实用肝脏病杂志
實用肝髒病雜誌
실용간장병잡지
JOURNAL OF CLINICAL HEPATOLOGY
2015年
5期
530-533
,共4页
关永霞%李晓梅%张永霞%李晓丽%王平平%张贵民
關永霞%李曉梅%張永霞%李曉麗%王平平%張貴民
관영하%리효매%장영하%리효려%왕평평%장귀민
酒精性肝炎%化滞柔肝颗粒%脂多糖%小鼠
酒精性肝炎%化滯柔肝顆粒%脂多糖%小鼠
주정성간염%화체유간과립%지다당%소서
Alcoholic hepatitis%Huazhi Rougan granule%Lipopolysaccharide%Mice
目的:观察化滞柔肝颗粒对酒精联合脂多糖诱导的酒精性肝炎小鼠的保护作用。方法将80只ICR小鼠随机分成正常组、模型组、小、中、大剂量化滞柔肝组和护肝片处理组,通过灌胃给予56%北京红星二锅头(12 ml·kg-1.d-1)和脂多糖(5 mg·kg-1,2次/w)腹腔注射,建立酒精性肝炎小鼠模型,同时给予相应的药物灌胃,连续10 w。在末次给药后,解剖动物,取血清和肝组织,进行相应的检查。结果在实验10 w末,模型组肝组织肝细胞水肿,胞浆疏松,其肝质量指数、血清ALT和AST水平分别为(5.77±0.67)%、(82.22±6.20) U/L和(93.43±17.30) U/L,均显著高于正常组[分别为(4.44±0.42)%、(35.83±3.84) U/L和(66.43±5.14) U/L,P<0.05];大剂量化滞柔肝组肝质量指数为(5.24±0.36)%,显著低于模型组[(5.77±0.67)%,P<0.05],小、中、大剂量化滞柔肝颗粒组和护肝片组ALT和AST水平均显著低于模型组(P<0.001);小、中、大剂量化滞柔肝颗粒组和护肝片组的CK分别为(118.93±10.15) U/L、(102.33±8.07) U/L、(119.45±19.26) U/L和(104.00±8.15) U/L,均显著低于模型组[(227.50±50.10) U/L,P<0.001];小、中、大剂量化滞柔肝组和护肝片组血清TBIL水平均显著低于模型组(P<0.01);各试验组之间血脂水平均无明显变化。结论化滞柔肝颗粒对酒精联合脂多糖诱导的酒精性肝炎小鼠有保护作用,为化滞柔肝颗粒将来用于临床治疗酒精性脂肪肝提供了试验支持。
目的:觀察化滯柔肝顆粒對酒精聯閤脂多糖誘導的酒精性肝炎小鼠的保護作用。方法將80隻ICR小鼠隨機分成正常組、模型組、小、中、大劑量化滯柔肝組和護肝片處理組,通過灌胃給予56%北京紅星二鍋頭(12 ml·kg-1.d-1)和脂多糖(5 mg·kg-1,2次/w)腹腔註射,建立酒精性肝炎小鼠模型,同時給予相應的藥物灌胃,連續10 w。在末次給藥後,解剖動物,取血清和肝組織,進行相應的檢查。結果在實驗10 w末,模型組肝組織肝細胞水腫,胞漿疏鬆,其肝質量指數、血清ALT和AST水平分彆為(5.77±0.67)%、(82.22±6.20) U/L和(93.43±17.30) U/L,均顯著高于正常組[分彆為(4.44±0.42)%、(35.83±3.84) U/L和(66.43±5.14) U/L,P<0.05];大劑量化滯柔肝組肝質量指數為(5.24±0.36)%,顯著低于模型組[(5.77±0.67)%,P<0.05],小、中、大劑量化滯柔肝顆粒組和護肝片組ALT和AST水平均顯著低于模型組(P<0.001);小、中、大劑量化滯柔肝顆粒組和護肝片組的CK分彆為(118.93±10.15) U/L、(102.33±8.07) U/L、(119.45±19.26) U/L和(104.00±8.15) U/L,均顯著低于模型組[(227.50±50.10) U/L,P<0.001];小、中、大劑量化滯柔肝組和護肝片組血清TBIL水平均顯著低于模型組(P<0.01);各試驗組之間血脂水平均無明顯變化。結論化滯柔肝顆粒對酒精聯閤脂多糖誘導的酒精性肝炎小鼠有保護作用,為化滯柔肝顆粒將來用于臨床治療酒精性脂肪肝提供瞭試驗支持。
목적:관찰화체유간과립대주정연합지다당유도적주정성간염소서적보호작용。방법장80지ICR소서수궤분성정상조、모형조、소、중、대제양화체유간조화호간편처리조,통과관위급여56%북경홍성이과두(12 ml·kg-1.d-1)화지다당(5 mg·kg-1,2차/w)복강주사,건립주정성간염소서모형,동시급여상응적약물관위,련속10 w。재말차급약후,해부동물,취혈청화간조직,진행상응적검사。결과재실험10 w말,모형조간조직간세포수종,포장소송,기간질량지수、혈청ALT화AST수평분별위(5.77±0.67)%、(82.22±6.20) U/L화(93.43±17.30) U/L,균현저고우정상조[분별위(4.44±0.42)%、(35.83±3.84) U/L화(66.43±5.14) U/L,P<0.05];대제양화체유간조간질량지수위(5.24±0.36)%,현저저우모형조[(5.77±0.67)%,P<0.05],소、중、대제양화체유간과립조화호간편조ALT화AST수평균현저저우모형조(P<0.001);소、중、대제양화체유간과립조화호간편조적CK분별위(118.93±10.15) U/L、(102.33±8.07) U/L、(119.45±19.26) U/L화(104.00±8.15) U/L,균현저저우모형조[(227.50±50.10) U/L,P<0.001];소、중、대제양화체유간조화호간편조혈청TBIL수평균현저저우모형조(P<0.01);각시험조지간혈지수평균무명현변화。결론화체유간과립대주정연합지다당유도적주정성간염소서유보호작용,위화체유간과립장래용우림상치료주정성지방간제공료시험지지。
Objective To study the protective effects of Huazhirougan granule on liver tissue injuries of mice with alcohol and lipopolysaccharide-induced alcoholic hepatitis. Methods Eighty mice were randomly divid-ed into control,model,and low,middle and high dose of Huazhirougan granule,and Hugan tablet group. Except in the control group,the mice in other five groups had 56% alcohol by intragastric administration once daily,and in-traperitoneal administration of lipopolysaccharide twice a week,and then intragastricly administered corresponding drugs in the afternoon for 10 weeks. The serum levels of ALT,AST,CK,γ-GT,ALP,TBIL,TG,TC,HDL-C and LDL-C were measured. The liver tissues were fixed by formaldehyde,routine paraffin section,and hematoxylin-eosin staining. Results The liver mass index,serum ALT and AST levels in the model group increased signifi-cantly [(5.77±0.67)%,(82.22±6.20) U/L and (93.43±17.30) U/L] vs. [(4.44±0.42)%,(35.83±3.84) U/L and (66.43±5.14) U/L,P<0.05] as compared with in control group; the serum levels of transaminase in the low,mid-dle,and high dose of Huazhirougan granule group,and Hugan tablet group decreased significantly as compared to those in model group (P<0.001);The serum CK levels in the low,middle,and high dose of Huazhirougan granule group,and Hugan tablet group were (118.93±10.15) U/L,(102.33±8.07) U/L,(119.45±19.26) U/L,(104.00±8.15) U/L,significantly decreased as compared with in model group [(227.50±50.10) U/L,P<0.001];The serum bilirubin levels also decreased significantly as compared with in model group (P<0.01). Conclusion Huazhirougan granule can protect the alcoholic liver injuries in mice with alcohol and lipopolysaccharide- induced alcoholic hepatitis.