郑州大学学报（医学版）
鄭州大學學報（醫學版）
정주대학학보（의학판）
JOURNAL OF ZHENGZHOU UNIVERSITY(MEDICAL SCIENCES)
2014年
3期
319-322
,共4页
徐宏平%贾宝辉%艾启帆%孙顾峰%汪嘉飞%刘浩%刘祥玉%程舒
徐宏平%賈寶輝%艾啟帆%孫顧峰%汪嘉飛%劉浩%劉祥玉%程舒
서굉평%가보휘%애계범%손고봉%왕가비%류호%류상옥%정서
人参皂甙Rb1%感染性休克%Toll样受体4%肿瘤坏死因子-α%大鼠
人參皂甙Rb1%感染性休剋%Toll樣受體4%腫瘤壞死因子-α%大鼠
인삼조대Rb1%감염성휴극%Toll양수체4%종류배사인자-α%대서
ginsenoside Rb1%septic shock%Toll like receptor 4%TNF-α%rat
目的：探讨人参皂甙Rb1对感染性休克大鼠重要器官的保护作用及其机制。方法：66只SD大鼠随机分为假手术组、模型组、Rb1治疗（0．04 mg/g）组，每组22只。模型组和Rb1治疗组大鼠建立感染性休克动物模型。观察3组大鼠肝、肺组织病理变化，检测血清肿瘤坏死因子-α（ TNF-α）含量和心肌组织Toll样受体4（ TLR4） mRNA表达的变化。结果：模型组肝细胞肿胀、变性、坏死，中性粒细胞浸润；Rb1治疗组肝细胞浊肿，轻度变性，未见明显坏死灶，肝血窦中中性粒细胞浸润较轻。模型组部分肺泡上皮细胞肿胀，肺泡隔增宽，毛细血管明显扩张淤血，微血栓形成，肺间质充血水肿，弥漫性中性粒细胞浸润，肺泡腔内大量炎性渗出；Rb1治疗组小血管及毛细血管内中性粒细胞浸润较轻，肺间质轻度水肿，肺泡隔增宽不明显，肺泡腔无渗出物。模型组血清TNF-α、心肌组织TLR4 mRNA水平高于假手术组，Rb1治疗组两指标低于模型组（P＜0．01）。结论：Rb1可保护感染性休克大鼠肝、肺组织，其机制可能与减少TLR4 mRNA表达水平，抑制TNF-α的产生有关。
目的：探討人參皂甙Rb1對感染性休剋大鼠重要器官的保護作用及其機製。方法：66隻SD大鼠隨機分為假手術組、模型組、Rb1治療（0．04 mg/g）組，每組22隻。模型組和Rb1治療組大鼠建立感染性休剋動物模型。觀察3組大鼠肝、肺組織病理變化，檢測血清腫瘤壞死因子-α（ TNF-α）含量和心肌組織Toll樣受體4（ TLR4） mRNA錶達的變化。結果：模型組肝細胞腫脹、變性、壞死，中性粒細胞浸潤；Rb1治療組肝細胞濁腫，輕度變性，未見明顯壞死竈，肝血竇中中性粒細胞浸潤較輕。模型組部分肺泡上皮細胞腫脹，肺泡隔增寬，毛細血管明顯擴張淤血，微血栓形成，肺間質充血水腫，瀰漫性中性粒細胞浸潤，肺泡腔內大量炎性滲齣；Rb1治療組小血管及毛細血管內中性粒細胞浸潤較輕，肺間質輕度水腫，肺泡隔增寬不明顯，肺泡腔無滲齣物。模型組血清TNF-α、心肌組織TLR4 mRNA水平高于假手術組，Rb1治療組兩指標低于模型組（P＜0．01）。結論：Rb1可保護感染性休剋大鼠肝、肺組織，其機製可能與減少TLR4 mRNA錶達水平，抑製TNF-α的產生有關。
목적：탐토인삼조대Rb1대감염성휴극대서중요기관적보호작용급기궤제。방법：66지SD대서수궤분위가수술조、모형조、Rb1치료（0．04 mg/g）조，매조22지。모형조화Rb1치료조대서건립감염성휴극동물모형。관찰3조대서간、폐조직병리변화，검측혈청종류배사인자-α（ TNF-α）함량화심기조직Toll양수체4（ TLR4） mRNA표체적변화。결과：모형조간세포종창、변성、배사，중성립세포침윤；Rb1치료조간세포탁종，경도변성，미견명현배사조，간혈두중중성립세포침윤교경。모형조부분폐포상피세포종창，폐포격증관，모세혈관명현확장어혈，미혈전형성，폐간질충혈수종，미만성중성립세포침윤，폐포강내대량염성삼출；Rb1치료조소혈관급모세혈관내중성립세포침윤교경，폐간질경도수종，폐포격증관불명현，폐포강무삼출물。모형조혈청TNF-α、심기조직TLR4 mRNA수평고우가수술조，Rb1치료조량지표저우모형조（P＜0．01）。결론：Rb1가보호감염성휴극대서간、폐조직，기궤제가능여감소TLR4 mRNA표체수평，억제TNF-α적산생유관。
Aim:To observe the protective effect of ginsenoside Rb 1 on vital organs in rats with septic shock .Meth-ods:The septic shock model was reproduced by CLP .Sixty-six SD rats were randomly divided into three groups ( 22 in each group):sham group, CLP group and ginsenoside Rb1 group(0.04 mg/g).The liver and lung samples were prepared for observation of pathological changes;the expression of Toll like receptor 4(TLR4) mRNA in myocardial tissue was deter-mined by RT-PCR;the serum tumor necrosis factor-α(TNF-α) was measured by ELISA.Results:In CLP group, patho-logical results showed swelling , degeneration , necrosis and neutrophil infiltration in the liver cells , which were milder in ginsenoside Rb1 group.Moreover, in CLP group, there were swelling in alveolar epithelial cells , thickening in alveolar septum, expansion and congestion in capillaries , microthrombosis, congestion and edema in pulmonary interstitial , diffuse infiltration of neutrophils and diminished alveolar space with heavy inflammatory exudation ,which were milder in ginsen-oside Rb1 group.The TLR4 mRNA in myocardial tissue and serum TNF-αin CLP group were significantly higher than those in sham group(P<0.01).The ginsenoside Rb1 group had markedly lower TLR4 mRNA expression and TNF-αlevel than the CLP group(P <0.01).Conclusion: Ginsenoside Rb1 could protect the liver and lung tissue of septic shock rats through down-regulating the expression of TLR 4 mRNA and inhibiting the produce of TNF-α.
