CAJ | 학술논문

目的:研究电针足三里(ST36)对脓毒症大鼠促炎症因子所致多脏器功能损害的影响.方法:雄性Wistar大鼠64只,采用盲肠结扎穿孔术(CLP)制备大鼠脓毒症模型,随机分为CLP+电针(EA)足三里组 (CLP/EA组)、CLP+假电针(sham EA)组(CLP/SEA组)、迷走神经切断(VA)+CLP+SEA组(VA/CLP/SEA组)和VA+CLP+EA组(VA/CLP/EA组),每组16只.CLP/EA组持续针刺双侧足三里穴30 min),强度为2 mA,2-100 Hz.CLP/SEA组采用相同频率和强度刺激非经非穴(足三里外侧旁开0.5 cm)30 min).VA组于CLP前切断双侧迷走神经干.各组大鼠于CLP术后12 h取血检测血浆谷丙转氨酶(ALT)和肌苷(Cr);然后处死动物,取肝、肾和空肠组织检测肿瘤坏死因子-α(TNF-α)含量、髓过氧化物酶(MPO)和二胺氧化酶(DAO)活性以及脏器组织含水率.结果:与CLP/SEA组比较,CLP/EA组TNF-α、MPO、ALT、 Cr水平和脏器组织含水率显著降低,肠组织DAO活性显著增加 (均P<0.05);VA/CLP组和VA/CLP/EA组TNF-α、MPO、ALT、 Cr水平和脏器组织含水率显著增加,DAO活性显著降低 (均P<0.05);VA/CLP/EA组与VA/CLP组比较,上述指标的变化无显著差异(P＞0.05).结论:电针足三里显著抑制CLP大鼠肝、肾和空肠组织TNF-α水平,减轻脏器水肿和功能损害;切断迷走神经能显著减轻或消除EA的作用,上调组织TNF-α水平、加重脏器损害.电针足三里的抗炎和减轻脏器损伤的机制可能与兴奋胆碱能抗炎通路有关.
목적:연구전침족삼리(ST36)대농독증대서촉염증인자소치다장기공능손해적영향.방법:웅성Wistar대서64지,채용맹장결찰천공술(CLP)제비대서농독증모형,수궤분위CLP+전침(EA)족삼리조 (CLP/EA조)、CLP+가전침(sham EA)조(CLP/SEA조)、미주신경절단(VA)+CLP+SEA조(VA/CLP/SEA조)화VA+CLP+EA조(VA/CLP/EA조),매조16지.CLP/EA조지속침자쌍측족삼리혈30 min),강도위2 mA,2-100 Hz.CLP/SEA조채용상동빈솔화강도자격비경비혈(족삼리외측방개0.5 cm)30 min).VA조우CLP전절단쌍측미주신경간.각조대서우CLP술후12 h취혈검측혈장곡병전안매(ALT)화기감(Cr);연후처사동물,취간、신화공장조직검측종류배사인자-α(TNF-α)함량、수과양화물매(MPO)화이알양화매(DAO)활성이급장기조직함수솔.결과:여CLP/SEA조비교,CLP/EA조TNF-α、MPO、ALT、 Cr수평화장기조직함수솔현저강저,장조직DAO활성현저증가 (균P<0.05);VA/CLP조화VA/CLP/EA조TNF-α、MPO、ALT、 Cr수평화장기조직함수솔현저증가,DAO활성현저강저 (균P<0.05);VA/CLP/EA조여VA/CLP조비교,상술지표적변화무현저차이(P＞0.05).결론:전침족삼리현저억제CLP대서간、신화공장조직TNF-α수평,감경장기수종화공능손해;절단미주신경능현저감경혹소제EA적작용,상조조직TNF-α수평、가중장기손해.전침족삼리적항염화감경장기손상적궤제가능여흥강담감능항염통로유관.
AIM: To investigate the effect of electro-acupuncture (EA) at Zusanli (ST36) on proinflammatory factors induced-multiple organ dysfunction in rats with sepsis. METHODS: Sixty four male Wastar rats were used to develop the sepsis model by cecal ligation and puncture (CLP). The animals were randomly divided into 4 groups (n=16 in each group): CLP+EA (CLP/EA), CLP+sham EA (CLP/SEA), vagotomy+ CLP+SEA (VA/CLP/SEA) and vagotomy+CLP+EA (VA/CLP/EA). Zusanli point (ST36) was electroacupunctured with constant voltage (2-100 Hz, 2 mA for 0.5 h) 20 min after CLP surgery. Bilateral cervical vagotomies were performed in rats in VA/CL/SEA and VA/CLP/EA groups. Twelve hours after CLP, animals were sacrificed and liver, kidney and jejunum were harvested for evaluating the contents of tumor necrosis factor-α (TNF-α), myeloperoxidase (MPO) and diamine oxidase (DAO). The rate of water content (WCR) of the organs was determined. At the same time, the plasma levels of alanine aminotransferase (ALT) and creatinine (Cr) in each group were also detected. RESULTS: The levels of ALT and Cr in plasma, as well as TNF-α, MPO and WCR in organ tissues were markedly lower, and the activity of DAO in jejunum tissue was obviously higher than that in CLP/SEA group at 12 h after CLP (all P<0.05). The levels of ALT, Cr, TNF-α, MPO and WCR in VA/CLP/SEA group and VA/CLP/EA group were significantly higher, the activity of DAO was obviously lower than that in CLP/SEA group (all P<0.05). No statistical difference in all above measurements between VA/CLP/EA group and VA/CLP/SEA) group was observed (all P>0.05). CONCLUSION: The results indicate that EA at Zusanli point obviously decreases the levels of TNF-α in liver, kidney and jejunum tissues after CLP, and alleviates the tissue edema and dysfunction of those organs. Vagotomy decreases or eliminates the effects of EA, suggesting that activation of cholinergic anti-inflammatory pathway is one of the main mechanisms to induce the effects of EA at ST36 on CLP sepsis.