浙江医学
浙江醫學
절강의학
ZHEJIANG MEDICAL JOURNAL
2015年
12期
1037-1040,1045
,共5页
沈淑蓉%朱静%张浩%曾静静%付瑶阳%王雅琪%王方岩
瀋淑蓉%硃靜%張浩%曾靜靜%付瑤暘%王雅琪%王方巖
침숙용%주정%장호%증정정%부요양%왕아기%왕방암
酪酸梭菌%阿司匹林%胃溃疡%氧化应激
酪痠梭菌%阿司匹林%胃潰瘍%氧化應激
락산사균%아사필림%위궤양%양화응격
Clostridium butyricum%Aspirin%Gastric ulcer%Oxidative stress
目的:观测酪酸梭菌是否对阿司匹林导致的胃溃疡具有预防效应,并对其机制进行初步探讨。方法取30只健康雄性ICR小鼠,随机分成3组,每组各10只,即模型组、酪酸梭菌组、奥美拉唑组。酪酸梭菌组以6×108cfu/只的菌量,模型组和奥美拉唑组均予以相同体积的无菌培养基,灌胃4d后再饥饿处理48h,然后以250mg/kg剂量的阿司匹林灌胃造模,奥美拉唑组小鼠于造模前30min,腹腔注射奥美拉唑(13mg/kg)。造模4h后,取胃组织分别测定SOD、CAT活力、MDA含量;进行常规HE染色观察胃黏膜组织结构变化,PAS染色判断黏液量的变化,免疫组化法测定Bcl-2、Bax表达水平。结果模型组的SOD、CAT活性明显降低,MDA含量显著增加,而酪酸梭菌预处理后逆转了该趋势(P<0.01),与奥美拉唑组比较无统计学差异。HE染色观察,酪酸梭菌能减轻胃黏膜的病理损伤,与奥美拉唑组无统计学差异。PAS结果提示酪酸梭菌能够增加黏液量。酪酸梭菌组的Bcl-2表达较模型组显著增多,同时Bax表达显著减少。结论酪酸梭菌预处理通过抗氧化应激、增加胃黏液量、上调Bcl-2/Bax表达比例,减轻阿司匹林造成的胃溃疡损伤。
目的:觀測酪痠梭菌是否對阿司匹林導緻的胃潰瘍具有預防效應,併對其機製進行初步探討。方法取30隻健康雄性ICR小鼠,隨機分成3組,每組各10隻,即模型組、酪痠梭菌組、奧美拉唑組。酪痠梭菌組以6×108cfu/隻的菌量,模型組和奧美拉唑組均予以相同體積的無菌培養基,灌胃4d後再饑餓處理48h,然後以250mg/kg劑量的阿司匹林灌胃造模,奧美拉唑組小鼠于造模前30min,腹腔註射奧美拉唑(13mg/kg)。造模4h後,取胃組織分彆測定SOD、CAT活力、MDA含量;進行常規HE染色觀察胃黏膜組織結構變化,PAS染色判斷黏液量的變化,免疫組化法測定Bcl-2、Bax錶達水平。結果模型組的SOD、CAT活性明顯降低,MDA含量顯著增加,而酪痠梭菌預處理後逆轉瞭該趨勢(P<0.01),與奧美拉唑組比較無統計學差異。HE染色觀察,酪痠梭菌能減輕胃黏膜的病理損傷,與奧美拉唑組無統計學差異。PAS結果提示酪痠梭菌能夠增加黏液量。酪痠梭菌組的Bcl-2錶達較模型組顯著增多,同時Bax錶達顯著減少。結論酪痠梭菌預處理通過抗氧化應激、增加胃黏液量、上調Bcl-2/Bax錶達比例,減輕阿司匹林造成的胃潰瘍損傷。
목적:관측락산사균시부대아사필림도치적위궤양구유예방효응,병대기궤제진행초보탐토。방법취30지건강웅성ICR소서,수궤분성3조,매조각10지,즉모형조、락산사균조、오미랍서조。락산사균조이6×108cfu/지적균량,모형조화오미랍서조균여이상동체적적무균배양기,관위4d후재기아처리48h,연후이250mg/kg제량적아사필림관위조모,오미랍서조소서우조모전30min,복강주사오미랍서(13mg/kg)。조모4h후,취위조직분별측정SOD、CAT활력、MDA함량;진행상규HE염색관찰위점막조직결구변화,PAS염색판단점액량적변화,면역조화법측정Bcl-2、Bax표체수평。결과모형조적SOD、CAT활성명현강저,MDA함량현저증가,이락산사균예처리후역전료해추세(P<0.01),여오미랍서조비교무통계학차이。HE염색관찰,락산사균능감경위점막적병리손상,여오미랍서조무통계학차이。PAS결과제시락산사균능구증가점액량。락산사균조적Bcl-2표체교모형조현저증다,동시Bax표체현저감소。결론락산사균예처리통과항양화응격、증가위점액량、상조Bcl-2/Bax표체비례,감경아사필림조성적위궤양손상。
Objective To investigate the effect of Clostridium butyricum (C. butyricum) in prevention of gastric ulcer (GU) induced by aspirin in mice. Methods Thirty ICR mice were randomly divided into model group, bacteria group andomeprazole group (n=10/group). After starvation for 48h, mice were given oral y with 250mg/kg aspirin to establish GU model.Mice in bacteria group were oral y pretreated with C. butyricum 6 ×108cfu for 4d before starvation, while mice in model group and omeprazole groupwere given the samevolume of sterile culture medium.Mice in omeprazole group were intraperitoneal y injected with 13mg/kg omeprazole 30 min priorto aspirin treatment. Modeling for 4 h, gastric tissue was to harvest for measuring the activity of SOD and CAT, the content ofMDA, Bcl- 2 and Bax, HE staining and PAS staining were performed. Results In model group, the activity of SOD, CAT were significantly reduced while the content of MDA was significantly increased. The activity of SOD,CAT were in-creased while the content of MDA was reduced in bacteria group (P<0.01), there was no significant difference between bacteria and omeprazole group. The Bcl- 2 expression increased and Bax expression reduced in bacteria group. PAS stainning showed that the mucus secretion was increased in bacteria group and HE staining showed that the mucosa injury was attenuated in bacte-ria gorup. Conclusion C. butyricum can effectively protect the gastric mucosa against damages caused by aspirin in mice.