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
1451-1455
,共5页
夏玲玲%周仲松%谢琴秀%朱启金
夏玲玲%週仲鬆%謝琴秀%硃啟金
하령령%주중송%사금수%주계금
糖尿病%肝脏%内质网应激%炎症%白芍总苷
糖尿病%肝髒%內質網應激%炎癥%白芍總苷
당뇨병%간장%내질망응격%염증%백작총감
diabetes%liver%endoplasmic reticulum stress%inflammation%total glucosides of paeony
目的 探讨白芍总苷( TGP)对糖尿病大鼠肝脏损害的保护作用是否与抑制内质网应激( ERS)有关. 方法 建立链脲佐菌素( STZ)诱导的糖尿病模型,随机分为对照组、模型组、TGP ( 50、100、200 mg/kg )给药组. 应用油红 O与Masson染色对肝组织行病理检查;采用免疫组化法检测肝组织ED-1表达;采用Western blot法检测GRP78、p-Perk及p-Eif2α的表达. 结果 TGP给药可降低糖尿病大鼠肝重增加及肝组织总胆固醇( TC)、三酰甘油( TG)及游离脂肪酸( FFA)水平. 模型组肝细胞油红O染色评分明显高于对照组( P <0. 01 );TGP 各给药组评分明显低于模型组( P <0. 01). Masson染色模型组肝纤维化评分明显高于对照组(P<0. 01);TGP 50、100、200 mg/kg给药组评分明显低于模型组( P<0. 01 ). 免疫组化显示模型组肝组织巨噬细胞浸润明显增加,各给药组均能抑制糖尿病肝组织巨噬细胞浸润的增加. Western blot显示糖尿病模型组肝组织GRP78、p-Perk及p-Eif2α表达明显高于对照组, TGP 给药组肝组织GRP78、p-Perk及p-Eif2α表达明显低于模型组. 结论 TGP对糖尿病肝损害有明显保护作用,其机制可能与其抗炎、抑制ERS有关.
目的 探討白芍總苷( TGP)對糖尿病大鼠肝髒損害的保護作用是否與抑製內質網應激( ERS)有關. 方法 建立鏈脲佐菌素( STZ)誘導的糖尿病模型,隨機分為對照組、模型組、TGP ( 50、100、200 mg/kg )給藥組. 應用油紅 O與Masson染色對肝組織行病理檢查;採用免疫組化法檢測肝組織ED-1錶達;採用Western blot法檢測GRP78、p-Perk及p-Eif2α的錶達. 結果 TGP給藥可降低糖尿病大鼠肝重增加及肝組織總膽固醇( TC)、三酰甘油( TG)及遊離脂肪痠( FFA)水平. 模型組肝細胞油紅O染色評分明顯高于對照組( P <0. 01 );TGP 各給藥組評分明顯低于模型組( P <0. 01). Masson染色模型組肝纖維化評分明顯高于對照組(P<0. 01);TGP 50、100、200 mg/kg給藥組評分明顯低于模型組( P<0. 01 ). 免疫組化顯示模型組肝組織巨噬細胞浸潤明顯增加,各給藥組均能抑製糖尿病肝組織巨噬細胞浸潤的增加. Western blot顯示糖尿病模型組肝組織GRP78、p-Perk及p-Eif2α錶達明顯高于對照組, TGP 給藥組肝組織GRP78、p-Perk及p-Eif2α錶達明顯低于模型組. 結論 TGP對糖尿病肝損害有明顯保護作用,其機製可能與其抗炎、抑製ERS有關.
목적 탐토백작총감( TGP)대당뇨병대서간장손해적보호작용시부여억제내질망응격( ERS)유관. 방법 건립련뇨좌균소( STZ)유도적당뇨병모형,수궤분위대조조、모형조、TGP ( 50、100、200 mg/kg )급약조. 응용유홍 O여Masson염색대간조직행병리검사;채용면역조화법검측간조직ED-1표체;채용Western blot법검측GRP78、p-Perk급p-Eif2α적표체. 결과 TGP급약가강저당뇨병대서간중증가급간조직총담고순( TC)、삼선감유( TG)급유리지방산( FFA)수평. 모형조간세포유홍O염색평분명현고우대조조( P <0. 01 );TGP 각급약조평분명현저우모형조( P <0. 01). Masson염색모형조간섬유화평분명현고우대조조(P<0. 01);TGP 50、100、200 mg/kg급약조평분명현저우모형조( P<0. 01 ). 면역조화현시모형조간조직거서세포침윤명현증가,각급약조균능억제당뇨병간조직거서세포침윤적증가. Western blot현시당뇨병모형조간조직GRP78、p-Perk급p-Eif2α표체명현고우대조조, TGP 급약조간조직GRP78、p-Perk급p-Eif2α표체명현저우모형조. 결론 TGP대당뇨병간손해유명현보호작용,기궤제가능여기항염、억제ERS유관.
Objective To investigate prevention of early liver injury by total glucosides of paeony ( TGP) in diabetic rats and whether its mechanism was related to the inhibition of endoplasmic reticulum stress. Methods TGP (50, 100, 200 mg/kg) was orally administered once a day for 8 weeks in STZ-induced diabetic rats. The levels of cho-lesterol, triglyceride and free fatty acid in liver tissue were determined by spetrophotometric method. Liver lesions were evaluated using oil red O and Masson staining. Expression of ED-1 was determined by immunohistochemistry and GRP78, p-Perk, p-Eif2αwere determined by Western blot analysis. Results TGP treatment in all three doses significantly reduced increased liver weight and liver lipid content in diabetic rats. Oil red O staining score in dia-betic group was significantly higher than that in the control group ( P<0. 01 ) , TGP 50 ,100 ,200 mg/kg treatment group scores were significantly lower than those in the diabetic group ( P<0. 01 ) . Masson staining showed hepatic fibrosis score was much higher than that in the control group ( P<0. 01 ) , hepatic fibrosis scores in TGP 50 ,100 , 200 mg/kg treatment group were significantly lower than those in the diabetic group. Compared with the control group, immunohistochemistry showed that macrophage infiltration in the liver tissue from diabetic significantly in-creased, which was inhibited by TGP treatment in all three doses. Expressions of GRP78, p-Perk and p-Eif2αde-termined by Western blot in liver tissue of diabetic group were significantly higher than that in the control group, which also were decreased by TGP administration (50, 100, 200 mg/kg). Conclusion Our results indicate that TGP has potential as a treatment for diabetic liver injury through attenuating liver lipid accumulation and inflamma-tion as well as ERS induced by diabetic condition.
