中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2014年
1期
38-40,封3
,共4页
袁昊%余保平%张丽%杨斌%潘陈为%胡锐%胡桂英%黄梦君%谢枝隽
袁昊%餘保平%張麗%楊斌%潘陳為%鬍銳%鬍桂英%黃夢君%謝枝雋
원호%여보평%장려%양빈%반진위%호예%호계영%황몽군%사지준
慢性胰腺炎%甘氨酸受体β亚基%疼痛
慢性胰腺炎%甘氨痠受體β亞基%疼痛
만성이선염%감안산수체β아기%동통
Chronic pancreatitis%Glycine receptor beta subunit%Pain
目的 观察抑制性神经递质甘氨酸受体β亚基(GLRB)在慢性胰腺炎(CP)疼痛模型中的表达,探讨其与CP炎疼痛发生的关系.方法 30只雄性Wistar大鼠随机分成正常对照组、磷酸盐缓冲液(PBS)胰管内注射假手术组、三硝基苯磺酸(TNBS)胰管内注射模型组3组,通过胰腺组织苏木素-伊红(HE)染色及疼痛阈值测定判定造模成功与否.荧光实时定量聚合酶链反应(FQ-PCR)检测脊髓背根神经节中GLRB基因表达水平,免疫组织化学检测其表达部位及强弱.根据GLRB表达水平分析其与疼痛相关性.结果 造模前后,3组疼痛阈值测定均成动态变化,先降低后升高,造模第4周,造模组疼痛阈值低于假手术组和对照组(3组比较:x2=4.279<x20.05(8),P>0.05;两两对比:P <0.05).在GLRB基凶表达层面上,造模组较假手术组和对照组表达上调,造模组GLRB相对表达量为4.545 2±1.886 0,假手术组GLRB相对表达量为1.841 0±1.0490,对照组GLRB相对表达量为1.4920±1.1370(上调约2.5倍,P<0.05).免疫组织化学结果示表达部位主要于神经节细胞胞质.结论 抑制性神经递质GLRB在CP脊髓背根神经节组织中表达增加,疼痛阈值呈先降低后升高至接近正常的动态变化,可能是自我保护机制的负反馈调节作用.
目的 觀察抑製性神經遞質甘氨痠受體β亞基(GLRB)在慢性胰腺炎(CP)疼痛模型中的錶達,探討其與CP炎疼痛髮生的關繫.方法 30隻雄性Wistar大鼠隨機分成正常對照組、燐痠鹽緩遲液(PBS)胰管內註射假手術組、三硝基苯磺痠(TNBS)胰管內註射模型組3組,通過胰腺組織囌木素-伊紅(HE)染色及疼痛閾值測定判定造模成功與否.熒光實時定量聚閤酶鏈反應(FQ-PCR)檢測脊髓揹根神經節中GLRB基因錶達水平,免疫組織化學檢測其錶達部位及彊弱.根據GLRB錶達水平分析其與疼痛相關性.結果 造模前後,3組疼痛閾值測定均成動態變化,先降低後升高,造模第4週,造模組疼痛閾值低于假手術組和對照組(3組比較:x2=4.279<x20.05(8),P>0.05;兩兩對比:P <0.05).在GLRB基兇錶達層麵上,造模組較假手術組和對照組錶達上調,造模組GLRB相對錶達量為4.545 2±1.886 0,假手術組GLRB相對錶達量為1.841 0±1.0490,對照組GLRB相對錶達量為1.4920±1.1370(上調約2.5倍,P<0.05).免疫組織化學結果示錶達部位主要于神經節細胞胞質.結論 抑製性神經遞質GLRB在CP脊髓揹根神經節組織中錶達增加,疼痛閾值呈先降低後升高至接近正常的動態變化,可能是自我保護機製的負反饋調節作用.
목적 관찰억제성신경체질감안산수체β아기(GLRB)재만성이선염(CP)동통모형중적표체,탐토기여CP염동통발생적관계.방법 30지웅성Wistar대서수궤분성정상대조조、린산염완충액(PBS)이관내주사가수술조、삼초기분광산(TNBS)이관내주사모형조3조,통과이선조직소목소-이홍(HE)염색급동통역치측정판정조모성공여부.형광실시정량취합매련반응(FQ-PCR)검측척수배근신경절중GLRB기인표체수평,면역조직화학검측기표체부위급강약.근거GLRB표체수평분석기여동통상관성.결과 조모전후,3조동통역치측정균성동태변화,선강저후승고,조모제4주,조모조동통역치저우가수술조화대조조(3조비교:x2=4.279<x20.05(8),P>0.05;량량대비:P <0.05).재GLRB기흉표체층면상,조모조교가수술조화대조조표체상조,조모조GLRB상대표체량위4.545 2±1.886 0,가수술조GLRB상대표체량위1.841 0±1.0490,대조조GLRB상대표체량위1.4920±1.1370(상조약2.5배,P<0.05).면역조직화학결과시표체부위주요우신경절세포포질.결론 억제성신경체질GLRB재CP척수배근신경절조직중표체증가,동통역치정선강저후승고지접근정상적동태변화,가능시자아보호궤제적부반궤조절작용.
Objective To study the expression of glycine receptor beta subunit in the model of chronic pancreatitis,and evaluate the relationship between glycine receptor beta subunit and pain in chronic pancreatitis.Methods Thirty male Wistar rats were randomly divided into three groups:normal group,phosphate buffer (PBS) perfusion group,and trinitrobenzene sulfonic acid perfusion group.Histopathological and pain examinations were done to confirm the establishment of chronic pancreatitis model.Real-time fluorescent quantitative polymerase chain reaction (FQ-PCR) was applied to detect the expression of glycine receptor beta subunit.Immunohistochemistry was used to localize the expression site of glycine receptor beta subunit.Results Pain examination in this model showed dynamic,decrease at first,increase at last.Compared with another groups,the trinitrobenzene sulfonic acid perfusion group is lower in the aspect about the pain during the fourth week (comparing the three groups:x2 =4.279<x0.05 (8),P > 0.05 ; comparing with each other:P <0.05),but higher than others in gene expression (2.5 times,P <0.05),and strongly expression was observed in cytoplasm.Conclusion Enhanced expression of glycine receptor beta subunit,the inhibitory neurotransmitter,is involved in the pain of chronic pancreatitis.For self-protection,it reduces the degree of pain below normal lever.