【目的】研究黄芪甲苷对 SD大鼠脓毒症致肝损伤的保护作用。【方法】采用盲肠结扎穿孔（Cecal ligation and puncture ，CLP）诱导形成脓毒症大鼠肝损伤模型，黄芪甲苷分别于大鼠 CLP术前1 h灌胃给药。30只SD大鼠随机分为三组，分别为...【目的】研究黄芪甲苷对 SD大鼠脓毒症致肝损伤的保护作用。【方法】采用盲肠结扎穿孔（Cecal ligation and puncture ，CLP）诱导形成脓毒症大鼠肝损伤模型，黄芪甲苷分别于大鼠 CLP术前1 h灌胃给药。30只SD大鼠随机分为三组，分别为假手术组、CLP模型组、CLP＋黄芪甲苷（50 mg／kg）治疗组。记录一般情况并检测CLP术后24 h各组大鼠的存活率，血清中谷丙转氨酶（ALT）、谷草转氨酶（AST）水平及各组大鼠肝脏组织中TNF‐α、IL‐6水平及其 HE染色的病理变化情况。【结果】各时间点假手术组大鼠均无死亡。术后12 h ，模型组、黄芪甲苷组大鼠存活率分别为80％和100％，术后24 h ，模型组大鼠无存活，而黄芪甲苷组大鼠存活率为40％，经比较有显著性差异（χ2＝8．4，P＜0．05），显示黄芪甲苷能提高实验性脓毒症大鼠的存活率；术后24 h ，大鼠血清AST、ALT值脓毒症模型组较假手术组显著升高（ P ＜0．05），黄芪甲苷治疗组则明显改善（ P ＜0．05）；脓毒症模型组较假手术组肝组织 TNF‐α、IL‐6值显著升高（ P ＜0．05），黄芪甲苷治疗组则明显改善（ P＜0．05）；病理切片显示假手术组大鼠肝脏结构轻微改变，脓毒症模型组肝组织点灶状坏死、混合炎细胞浸润、肝细胞脂肪变性，黄芪甲苷治疗组肝脏组织病理损伤情况均较模型组明显改善。【结论】黄芪甲苷对CLP诱导的SD大鼠肝损伤具有一定的保护作用。展开更多
AIM： To investigate the innate immune reactivity of tumor necrosis factor-alpha （TNF-α）, Toll-like receptor 4 （TLR4）, and CD14 in the liver of non-alcoholic steatohepatitis （NASH） model rats. METHODS： Male F3...AIM： To investigate the innate immune reactivity of tumor necrosis factor-alpha （TNF-α）, Toll-like receptor 4 （TLR4）, and CD14 in the liver of non-alcoholic steatohepatitis （NASH） model rats. METHODS： Male F344 rats were fed a cholinedeficient L-amino-acid-defined （CDAA） diet. The rats were killed after 4 or 8 wk of the diet, and their livers were removed for immunohistochemical investigation and RNA extraction. The liver specimens were immunostained for TNF-α, TLR4, and CD14. The gene expressions of TNF-α, TLR4, and CD14 were determined by reverse-transcriptase polymerase chain reaction （RT-PCR）. Kupffer cells were isolated from the liver by Percoll gradient centrifugation, and were then cultured to measure TNF-α production. RESULTS： The serum and liver levels of TNF-~ in the CDAA-fed rats increased significantly as compared with the control group, as did the immunohistochemical values and gene expressions of TNF-α, TLR4, and CD14 with the progression of steatohepatitis. TNF-α production from the isolated Kupffer cells of the CDAAfed rats was elevated by lipopolysaccharide stimulation. CONCLUSION： The expressions of TNF-α, TLR4, and CD14 increased in the NASH model, suggesting that展开更多
目的探讨乌司他丁(UTI)对脂多糖(LPS)致大鼠急性肺损伤(ALI)组织糖皮质激素受体(GR)的影响,并了解其可能机制。方法清洁级成年雄性SD大鼠54只,随机分为3组:空白对照组(Con组,n=18),LPS组(n=18),脂多糖+乌司他丁组(LPS+UTI组,n=18)。各...目的探讨乌司他丁(UTI)对脂多糖(LPS)致大鼠急性肺损伤(ALI)组织糖皮质激素受体(GR)的影响,并了解其可能机制。方法清洁级成年雄性SD大鼠54只,随机分为3组:空白对照组(Con组,n=18),LPS组(n=18),脂多糖+乌司他丁组(LPS+UTI组,n=18)。各组又按照不同的时间点被分为4 h、8 h、12 h三个亚组。在各时间点处死大鼠,利用Western blot检测大鼠肺组织中GR的表达,实时荧光定量PCR检测GR m RNA的表达,同时酶联免疫吸附法(ELISA)检测肺组织匀浆液中肿瘤坏死因子(TNF)-α和白细胞介素(IL)-10的浓度以及肺组织病理学的变化。结果与对照组相比,LPS组GR蛋白表达在各时间点降低(P<0.05),LPS+UTI组GR蛋白在各时间点的表达水平高于LPS组,低于Con组(P<0.05);与对照组相比,LPS组GR m RNA表达降低(P<0.05),LPS+UTI组GR m RNA在各时间点的表达水平略高于LPS组(P>0.05),低于Con组(P<0.05);与对照组相比,LPS组TNF-α的表达在各时间点升高(P<0.05),LPS+UTI组TNF-α的表达水平在各时间点低于LPS组,高于Con组(P<0.05);与对照组相比,LPS组IL-10的表达在各时间点升高(P<0.05),LPS+UTI组IL-10的表达水平在各时间点高于LPS组(P<0.05)。组织病理学检查显示:LPS组肺组织见肺泡结构破坏,炎性细胞浸润,肺泡间隔增宽,出血,水肿,LPS+UTI组肺组织病理损害较LPS组明显减轻。结论 UTI能提高GR的表达;TNF-α和IL-10出现高峰的时间不同。展开更多
OBJECTIVE: To investigate effects of Xinfeng capsule(XFC) on cardiac function in rats with adjuvant arthritis(AA) and explore the mechanism of these effects.METHODS: Forty-eight rats were randomly divided into normal ...OBJECTIVE: To investigate effects of Xinfeng capsule(XFC) on cardiac function in rats with adjuvant arthritis(AA) and explore the mechanism of these effects.METHODS: Forty-eight rats were randomly divided into normal control(NC), model control(MC), methotrexate(MTX) and XFC groups of equal size. In all groups except for the NC group, 0.1 m L Freund's complete adjuvant(FCA) was intracutaneously injected in the right rear vola pedis to induce inflammation. Drugs were applied beginning 19 days after induction of inflammation. Normal saline was administered to the NC and MC groups and 1 mg/100 g MTX(weekly) and 0.12 g/100 g XFC(daily) to the MTX and XFC groups, respectively. Rats were sacrificed after 30 day of treatment. Toe swelling degree(TSD), arthritis index(AI), cardiac function and expression of nuclear factor kappa B(NF-κB) / tumor necrosis factor alpha(TNF-α) and transforming growth factor beta 1(TGF-β1)/Smads pathway proteins were measured.RESULTS: In the MC group, TSD and AI were greatly increased, while parameters of cardiac function were decreased and morphological analysis showed myocardial cell damage. Expression of TNF-α, NF-κB, Smad2, P-Smad2, Smad4 and TGF-β1 proteins were elevated in cardiac tissue, while Smad7 expression was decreased.TSD and AI values closely correlated to parameters of cardiac function and to levels of proteins in the NF-κB/TNF-α and TGF-β1/Smads pathways. Certain correlations were identified among TGF-β1 and NF-κB, Smad2, P-Smad2 and Smad4.With XFC intervention, both TSD and AI were decreased and parameters of cardiac function and ultrastructure of myocardial cells improved.Expressions of NF-κB, Smad2, and Smad4 proteins were greatly decreased and Smad7 expression was elevated, as compared with levels in the MC and MTX groups.CONCLUSION: XFC regulates expression of proteins in the NF-κB/TNF-α and TGF-β1/Smads pathways, decreases immune complex deposition in cardiac tissue and improves cardiac function in AA rats via upregulation of Smad7.展开更多
文摘【目的】研究黄芪甲苷对 SD大鼠脓毒症致肝损伤的保护作用。【方法】采用盲肠结扎穿孔（Cecal ligation and puncture ，CLP）诱导形成脓毒症大鼠肝损伤模型，黄芪甲苷分别于大鼠 CLP术前1 h灌胃给药。30只SD大鼠随机分为三组，分别为假手术组、CLP模型组、CLP＋黄芪甲苷（50 mg／kg）治疗组。记录一般情况并检测CLP术后24 h各组大鼠的存活率，血清中谷丙转氨酶（ALT）、谷草转氨酶（AST）水平及各组大鼠肝脏组织中TNF‐α、IL‐6水平及其 HE染色的病理变化情况。【结果】各时间点假手术组大鼠均无死亡。术后12 h ，模型组、黄芪甲苷组大鼠存活率分别为80％和100％，术后24 h ，模型组大鼠无存活，而黄芪甲苷组大鼠存活率为40％，经比较有显著性差异（χ2＝8．4，P＜0．05），显示黄芪甲苷能提高实验性脓毒症大鼠的存活率；术后24 h ，大鼠血清AST、ALT值脓毒症模型组较假手术组显著升高（ P ＜0．05），黄芪甲苷治疗组则明显改善（ P ＜0．05）；脓毒症模型组较假手术组肝组织 TNF‐α、IL‐6值显著升高（ P ＜0．05），黄芪甲苷治疗组则明显改善（ P＜0．05）；病理切片显示假手术组大鼠肝脏结构轻微改变，脓毒症模型组肝组织点灶状坏死、混合炎细胞浸润、肝细胞脂肪变性，黄芪甲苷治疗组肝脏组织病理损伤情况均较模型组明显改善。【结论】黄芪甲苷对CLP诱导的SD大鼠肝损伤具有一定的保护作用。
基金Supported by Grant-in-Aid for Scientific Research from the Ministry of Education,Culture,Sports,Science,and Technology of Japan,No.19590784
文摘AIM： To investigate the innate immune reactivity of tumor necrosis factor-alpha （TNF-α）, Toll-like receptor 4 （TLR4）, and CD14 in the liver of non-alcoholic steatohepatitis （NASH） model rats. METHODS： Male F344 rats were fed a cholinedeficient L-amino-acid-defined （CDAA） diet. The rats were killed after 4 or 8 wk of the diet, and their livers were removed for immunohistochemical investigation and RNA extraction. The liver specimens were immunostained for TNF-α, TLR4, and CD14. The gene expressions of TNF-α, TLR4, and CD14 were determined by reverse-transcriptase polymerase chain reaction （RT-PCR）. Kupffer cells were isolated from the liver by Percoll gradient centrifugation, and were then cultured to measure TNF-α production. RESULTS： The serum and liver levels of TNF-~ in the CDAA-fed rats increased significantly as compared with the control group, as did the immunohistochemical values and gene expressions of TNF-α, TLR4, and CD14 with the progression of steatohepatitis. TNF-α production from the isolated Kupffer cells of the CDAAfed rats was elevated by lipopolysaccharide stimulation. CONCLUSION： The expressions of TNF-α, TLR4, and CD14 increased in the NASH model, suggesting that
文摘目的探讨乌司他丁(UTI)对脂多糖(LPS)致大鼠急性肺损伤(ALI)组织糖皮质激素受体(GR)的影响,并了解其可能机制。方法清洁级成年雄性SD大鼠54只,随机分为3组:空白对照组(Con组,n=18),LPS组(n=18),脂多糖+乌司他丁组(LPS+UTI组,n=18)。各组又按照不同的时间点被分为4 h、8 h、12 h三个亚组。在各时间点处死大鼠,利用Western blot检测大鼠肺组织中GR的表达,实时荧光定量PCR检测GR m RNA的表达,同时酶联免疫吸附法(ELISA)检测肺组织匀浆液中肿瘤坏死因子(TNF)-α和白细胞介素(IL)-10的浓度以及肺组织病理学的变化。结果与对照组相比,LPS组GR蛋白表达在各时间点降低(P<0.05),LPS+UTI组GR蛋白在各时间点的表达水平高于LPS组,低于Con组(P<0.05);与对照组相比,LPS组GR m RNA表达降低(P<0.05),LPS+UTI组GR m RNA在各时间点的表达水平略高于LPS组(P>0.05),低于Con组(P<0.05);与对照组相比,LPS组TNF-α的表达在各时间点升高(P<0.05),LPS+UTI组TNF-α的表达水平在各时间点低于LPS组,高于Con组(P<0.05);与对照组相比,LPS组IL-10的表达在各时间点升高(P<0.05),LPS+UTI组IL-10的表达水平在各时间点高于LPS组(P<0.05)。组织病理学检查显示:LPS组肺组织见肺泡结构破坏,炎性细胞浸润,肺泡间隔增宽,出血,水肿,LPS+UTI组肺组织病理损害较LPS组明显减轻。结论 UTI能提高GR的表达;TNF-α和IL-10出现高峰的时间不同。
基金Supported by Natural Science Foundation of China(Mechanism Research of Xinfeng Capsule through the NF-kappa B/TNF Alpha and Beta 1/Smads TGF-Pathways,No.81173211)National Sci-tech Support Plan(Clinical Research on Intractable Diseases of Traditional Chinese Medicine Treated by Xi'an Medicine,No.2012BA126B02)+1 种基金Construction Program of Study of Bi Syndrome in Traditional Chinese Medicine of State Key Subject[State Traditional Chinese Medicine Issue(2009)No.30]Natural Science Foundation of Anhui Province(Mechanism Research of Xinfeng capsules Improve Cardiopulmonary Based on the NF-kappa B/TNF Alpha and TGF-beta 1/Smads Pathways in AA Rats,No.1208085MH180)
文摘OBJECTIVE: To investigate effects of Xinfeng capsule(XFC) on cardiac function in rats with adjuvant arthritis(AA) and explore the mechanism of these effects.METHODS: Forty-eight rats were randomly divided into normal control(NC), model control(MC), methotrexate(MTX) and XFC groups of equal size. In all groups except for the NC group, 0.1 m L Freund's complete adjuvant(FCA) was intracutaneously injected in the right rear vola pedis to induce inflammation. Drugs were applied beginning 19 days after induction of inflammation. Normal saline was administered to the NC and MC groups and 1 mg/100 g MTX(weekly) and 0.12 g/100 g XFC(daily) to the MTX and XFC groups, respectively. Rats were sacrificed after 30 day of treatment. Toe swelling degree(TSD), arthritis index(AI), cardiac function and expression of nuclear factor kappa B(NF-κB) / tumor necrosis factor alpha(TNF-α) and transforming growth factor beta 1(TGF-β1)/Smads pathway proteins were measured.RESULTS: In the MC group, TSD and AI were greatly increased, while parameters of cardiac function were decreased and morphological analysis showed myocardial cell damage. Expression of TNF-α, NF-κB, Smad2, P-Smad2, Smad4 and TGF-β1 proteins were elevated in cardiac tissue, while Smad7 expression was decreased.TSD and AI values closely correlated to parameters of cardiac function and to levels of proteins in the NF-κB/TNF-α and TGF-β1/Smads pathways. Certain correlations were identified among TGF-β1 and NF-κB, Smad2, P-Smad2 and Smad4.With XFC intervention, both TSD and AI were decreased and parameters of cardiac function and ultrastructure of myocardial cells improved.Expressions of NF-κB, Smad2, and Smad4 proteins were greatly decreased and Smad7 expression was elevated, as compared with levels in the MC and MTX groups.CONCLUSION: XFC regulates expression of proteins in the NF-κB/TNF-α and TGF-β1/Smads pathways, decreases immune complex deposition in cardiac tissue and improves cardiac function in AA rats via upregulation of Smad7.
