CAJ | 학술논문

目的：探讨电针足三里穴对肠缺血/再灌注（I/R）大鼠小肠促炎细胞因子引起的肠绒毛损伤及肠通透性的保护作用。方法将30只SD大鼠按随机数字表法分为肠I/R组（模型组）、肠I/R+电针足三里穴组（电针足三里穴组）、肠I/R+电针非经非穴组（电针非经非穴组），每组10只。采用夹闭肠系膜上动脉根部30 min、恢复灌注60 min的方法复制小鼠肠I/R损伤模型。电针足三里穴组于缺血后即刻电针双侧足三里穴30 min，强度为2～3 mA，频率2～100 Hz；电针非经非穴组采用相同频率和强度刺激足三里穴外侧旁开0.5 cm处30 min；模型组不进行任何治疗。于再灌注60 min处死各组动物，取远端回肠组织，检测肿瘤坏死因子-α（TNF-α）和白细胞介素-6（IL-6）含量，光镜下观察肠组织病理改变并进行肠损伤评分。于再灌注30 min在肠袋中注入异硫氰酸荧光素（FITC）标记的葡聚糖，再灌注60 min后腹主动脉取血，测定血中FITC-葡聚糖含量，观察肠黏膜通透性的改变。结果与模型组和电针非经非穴组比较，电针足三里穴可显著抑制肠道TNF-α（pg/mg：3.01±0.50比8.65±1.02、8.42±1.41，均P＜0.05）和IL-6（pg/mg：2.51±0.15比6.34±0.86、6.13±1.12，均P＜0.05）水平，降低I/R造成的肠绒毛损伤评分（分：1.50±0.33比3.18±0.39、3.04±0.37，均P＜0.05）及肠黏膜FITC-葡聚糖含量（μg/L：282.42±73.92比856.22±229.47、844.22±239.47，均P＜0.05），模型组与电针非经非穴组上述指标比较差异无统计学意义（均P＞0.05）。模型组与电针非经非穴组肠组织病理改变无明显差异，肠绒毛顶端坏死、变钝、塌陷；电针足三里穴组动物肠绒毛损伤较模型组与电针非经非穴组减轻。结论电针足三里穴能显著抑制肠I/R大鼠肠道促炎细胞因子水平、减轻肠黏膜损伤，其对肠道的保护作用可能与电针足三里穴降低肠黏膜通透性有关。目的：探討電針足三裏穴對腸缺血/再灌註（I/R）大鼠小腸促炎細胞因子引起的腸絨毛損傷及腸通透性的保護作用。方法將30隻SD大鼠按隨機數字錶法分為腸I/R組（模型組）、腸I/R+電針足三裏穴組（電針足三裏穴組）、腸I/R+電針非經非穴組（電針非經非穴組），每組10隻。採用夾閉腸繫膜上動脈根部30 min、恢複灌註60 min的方法複製小鼠腸I/R損傷模型。電針足三裏穴組于缺血後即刻電針雙側足三裏穴30 min，彊度為2～3 mA，頻率2～100 Hz；電針非經非穴組採用相同頻率和彊度刺激足三裏穴外側徬開0.5 cm處30 min；模型組不進行任何治療。于再灌註60 min處死各組動物，取遠耑迴腸組織，檢測腫瘤壞死因子-α（TNF-α）和白細胞介素-6（IL-6）含量，光鏡下觀察腸組織病理改變併進行腸損傷評分。于再灌註30 min在腸袋中註入異硫氰痠熒光素（FITC）標記的葡聚糖，再灌註60 min後腹主動脈取血，測定血中FITC-葡聚糖含量，觀察腸黏膜通透性的改變。結果與模型組和電針非經非穴組比較，電針足三裏穴可顯著抑製腸道TNF-α（pg/mg：3.01±0.50比8.65±1.02、8.42±1.41，均P＜0.05）和IL-6（pg/mg：2.51±0.15比6.34±0.86、6.13±1.12，均P＜0.05）水平，降低I/R造成的腸絨毛損傷評分（分：1.50±0.33比3.18±0.39、3.04±0.37，均P＜0.05）及腸黏膜FITC-葡聚糖含量（μg/L：282.42±73.92比856.22±229.47、844.22±239.47，均P＜0.05），模型組與電針非經非穴組上述指標比較差異無統計學意義（均P＞0.05）。模型組與電針非經非穴組腸組織病理改變無明顯差異，腸絨毛頂耑壞死、變鈍、塌陷；電針足三裏穴組動物腸絨毛損傷較模型組與電針非經非穴組減輕。結論電針足三裏穴能顯著抑製腸I/R大鼠腸道促炎細胞因子水平、減輕腸黏膜損傷，其對腸道的保護作用可能與電針足三裏穴降低腸黏膜通透性有關。
목적：탐토전침족삼리혈대장결혈/재관주（I/R）대서소장촉염세포인자인기적장융모손상급장통투성적보호작용。방법장30지SD대서안수궤수자표법분위장I/R조（모형조）、장I/R+전침족삼리혈조（전침족삼리혈조）、장I/R+전침비경비혈조（전침비경비혈조），매조10지。채용협폐장계막상동맥근부30 min、회복관주60 min적방법복제소서장I/R손상모형。전침족삼리혈조우결혈후즉각전침쌍측족삼리혈30 min，강도위2～3 mA，빈솔2～100 Hz；전침비경비혈조채용상동빈솔화강도자격족삼리혈외측방개0.5 cm처30 min；모형조불진행임하치료。우재관주60 min처사각조동물，취원단회장조직，검측종류배사인자-α（TNF-α）화백세포개소-6（IL-6）함량，광경하관찰장조직병리개변병진행장손상평분。우재관주30 min재장대중주입이류청산형광소（FITC）표기적포취당，재관주60 min후복주동맥취혈，측정혈중FITC-포취당함량，관찰장점막통투성적개변。결과여모형조화전침비경비혈조비교，전침족삼리혈가현저억제장도TNF-α（pg/mg：3.01±0.50비8.65±1.02、8.42±1.41，균P＜0.05）화IL-6（pg/mg：2.51±0.15비6.34±0.86、6.13±1.12，균P＜0.05）수평，강저I/R조성적장융모손상평분（분：1.50±0.33비3.18±0.39、3.04±0.37，균P＜0.05）급장점막FITC-포취당함량（μg/L：282.42±73.92비856.22±229.47、844.22±239.47，균P＜0.05），모형조여전침비경비혈조상술지표비교차이무통계학의의（균P＞0.05）。모형조여전침비경비혈조장조직병리개변무명현차이，장융모정단배사、변둔、탑함；전침족삼리혈조동물장융모손상교모형조여전침비경비혈조감경。결론전침족삼리혈능현저억제장I/R대서장도촉염세포인자수평、감경장점막손상，기대장도적보호작용가능여전침족삼리혈강저장점막통투성유관。
Objective To investigate the protective effects of elctroacupuncture(EA)at Zusanli(ST36) points on intestinal villas damage and mucosal permeability induced by small intestine pro-inflammatory factors in rats with intestinal ischemia/reperfusion(I/R). Methods 30 Sprague-Dawley(SD)rats were randomly divided into three groups(each,n=10):intestinal I/R group(model group),intestinal I/R+EA ST36 group(EA group)and intestinal I/R+sham EA group(SEA group). Rats were subjected to superior mesenteric artery(SMA)clamping at its root part to occlude the vessel for 30 minutes,followed by reperfusion for 60 minutes to form intestinal I/R models. Rats in EA group received EA at the bilateral ST36 points(2-3 mA,2-100 Hz)for 30 minutes immediately after ischemia,those in SEA group received EA at bilateral sham points(the point was located at 0.5 cm away from ST36 point in its lateral side)with the same frequency and intensity of stimulation as EA group for 30 minutes,and those in model group received no treatment. Animals were sacrificed 60 minutes after reperfusion and segments of distal part of ileum were harvested,then the levels of tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)in intestinal tissue were measured. Histopathologic changes were viewed and graded via light microscopy. A solution of fluorescein isothiocyanate(FITC)-dextran was injected into the lumen of the segment of intestine 30 minutes after reperfusion,systemic blood was drawn via abdominal aorta puncture at 60 minutes after reperfusion,and then the level of FITC-dextran in blood was measured to determine the changes in intestinal permeability. Results Compared to the model group and SEA group,EA ST36 significantly attenuated intestine TNF-α(pg/mg:3.01±0.50 vs. 8.65±1.02,8.42±1.41,both P<0.05)and IL-6 levels(pg/mg:2.51±0.15 vs. 6.34±0.86,6.13±1.12,both P<0.05),successfully maintained low gut injury scores(1.50±0.33 vs. 3.18±0.39,3.04±0.37,both P<0.05), and significantly reduced permeability of the distal ileum and the content of FITC-dextran(μg/L:282.42±73.92 vs. 856.22±229.47,844.22±239.47,both P<0.05). However,there were no significant differences in all above variables between SEA and model group(all P>0.05). Sections of distal ileum from animals in the model group and SEA group showed no obvious difference histologically,and the pathological manifestations were villous tip necrosis, blunt-shaped and collapse. Compared to the model group and SEA group,the intestinal villous injury in animals of EA group was much milder. Conclusion In rats with intestinal I/R injury,EA ST36 points has protective effect on the gut that is possibly due to the fact it may obviously lower the levels of the pro-inflammatory factors of small intestinal tissue,alleviate mucosal insult of gut and reduce the mucosal permeability.