安徽医科大学学报
安徽醫科大學學報
안휘의과대학학보
Acta Universitatis Medicinalis Anhui
2015年
10期
1443-1447
,共5页
吴永琴%关存杰%刘洪茂%姬艳丽%徐德祥
吳永琴%關存傑%劉洪茂%姬豔麗%徐德祥
오영금%관존걸%류홍무%희염려%서덕상
氯化镉%急性肝损伤%动物模型%MDA%NO%GSH
氯化鎘%急性肝損傷%動物模型%MDA%NO%GSH
록화력%급성간손상%동물모형%MDA%NO%GSH
cadmium chloride%acute liver injury%animal model%MDA%NO%GSH
目的 通过腹腔注射氯化镉( CdCl2 )建立小鼠急性肝损伤模型,初步阐明其分子机制. 方法 以4 mg/kg CdCl2腹腔注射小鼠,观察各时间点小鼠肝组织病理变化和血清丙氨酸氨基转移酶( ALT)、天冬氨酸氨基转移酶( AST)的变化,探索CdCl2 引起明显肝损伤的染毒时间;以1、2、4 mg/kg CdCl2 对小鼠腹腔注射染毒,筛选出CdCl2 诱导急性肝损伤的最佳染毒剂量;检测血清丙二醛( MDA)以及肝匀浆MDA、一氧化氮( NO )、谷胱甘肽( GSH )、谷胱甘肽过氧化物酶( GSH-PX)含量,观察氧化应激在CdCl2 诱导的小鼠肝损伤中的作用. 结果 以4 mg/kg CdCl2 腹腔注射18 h后,肝脏组织出现片状坏死,肝细胞严重气球样变,血清ALT和AST明显升高. 此外,与对照组比较,CdCl2 处理18 h后,血清与肝脏MDA及肝脏NO水平显著升高,肝脏GSH、GSH-PX活性明显降低. 结论 4 mg/kg CdCl2 腹腔注射18 h后可成功建立小鼠急性肝损伤模型,其发生可能与MDA和NO升高,肝组织GSH含量、GSH-PX活性降低相关.
目的 通過腹腔註射氯化鎘( CdCl2 )建立小鼠急性肝損傷模型,初步闡明其分子機製. 方法 以4 mg/kg CdCl2腹腔註射小鼠,觀察各時間點小鼠肝組織病理變化和血清丙氨痠氨基轉移酶( ALT)、天鼕氨痠氨基轉移酶( AST)的變化,探索CdCl2 引起明顯肝損傷的染毒時間;以1、2、4 mg/kg CdCl2 對小鼠腹腔註射染毒,篩選齣CdCl2 誘導急性肝損傷的最佳染毒劑量;檢測血清丙二醛( MDA)以及肝勻漿MDA、一氧化氮( NO )、穀胱甘肽( GSH )、穀胱甘肽過氧化物酶( GSH-PX)含量,觀察氧化應激在CdCl2 誘導的小鼠肝損傷中的作用. 結果 以4 mg/kg CdCl2 腹腔註射18 h後,肝髒組織齣現片狀壞死,肝細胞嚴重氣毬樣變,血清ALT和AST明顯升高. 此外,與對照組比較,CdCl2 處理18 h後,血清與肝髒MDA及肝髒NO水平顯著升高,肝髒GSH、GSH-PX活性明顯降低. 結論 4 mg/kg CdCl2 腹腔註射18 h後可成功建立小鼠急性肝損傷模型,其髮生可能與MDA和NO升高,肝組織GSH含量、GSH-PX活性降低相關.
목적 통과복강주사록화력( CdCl2 )건립소서급성간손상모형,초보천명기분자궤제. 방법 이4 mg/kg CdCl2복강주사소서,관찰각시간점소서간조직병리변화화혈청병안산안기전이매( ALT)、천동안산안기전이매( AST)적변화,탐색CdCl2 인기명현간손상적염독시간;이1、2、4 mg/kg CdCl2 대소서복강주사염독,사선출CdCl2 유도급성간손상적최가염독제량;검측혈청병이철( MDA)이급간균장MDA、일양화담( NO )、곡광감태( GSH )、곡광감태과양화물매( GSH-PX)함량,관찰양화응격재CdCl2 유도적소서간손상중적작용. 결과 이4 mg/kg CdCl2 복강주사18 h후,간장조직출현편상배사,간세포엄중기구양변,혈청ALT화AST명현승고. 차외,여대조조비교,CdCl2 처리18 h후,혈청여간장MDA급간장NO수평현저승고,간장GSH、GSH-PX활성명현강저. 결론 4 mg/kg CdCl2 복강주사18 h후가성공건립소서급성간손상모형,기발생가능여MDA화NO승고,간조직GSH함량、GSH-PX활성강저상관.
Objective To establish the mouse model of acute liver damage induced cadmium chloride and elucidate the mechanism of Cd-induced-liver injury. Methods The adult male mice were intraperitoneally ( i. p. ) injected with a single dose of CdCl2 (4 mg/kg) and killed at different time(6, 12, 18, 24 h) after Cd treatment, or admin-istrated with different doses of CdCl2 (1, 2 or 4 mg/kg) i. p. and sacrificed at 18 h after Cd exposure. The control group received only equal volumes of normal saline. Histopathology of liver tissues, serum of ALT, AST and MDA, and MDA,NO,GSH,GSH-PX of liver tissues were observed. Results 18 hours after the treatment of using 4 mg/kg dosage, i. p, liver tissues appeared visible pathological changes with severe ballooning degeneration and necro-sis, the levels of ALT and AST in serum were obviously higher. In addition, at 18 h after Cd treatment, the levels of MDA and NO in liver tissues significantly increased in the cadmium group, however, the level of GSH and the activity of GSH-PX in liver tissues significantly decreased. Conclusion A mouse model of acute liver injury is successfully established by intraperitoneal injection with 4 mg/kg CdCl2 at 18 hours after Cd treatment. The mecha-nism might be associated with the increase of MDA and NO and the decrease of the level of GSH and the activity of GSH-PX in liver tissues.
