Objective： To study the structural shifts of gut flora in rats with acute alcoholic liver injury （AALI）, and the effect of Jianpi Huoxue Decoction （健脾活血汤, JPHXD） on the gut flora. Methods： Thirty-six Spragu...Objective： To study the structural shifts of gut flora in rats with acute alcoholic liver injury （AALI）, and the effect of Jianpi Huoxue Decoction （健脾活血汤, JPHXD） on the gut flora. Methods： Thirty-six Sprague- Dawley rats were randomly allocated to the control, AALI and JPHXD groups equally. The rats in the control group were given water and those in AALI and JPHXD groups were given ethanol by intragastric gavage for 5 days, while rats in the JPHXD group were administered JPHXD simultaneously. The blood and liver tissue were collected at the end of the experiment. The activities of serum alkaline aminotransferase （ALT）, aspartate aminotransferase （AST）, hepatic γ/-glutamyitranspetidase （γ-GT） and hepatic tdglyceride （TG） levels were determined. Plasma endotoxin level in the portal vein was measured. Pathological changes of liver tissues were determined by hematoxylin and Eosin （HE） staining and oil red O staining. The total DNA of gut flora were extracted from fecal samples by Bead-beating method and determined by ERIC-PCR fingerprint method. The similarity cluster analysis and principal component analysis were performed to analyze the ERIC-PCR fingerprint respectively. Results： In the AALI group, the ratio of liver/body weight, activities of ALT, AST and hepatic γ-GT, amount of hepatic TG were elevated significantly compared with those in the control group （all P〈0.01）. JPHXD decreased the ratio, activities of ALT, AST, γ-GT and TG significantly compared with those in the AALI group （P〈0.05 or P〈0.01）. HE and oil red O staining showed that fat deposited markedly in liver tissue, while JPHXD alleviated pathological changes markedly. Plasma LPS level in rat portal vein in the AALI group increased significantly （P〈0.01）, but it was decreased significantly in the JPHXD group （P〈0.01）. The cluster analysis and principal component analysis of ERIC-PCR fingerprint showed that gut flora in the hALl group changed markedly, and JPHXD could recover gu展开更多
目的:通过观察健脾活血方对胃癌前病变大鼠胃黏膜组织中CD44V6、MLH1及MSH2表达的影响,探讨健脾活血方对其干预的作用机制.方法:除正常组外,其他大鼠采用以N-甲基-N-硝基-N-亚硝基胍(N-methyl-N-nitro N-nitrosoguanidine,MNNG)为主同...目的:通过观察健脾活血方对胃癌前病变大鼠胃黏膜组织中CD44V6、MLH1及MSH2表达的影响,探讨健脾活血方对其干预的作用机制.方法:除正常组外,其他大鼠采用以N-甲基-N-硝基-N-亚硝基胍(N-methyl-N-nitro N-nitrosoguanidine,MNNG)为主同时配合0.3g/L雷尼替丁、400 mL/L乙醇及饥饱失常的多因素造模法建立胃癌前病变动物模型.将造模成功的40只大鼠随机分为模型组(0.9%氯化钠溶液)、胃复春组(0.86 g/kg)、健脾活血方高、中、低剂量组(32、16、8 g/kg),每组8只,每组每天给予等量(10 mL/kg)的不同药物灌胃一次,连续10 wk.实验末处死大鼠,给予相应处理后,快速免疫组织化学检测CD44V6、MLH1及MSH2表达情况.结果:模型组CD44V6表达与正常组相比明显升高(5.12±1.96 vs 0.25±0.46,P<0.01);健脾活血方高、中剂量组CD44V6表达与模型组相比均明显降低(2.25±0.71,3.25±0.31vs 5.12±1.96,P<0.01或P<0.05),低剂量组C D44V6表达与模型组比较差异无统计学意义(P>0.05);健脾活血方高剂量组CD44V6表达与胃复春组相比明显降低(2.25±0.71 vs4.62±1.19,P<0.01),中、低剂量组CD44V6表达与胃复春组比较差异无统计学意义(P>0.05).模型组MLH1、MSH2表达与正常组相比均明显降低(3.75±1.04 vs 8.00±0.926;3.62±1.69 vs 7.25±2.12,P<0.01);健脾活血方高、中、低剂量组MLH1、MSH2表达与模型组相比均明显升高(6.50±0.93,5.25±1.49,5.12±1.25 vs 3.75±1.04;6.62±2.13,6.00±1.51,5.50±1.41 vs 3.62±1.69,P<0.01或P<0.05);健脾活血方高剂量组MLH1表达与胃复春组相比明显升高(6.50±0.93 vs 4.88±1.25,P<0.05),中、低剂量组MLH1及高、中、低剂量组MSH2表达与胃复春组比较差异无统计学意义(P>0.05).结论:健脾活血方可通过降低CD44V6表达,上调MLH1、MSH2表达,减少细胞的非正常侵袭和转移,增强基因的错配修复功能,减少细胞的异常增殖和分化,发挥对大鼠胃癌前病变的治疗作用.展开更多
基金Supported by Shanghai Rising-Star Program(No.07QA14052)E-Institutes of Shanghai Municipal Education Commission (E03008)+1 种基金Innovative Research Team in Universities,Shanghai Municipal Education Commissionand Shanghai Leading Academic Discipline Project of Shanghai Municipal Education Commission
文摘Objective： To study the structural shifts of gut flora in rats with acute alcoholic liver injury （AALI）, and the effect of Jianpi Huoxue Decoction （健脾活血汤, JPHXD） on the gut flora. Methods： Thirty-six Sprague- Dawley rats were randomly allocated to the control, AALI and JPHXD groups equally. The rats in the control group were given water and those in AALI and JPHXD groups were given ethanol by intragastric gavage for 5 days, while rats in the JPHXD group were administered JPHXD simultaneously. The blood and liver tissue were collected at the end of the experiment. The activities of serum alkaline aminotransferase （ALT）, aspartate aminotransferase （AST）, hepatic γ/-glutamyitranspetidase （γ-GT） and hepatic tdglyceride （TG） levels were determined. Plasma endotoxin level in the portal vein was measured. Pathological changes of liver tissues were determined by hematoxylin and Eosin （HE） staining and oil red O staining. The total DNA of gut flora were extracted from fecal samples by Bead-beating method and determined by ERIC-PCR fingerprint method. The similarity cluster analysis and principal component analysis were performed to analyze the ERIC-PCR fingerprint respectively. Results： In the AALI group, the ratio of liver/body weight, activities of ALT, AST and hepatic γ-GT, amount of hepatic TG were elevated significantly compared with those in the control group （all P〈0.01）. JPHXD decreased the ratio, activities of ALT, AST, γ-GT and TG significantly compared with those in the AALI group （P〈0.05 or P〈0.01）. HE and oil red O staining showed that fat deposited markedly in liver tissue, while JPHXD alleviated pathological changes markedly. Plasma LPS level in rat portal vein in the AALI group increased significantly （P〈0.01）, but it was decreased significantly in the JPHXD group （P〈0.01）. The cluster analysis and principal component analysis of ERIC-PCR fingerprint showed that gut flora in the hALl group changed markedly, and JPHXD could recover gu
文摘目的:通过观察健脾活血方对胃癌前病变大鼠胃黏膜组织中CD44V6、MLH1及MSH2表达的影响,探讨健脾活血方对其干预的作用机制.方法:除正常组外,其他大鼠采用以N-甲基-N-硝基-N-亚硝基胍(N-methyl-N-nitro N-nitrosoguanidine,MNNG)为主同时配合0.3g/L雷尼替丁、400 mL/L乙醇及饥饱失常的多因素造模法建立胃癌前病变动物模型.将造模成功的40只大鼠随机分为模型组(0.9%氯化钠溶液)、胃复春组(0.86 g/kg)、健脾活血方高、中、低剂量组(32、16、8 g/kg),每组8只,每组每天给予等量(10 mL/kg)的不同药物灌胃一次,连续10 wk.实验末处死大鼠,给予相应处理后,快速免疫组织化学检测CD44V6、MLH1及MSH2表达情况.结果:模型组CD44V6表达与正常组相比明显升高(5.12±1.96 vs 0.25±0.46,P<0.01);健脾活血方高、中剂量组CD44V6表达与模型组相比均明显降低(2.25±0.71,3.25±0.31vs 5.12±1.96,P<0.01或P<0.05),低剂量组C D44V6表达与模型组比较差异无统计学意义(P>0.05);健脾活血方高剂量组CD44V6表达与胃复春组相比明显降低(2.25±0.71 vs4.62±1.19,P<0.01),中、低剂量组CD44V6表达与胃复春组比较差异无统计学意义(P>0.05).模型组MLH1、MSH2表达与正常组相比均明显降低(3.75±1.04 vs 8.00±0.926;3.62±1.69 vs 7.25±2.12,P<0.01);健脾活血方高、中、低剂量组MLH1、MSH2表达与模型组相比均明显升高(6.50±0.93,5.25±1.49,5.12±1.25 vs 3.75±1.04;6.62±2.13,6.00±1.51,5.50±1.41 vs 3.62±1.69,P<0.01或P<0.05);健脾活血方高剂量组MLH1表达与胃复春组相比明显升高(6.50±0.93 vs 4.88±1.25,P<0.05),中、低剂量组MLH1及高、中、低剂量组MSH2表达与胃复春组比较差异无统计学意义(P>0.05).结论:健脾活血方可通过降低CD44V6表达,上调MLH1、MSH2表达,减少细胞的非正常侵袭和转移,增强基因的错配修复功能,减少细胞的异常增殖和分化,发挥对大鼠胃癌前病变的治疗作用.
