Xie Cancan, Wu Shuanghua, Li Zhengrong, Huang Bing, Zeng Weizhong
Department of Critical Medicine, Zhuzhou Central Hospital, Zhuzhou 412000, China.
Nan Fang Yi Ke Da Xue Xue Bao. 2020 Nov 30;40(11):1662-1667. doi: 10.12122/j.issn.1673-4254.2020.11.20.
To explore the protective effect of electroacupuncture against acute lung injury (ALI) in septic rats and explore the mechanism.
Sixty male SD rats were randomly divided into cecal ligation and puncture (CLP)-induced sepsis group (=45) and sham operation group (=15; with laparotomy but without CLP). The rat models of sepsis were randomized into ALI group (=15) without further treatment, ALI + SEA group (=15) treated with electroacupuncture at the point far from the Zusanli acupoint for 30 min, and ALI + EA group (=15) with electroacupuncture at Zusanli with identical frequency, intensity and duration of electrical stimulation. All the rats were sacrificed at 12 h after CLP for measurement of the weight and the wet/dry weight (W/D) ratio of the lungs. Pathological changes of the lung tissues were examined using HE staining, and the contents of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the homogenate of the lung tissues were detected using enzyme-linked immunosorbent assay (ELISA). TUNEL staining was used to detect the apoptotic cells, and the expressions of Bax, caspase-3 and the important proteins in the JAK1/STAT3 signaling pathway (JAK1 and STAT3) were detected with Western blotting.
Compared with those in the sham operation group, the rats in ALI group showed obvious lung pathologies with significantly increased lung W/D ratio ( < 0.01), pulmonary expressions of TNF-α and IL-6 ( < 0.01), and obvious up-regulation of JAK1, STAT3, caspase-3, and Bax expressions ( < 0.01); similar changes were also observed in ALI+SEA group ( > 0.05). Compared with those in ALI+SEA group, the rats in ALI+EA group showed significantly milder lung pathologies, lowered lung W/D ratio ( < 0.01) and decreased pulmonary expressions of TNF-α, IL-6, JAK1, STAT3, caspase-3 and Bax ( < 0.01).
Electroacupuncture can inhibit the release of inflammatory mediators and cell apoptosis via the JAK1/STAT3 pathway to reduce lung injuries in septic rats.
探讨电针预处理对脓毒症大鼠急性肺损伤（ALI）的保护作用及其机制。
将60只雄性SD大鼠随机分为盲肠结扎穿孔（CLP）诱导的脓毒症组（n = 45）和假手术组（n = 15；仅行剖腹术，不进行CLP）。将脓毒症大鼠模型随机分为未进一步处理的ALI组（n = 15）、在远离足三里穴位处进行电针治疗30分钟的ALI + SEA组（n = 15）和在足三里穴位处进行相同频率、强度和持续时间电针刺激的ALI + EA组（n = 15）。所有大鼠在CLP术后12小时处死，测量肺组织重量及湿/干重（W/D）比值。采用苏木精-伊红（HE）染色观察肺组织病理变化，采用酶联免疫吸附测定（ELISA）法检测肺组织匀浆中肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）的含量。采用末端脱氧核苷酸转移酶介导的缺口末端标记（TUNEL）染色检测凋亡细胞，采用蛋白质免疫印迹法检测Bax、半胱天冬酶-3（caspase-3）及JAK1/信号转导子和转录激活子3（STAT3）信号通路中重要蛋白（JAK1和STAT3）的表达。
与假手术组相比，ALI组大鼠肺组织病变明显，肺W/D比值显著升高（P < 0.01），肺组织TNF-α和IL-6表达显著升高（P < 0.01），JAK1、STAT3、caspase-3及Bax表达明显上调（P < 0.01）；ALI + SEA组大鼠也观察到类似变化（P > 0.05）。与ALI + SEA组相比，ALI + EA组大鼠肺组织病变明显减轻，肺W/D比值降低（P < 0.01），肺组织TNF-α、IL-6、JAK1、STAT3、caspase-3及Bax表达降低（P < 0.01）。
电针预处理可通过JAK1/STAT3信号通路抑制炎症介质释放及细胞凋亡，减轻脓毒症大鼠肺损伤。
