatric Orthopedic Surgery, Chinese PLA General Hospital, Beijing, China.
Research Laboratory of Shock and Multiple Organ Dysfunction, Burns Institute, First Hospital Affiliated to the PLA General Hospital, Beijing, China; Department of Burns, Guangdong General Hospital, Guangzhou, China.
J Surg Res. 2015 May 1;195(1):89-98. doi: 10.1016/j.jss.2014.12.043. Epub 2014 Dec 31.
We have recently proved electroacupuncture (EA) ST36 exerted an anti-inflammatory effect in the early phase of intra-abdominal adhesion formation. Evidences indicate that the anti-inflammatory effect of EA ST36 involves a cholinergic anti-inflammatory pathway-dependent mechanism via the vagus nerve. However, the exact effects and accurate vagal modulation of acupuncture in prevention of postoperative intra-abdominal adhesion formation has not been thoroughly evaluated.
Sprague-Dawley rats subjected to abdominal adhesion lesions operation at the cecum and abdominal wall were randomly divided into six groups as follows: (a) EAN: EA non-channel acupoints; (b) EA: EA ST36 after abdominal lesions; (c) VGX/EA: vagotomy (VGX) after abdominal lesions, then EA ST36; (d) VGX/EAN: VGX after abdominal lesions, then EAN; (e) α-BGT/EA: intraperitoneal injection of α-bungarotoxin (α-BGT, an antagonist of α7 subunit of cholinergic nicotinic receptor) before EA ST36, and (f) α-BGT/EAN group: α-BGT injection before EAN. Seven days after abdominal surgical lesions, the levels of tumor necrosis factor-α (TNF-α) and vascular endothelial growth factor (VEGF) in the adhesive tissue were evaluated, macroscopic observation and histopathologic evaluation of adhesion formation and assessment of angiogenesis by immunohistochemical staining of platelet endothelial cell adhesion molecule-1 (CD31) were performed.
EA ST36 reduced TNF-α and VEGF levels in adhesive tissue homogenates 7 d after surgery, whereas vagotomy or intraperitoneal injection of α-BGT before EA ST36 reversed its suppressive effects. EA at non-channel acupoints with or without vagotomy or intraperitoneal injection of α-BGT before EA had no suppressive effects on TNF-α and VEGF levels. EA ST36 alleviated the adhesion formation, with both of macroscopic and histopathologic adhesion scores significantly lower than those of the EAN group (1.56 ± 0.29 versus 3.00 ± 0.82, 1.35 ± 0.4 versus 3.91 ± 0.8, respectively, both P < 0.05). Compared with the EAN group, EA ST36 significantly decreased angiogenesis evidenced by reduced CD31 positive microvessel density in adhesive tissue.
EA ST36 might reduce the postoperative local inflammatory response, attenuate the angiogenesis, and alleviate the adhesion formation partly via activating the cholinergic anti-inflammatory mechanism.
我们最近证明电针足三里(ST36)在腹腔粘连形成的早期发挥抗炎作用。有证据表明,电针足三里的抗炎作用涉及通过迷走神经的胆碱能抗炎途径依赖性机制。然而,针刺在预防术后腹腔粘连形成的确切作用和精确的迷走神经调节尚未得到充分评估。
将接受盲肠与腹壁粘连损伤手术的Sprague-Dawley大鼠随机分为六组,如下:(a)EAN组:电针非经穴;(b)EA组:腹部损伤后电针足三里;(c)VGX/EA组:腹部损伤后切断迷走神经(VGX),然后电针足三里;(d)VGX/EAN组:腹部损伤后VGX,然后电针非经穴;(e)α-BGT/EA组:在电针足三里之前腹腔注射α-银环蛇毒素(α-BGT,胆碱能烟碱受体α7亚基拮抗剂);(f)α-BGT/EAN组:在电针非经穴之前注射α-BGT。腹部手术损伤7天后,评估粘连组织中肿瘤坏死因子-α(TNF-α)和血管内皮生长因子(VEGF)水平,进行粘连形成的宏观观察和组织病理学评估,并通过血小板内皮细胞黏附分子-1(CD31)免疫组化染色评估血管生成。
术后7天,电针足三里降低了粘连组织匀浆中TNF-α和VEGF水平,而在电针足三里之前切断迷走神经或腹腔注射α-BGT可逆转其抑制作用。在电针之前,无论有无切断迷走神经或腹腔注射α-BGT,电针非经穴对TNF-α和VEGF水平均无抑制作用。电针足三里减轻了粘连形成,宏观和组织病理学粘连评分均显著低于EAN组(分别为1.56±0.29对3.00±0.82,1.35±0.4对3.91±0.8,均P<0.05)。与EAN组相比,电针足三里显著减少了血管生成,表现为粘连组织中CD31阳性微血管密度降低。
电针足三里可能通过激活胆碱能抗炎机制部分降低术后局部炎症反应、减轻血管生成并缓解粘连形成。