Exp Biol Med (Maywood). 2013 Jun;238(6):705-12. doi: 10.1177/1535370213489487.
Heme oxygenase (HO)-1 has been reported to play a great role in attenuating lung injury during endotoxic shock in our previous research. Although electro-acupuncture has been explored to reduce oxidative stress and decrease inflammatory reaction in animals with endotoxic shock, the mechanism of this effect is still unclear. The aim of this study was to determine whether HO-1 is involved in the effect of electro-acupuncture on the injured lung during endotoxic shock in rabbits. Sixty New England white rabbits were randomly divided into groups C, Z, ES, EA, AP, and EAZ. Before inducing endotoxic shock, group ES received no electro-acupuncture, while group EA received electro-acupuncture at ST36 (zusanli) and BL13 (feishu) acupoints on both sides for five days and group AP received electro-acupuncture (EA) stimulation at a non-acupoint. Groups ES, AP, EA, and EAZ received LPS to replicate the experimental model of injured lung induced by endotoxic shock, and electro-acupuncture was performed throughout the procedure with the same parameter. Groups EAZ and Z received the HO-1 inhibitor, ZnPP-IX, intraperitoneally. The animals were sacrificed by blood-letting at 6 h after LPS administration. The blood samples were collected for serum examination, and the lungs were removed for pathology examination, detection of alveolaer epithelial cell apoptosis by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay (TUNEL assay), determination of wet to dry ratio, measurement of Evans blue (EB) contents, and determination of HO-1protein and mRNA expression. According to the results, EA at ST36 and BL13 could increase the expression of HO-1. At the same time, index of quantitative assessment (IQA) score and the number of TUNEL-positive cells decreased, while electro-acupuncture at the other points did not exert this effect, and pretreatment with ZnPP-IX in group EAZ suppressed the efficacy of electro-acupuncture preconditioning. In summary, electro-acupuncture stimulation at ST36 and BL13, while not the non-acupoint, could attenuate the lung injury during the endotoxic shock, and this effect was due to increased expression of HO-1.
血红素加氧酶-1（HO-1）在我们之前的研究中已被报道在脓毒性休克期间减轻肺损伤方面发挥重要作用。尽管电针对脓毒性休克动物的氧化应激和炎症反应减少已有研究探索，但这种效应的机制仍不清楚。本研究旨在确定 HO-1 是否参与电针对脓毒性休克兔受损肺的作用。
将 60 只新英格兰白兔随机分为 C、Z、ES、EA、AP 和 EAZ 组。在诱导脓毒性休克之前，ES 组未接受电针，而 EA 组在双侧 ST36（足三里）和 BL13（肺俞）穴位接受电针刺激 5 天，AP 组在非穴位接受电针刺激。ES、AP、EA 和 EAZ 组接受 LPS 复制脓毒性休克引起的受损肺实验模型，整个过程中采用相同参数进行电针刺激。EAZ 和 Z 组腹腔内注射 HO-1 抑制剂 ZnPP-IX。LPS 给药后 6 h 采血，取肺进行病理检查、末端脱氧核苷酸转移酶介导的 dUTP 生物素缺口末端标记法（TUNEL 法）检测肺泡上皮细胞凋亡、湿干比测定、伊文思蓝（EB）含量测定和 HO-1 蛋白和 mRNA 表达测定。
结果显示，ST36 和 BL13 处的电针刺激可增加 HO-1 的表达。同时，定量评估指数（IQA）评分和 TUNEL 阳性细胞数减少，而其他部位的电针刺激则没有这种作用，并且 EAZ 组中 ZnPP-IX 的预处理抑制了电针预处理的效果。
总之，ST36 和 BL13 处的电针刺激，而非非穴位，可减轻脓毒性休克期间的肺损伤，这种效应是由于 HO-1 的表达增加所致。
