中国药理学通报
中國藥理學通報
중국약이학통보
CHINESE PHARMACOLOGICAL BULLETIN
2014年
12期
1677-1680,1681
,共5页
孙阿宁%任改艳%邓超%张晶晶%王峥涛%窦薇
孫阿寧%任改豔%鄧超%張晶晶%王崢濤%竇薇
손아저%임개염%산초%장정정%왕쟁도%두미
牡荆素%溃疡性结肠炎%葡聚糖硫酸钠%MPO%TNF-α%IL-6%COX-2
牡荊素%潰瘍性結腸炎%葡聚糖硫痠鈉%MPO%TNF-α%IL-6%COX-2
모형소%궤양성결장염%포취당류산납%MPO%TNF-α%IL-6%COX-2
vitexin%ulcerative colitis%dextran sul-phate sodium%MPO%TNF-α%IL-6%COX-2
目的：探讨牡荆素对葡聚糖硫酸钠（dextran sulfate so-dium，DSS）诱导的小鼠溃疡性结肠炎（ulcerative colitis， UC）的药效作用及机制。方法将 C57BL／6小鼠随机分成3组（n ＝10）：正常对照组、模型组（4％ DSS）和牡荆素组（4％ DSS ＋牡荆素，50 mg·kg －1）。除正常对照组外，其他组小鼠饮用水中加入4％ DSS 造模，造模同时牡荆素灌胃给药，每天1次，并每天称重和观察血便等症状，直到实验结束。于造模7 d 处死小鼠，截取结肠做 HE 染色并进行组织损伤和炎性细胞浸润评分；ELISA 方法检测小鼠结肠黏膜髓过氧化物酶（myeloperoxidase，MPO）活性；反转录荧光定量PCR 方法检测小鼠结肠组织肿瘤坏死因子α（tumor necrosis factor-α，TNF-α）、白介素6（interleukin-6，IL-6）及环氧合酶-2（cyclooxygenase 2，COX-2）mRNA 的表达水平。结果与正常对照组相比，模型组小鼠体重明显减轻，组织病理评分增高，同时结肠匀浆 MPO 水平明显升高，结肠组织 TNF-α、IL-6和 COX-2表达升高。与模型组比较，牡荆素组小鼠上述指标明显改善。结论牡荆素能有效减轻小鼠实验性溃疡性结肠炎，缓解炎症反应，其机制可能与抑制中性粒细胞浸润和减少炎症因子释放有关。
目的：探討牡荊素對葡聚糖硫痠鈉（dextran sulfate so-dium，DSS）誘導的小鼠潰瘍性結腸炎（ulcerative colitis， UC）的藥效作用及機製。方法將 C57BL／6小鼠隨機分成3組（n ＝10）：正常對照組、模型組（4％ DSS）和牡荊素組（4％ DSS ＋牡荊素，50 mg·kg －1）。除正常對照組外，其他組小鼠飲用水中加入4％ DSS 造模，造模同時牡荊素灌胃給藥，每天1次，併每天稱重和觀察血便等癥狀，直到實驗結束。于造模7 d 處死小鼠，截取結腸做 HE 染色併進行組織損傷和炎性細胞浸潤評分；ELISA 方法檢測小鼠結腸黏膜髓過氧化物酶（myeloperoxidase，MPO）活性；反轉錄熒光定量PCR 方法檢測小鼠結腸組織腫瘤壞死因子α（tumor necrosis factor-α，TNF-α）、白介素6（interleukin-6，IL-6）及環氧閤酶-2（cyclooxygenase 2，COX-2）mRNA 的錶達水平。結果與正常對照組相比，模型組小鼠體重明顯減輕，組織病理評分增高，同時結腸勻漿 MPO 水平明顯升高，結腸組織 TNF-α、IL-6和 COX-2錶達升高。與模型組比較，牡荊素組小鼠上述指標明顯改善。結論牡荊素能有效減輕小鼠實驗性潰瘍性結腸炎，緩解炎癥反應，其機製可能與抑製中性粒細胞浸潤和減少炎癥因子釋放有關。
목적：탐토모형소대포취당류산납（dextran sulfate so-dium，DSS）유도적소서궤양성결장염（ulcerative colitis， UC）적약효작용급궤제。방법장 C57BL／6소서수궤분성3조（n ＝10）：정상대조조、모형조（4％ DSS）화모형소조（4％ DSS ＋모형소，50 mg·kg －1）。제정상대조조외，기타조소서음용수중가입4％ DSS 조모，조모동시모형소관위급약，매천1차，병매천칭중화관찰혈편등증상，직도실험결속。우조모7 d 처사소서，절취결장주 HE 염색병진행조직손상화염성세포침윤평분；ELISA 방법검측소서결장점막수과양화물매（myeloperoxidase，MPO）활성；반전록형광정량PCR 방법검측소서결장조직종류배사인자α（tumor necrosis factor-α，TNF-α）、백개소6（interleukin-6，IL-6）급배양합매-2（cyclooxygenase 2，COX-2）mRNA 적표체수평。결과여정상대조조상비，모형조소서체중명현감경，조직병리평분증고，동시결장균장 MPO 수평명현승고，결장조직 TNF-α、IL-6화 COX-2표체승고。여모형조비교，모형소조소서상술지표명현개선。결론모형소능유효감경소서실험성궤양성결장염，완해염증반응，기궤제가능여억제중성립세포침윤화감소염증인자석방유관。
Aim To evaluate the effect and mecha-nism of vitexin in a mouse model of DSS-induced ulcer-ative colitis (UC).Methods C57BL/6 mice were randomly placed into three groups: normal control group,DSS group and DSS +Vitexin group.Mice coli-tis was induced by adding 4% dextran sulphate sodium (DSS)into the drinking water for seven days.Vitexin was administered once a day along with DSS treatment. Mice were monitored daily with body weight change and diarrhea symptoms.After sacrifice,colon was re-moved and fixed in 1 0% (W/V)buffered formalin for hematoxylin-eosin (H&E)staining.Histological dam-age was assessed as a combined score of inflammatory cell infiltration and mucosal damage.The remaining colon pieces were collected to measure the activity of myeloperoxidase (MPO)by ELISA method and to de-termine the mRNA expression of TNF-α,IL-6 and COX-2.Results None of the mice receiving vehicle alone exhibited body weight loss and mucosal disrup-tion at any point during the study.Vitexin treatment significantly ameliorated DSS-induced body weight loss and histological score.The activity of MPO and the mRNA expression of TNF-α,IL-6 and COX-2 were markedly inhibited by vitexin treatment.Conclusion Vitexin ameliorates DSS-induced colitis through sup-pressing leukocyte infiltration and pro-inflammatory mediators production.
