重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2015年
10期
1308-1310
,共3页
李小花%黎晓%万群雄%李和%李良东%黄志华%曾靖
李小花%黎曉%萬群雄%李和%李良東%黃誌華%曾靖
리소화%려효%만군웅%리화%리량동%황지화%증정
染料木素磺酸钠%慢性肝损伤%α7 尼古丁受体%白细胞介素 1β
染料木素磺痠鈉%慢性肝損傷%α7 尼古丁受體%白細胞介素 1β
염료목소광산납%만성간손상%α7 니고정수체%백세포개소 1β
genistein sodium sulfonate%chronic hepatic injury%α7 nicotinic acetylcholine receptor%interleukin-1beta
目的:观察染料木素磺酸钠(GSS)对小鼠慢性肝损伤的保护作用,以及其对肝组织α7尼古丁受体(α7nAChR)和白细胞介素1β(IL-1β)蛋白表达的影响。方法取 SPF 级雄性昆明种小鼠60只分成5组,分别为对照组、模型组、GSS 低剂量组、GSS 高剂量组及阳性药物组,每组12只。除对照组外其余4组采用腹腔注射10%四氯化碳(CCl4),体积为0.1 mL/10 g,持续6周,制备小鼠慢性肝损伤动物模型。同时 GSS 高、低剂量组分别灌胃给予不同剂量的 GSS(0.30、0.10 mg/kg),阳性药物组给予联苯双酯2.50 mg/kg,对照组及模型组给予等体积生理盐水,连续6 周。测定小鼠血清 AST 及 ALT 活性,并计算 AST/ALT 比值;Western blot 方法检测α7nAChR、IL-1β蛋白表达水平。结果模型组小鼠血清 ALT、AST 水平较对照组升高(P <0.05),肝组织α7nAChR 蛋白表达水平降低(P <0.01),IL-1β的表达水平升高(P <0.05);经 GSS 治疗后,血清 AST、ALT 水平明显低于模型组(P <0.05),α7nAChR 表达水平升高(P <0.01),IL-1β表达水平降低(P <0.05)。结论 GSS 可升高损伤的肝组织α7nAChR 的表达,激活胆碱能抗炎通路,从而减少致炎细胞因子的表达,可通过抑制炎症反应对抗小鼠慢性肝损伤。
目的:觀察染料木素磺痠鈉(GSS)對小鼠慢性肝損傷的保護作用,以及其對肝組織α7尼古丁受體(α7nAChR)和白細胞介素1β(IL-1β)蛋白錶達的影響。方法取 SPF 級雄性昆明種小鼠60隻分成5組,分彆為對照組、模型組、GSS 低劑量組、GSS 高劑量組及暘性藥物組,每組12隻。除對照組外其餘4組採用腹腔註射10%四氯化碳(CCl4),體積為0.1 mL/10 g,持續6週,製備小鼠慢性肝損傷動物模型。同時 GSS 高、低劑量組分彆灌胃給予不同劑量的 GSS(0.30、0.10 mg/kg),暘性藥物組給予聯苯雙酯2.50 mg/kg,對照組及模型組給予等體積生理鹽水,連續6 週。測定小鼠血清 AST 及 ALT 活性,併計算 AST/ALT 比值;Western blot 方法檢測α7nAChR、IL-1β蛋白錶達水平。結果模型組小鼠血清 ALT、AST 水平較對照組升高(P <0.05),肝組織α7nAChR 蛋白錶達水平降低(P <0.01),IL-1β的錶達水平升高(P <0.05);經 GSS 治療後,血清 AST、ALT 水平明顯低于模型組(P <0.05),α7nAChR 錶達水平升高(P <0.01),IL-1β錶達水平降低(P <0.05)。結論 GSS 可升高損傷的肝組織α7nAChR 的錶達,激活膽堿能抗炎通路,從而減少緻炎細胞因子的錶達,可通過抑製炎癥反應對抗小鼠慢性肝損傷。
목적:관찰염료목소광산납(GSS)대소서만성간손상적보호작용,이급기대간조직α7니고정수체(α7nAChR)화백세포개소1β(IL-1β)단백표체적영향。방법취 SPF 급웅성곤명충소서60지분성5조,분별위대조조、모형조、GSS 저제량조、GSS 고제량조급양성약물조,매조12지。제대조조외기여4조채용복강주사10%사록화탄(CCl4),체적위0.1 mL/10 g,지속6주,제비소서만성간손상동물모형。동시 GSS 고、저제량조분별관위급여불동제량적 GSS(0.30、0.10 mg/kg),양성약물조급여련분쌍지2.50 mg/kg,대조조급모형조급여등체적생리염수,련속6 주。측정소서혈청 AST 급 ALT 활성,병계산 AST/ALT 비치;Western blot 방법검측α7nAChR、IL-1β단백표체수평。결과모형조소서혈청 ALT、AST 수평교대조조승고(P <0.05),간조직α7nAChR 단백표체수평강저(P <0.01),IL-1β적표체수평승고(P <0.05);경 GSS 치료후,혈청 AST、ALT 수평명현저우모형조(P <0.05),α7nAChR 표체수평승고(P <0.01),IL-1β표체수평강저(P <0.05)。결론 GSS 가승고손상적간조직α7nAChR 적표체,격활담감능항염통로,종이감소치염세포인자적표체,가통과억제염증반응대항소서만성간손상。
Objective To observe the protective effects of genistein sodium sulfonate(GSS)on mice chronic hepatic injury in-duced by carbon tetrachloride(CCl4 )and its influence on the protein expression of α7 nicotinic acetylcholine receptor(α7nAChR) and interleukin-1 beta (IL-1β)in liver tissue.Methods 60 SPF grade male Kunming mice were randomly divided into 5 groups,in-cluding the control group,model group,low and high doses GSS groups,and positive control group,12 cases in each group.Except for the control group,the other 4 groups were intra peritoneally injected by 10 % CCl4 with a volume of 0.1 mL/10 g for 6 weeks. The mice chronic liver injury was prepared.At the same time,the high and low doses DSS groups were given the different doses of GSS(0.30,0.10 mg/kg),the positive control group was given bifendate(DDB,2.5mg/kg),the control group and the model group were given the equal volume of normal saline for 6 consecutive weeks.The AST and ALT activity was detect and the ratio of ALT/AST was calculated;the Western blot method was used to detect the expression levels ofα7nAChR and IL-1βprotein in liver.Re-sults The serum levels of ALT and AST in the model group were increased obviously,and the expression level ofα7nAChR in the liver tissue was decreased,while the expression level of IL-1βwas increased;after the GSS treatment,the serum AST and ALT lev-els were significantly lower than those in the model group(P <0.05),while the expression level ofα7nAChR was increased (P <0.01)and the expression level of IL-1βwas decreased(P <0.05).Conclusion GSS might increase the expression ofα7nAChR in injured liver tissue,activates the cholinergic anti-inflammatory pathway,thus decreases the expression of inflammatory cytokines and antagonizes the mice chronic liver injury by inhibiting the inflammatory reaction.