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目的:观察二氢杨梅素对四氯化碳(CCL.)诱导的肝纤维化大鼠的防治作用及对转化生长因子β1(TGF—β1)表达的影响。方法:56只雄性SD大鼠被随机分为正常组、模型组、二氢杨梅素治疗组及复方鳖甲阳性对照组,采用CCL4皮下注射诱导大鼠肝纤维化模型。于第13周末检测大鼠血清TGF—β1、I、PCⅢ及ClV的水平,免疫组织化学方法检测肝组织TGF-β1表达。结果:与模型组相比,二氢杨梅素治疗组血清TGF—β1、I、PCⅢ、CⅣ水平显著下降(P〈0.05),肝组织内TGF—β1阳性面积的表达明显下降(P〈0.05)。结论:二氢杨梅素对CCL4诱导的肝纤维化大鼠有较好的保护作用,对TGF—β1表达的影响可能是其作用机制之一。 相似文献
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有文献报道, SIRT1-AMPK信号通路可能在DHM改善肝脏细胞甘油三酯蓄积、胰岛素抵抗等作用中发挥作用。为此,本课题拟进一步观察DHM对高脂饮食诱导的肥胖小鼠肝脏脂肪沉积的影响,并探讨其可能机制。C57BL/6J小鼠采用普通饲料和高脂饲料喂养,同时分别用或不用低剂量(125 mg/kg)或高剂量(250 mg/kg)的DHM处理16周。实验期间,每两周检测体重一次。16周后,眼眶静脉取血并处死动物,同时取肩胛下、附睾与腹股沟的脂肪并用电子秤进行称重,并记录脂肪重量。全自动生化分析仪检测:血清甘油三酯(triglyceride,TG)、血清总胆固醇(totalcholesterol,TC)、血清高密度脂蛋白(high-densitylipoprotein,HDL)、血清低密度脂蛋白(low-densitylipoprotein,LDL)。取肝脏甲醛固定、HE和油红O染色检测肝脏脂肪沉积情况;比色法检测肝脏MDA和SOD含量; Realtime PCR检测相关指标的基因表达:IL-6、IL-8、TNF-α、乙酰辅酶A羧化酶(acetyl-Co A carboxylase, ACC)、固... 相似文献
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背景与目的:二氢杨梅素(dihydromyricetin,DHM)通过抑制细胞周期、促进细胞凋亡和抑制新生血管生成等机制发挥抗肿瘤作用。探讨DHM对胃癌的抗癌作用,并研究其可能作用机制。方法:不同剂量DHM作用体外人脐静脉内皮细胞(human umbilical vein endothelial cells, HUVEC)和胃癌细胞系MKN28后,采用细胞计数试剂盒(cell counting kit-8,CCK-8)法筛选无毒剂量的DHM,Transwell小室实验测定细胞侵袭;小管形成实验测定HUVEC体外血管生成能力;采用蛋白质印迹法(Western blot)检测血管内皮生长因子A(vascular endothelial growth factor A, VEGFA)、phospho-血管内皮生长因子受体(vascular endothelial growth factor receptor, VEGFR)2、细胞外信号调节激酶(extracellular signal-regulated kinase,ERK)、phospho-c-Jun氨基端激酶(c-Jun NH2-terminal kinase,JNK)和phospho-p38表达水平;基质胶塞实验测定DHM对体内血管形成的影响;通过皮下肿瘤细胞注射法建立MKN28裸鼠异种移植瘤模型,观察DHM给药对体内胃癌生长的影响,Ki-67增殖指数及CD34、VEGFA在移植瘤组织中的表达通过免疫组织化学法测定。结果:(0.5~2.5 μmol/L)的DHM对HUVEC和MKN28细胞生长无明显抑制作用,该浓度范围的DHM呈浓度依赖性地抑制HUVEC侵袭和小管形成,VEGFA(20 μg/L)可明显逆转DHM对HUVEC侵袭和小管形成的抑制效果;DHM处理可导致MKN28细胞中VEGFA和phospho-ERK表达呈剂量依赖性下降,而对p-p38和p-JNK的表达无明显影响;DHM处理可导致HUVEC中phospho-VEGFR2表达呈剂量依赖性下降;低剂量(30 mg/kg)DHM对裸鼠无明显的不良反应,但可抑制体内血管形成,同时有效延缓体内胃癌生长,体内肿瘤组织中的CD34和VEGFA的表达受到DHM的显著下调作用,但低剂量DHM对Ki-67无明显作用。结论:低剂量的DHM可有效抑制体内外血管生成和体内胃癌生长,该作用至少部分是通过ERK/VEGFA/VEGFR2信号通路来实现的。 相似文献
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目的 探讨二氢杨梅素(DMY)对绒毛膜癌(绒癌)JEG-3及JAR细胞增殖和迁移能力的影响。 方法 MTT法检测不同浓度的二氢杨梅素(0 mg/L, 20 mg/L, 40 mg/L, 60 mg/L, 80 mg/L)作用一定时间后,对绒癌JEG-3和JAR细胞增殖能力的影响;细胞划痕实验和Transwell法检测不同浓度二氢杨梅素(0 mg/L, 40 mg/L, 60 mg/L, 80 mg/L)分别作用绒癌JEG-3细胞及JAR细胞一定时间后,对其迁移能力的影响;Real-time PCR和Western blotting方法分别检测不同浓度二氢杨梅素(0 mg/L, 40 mg/L, 60 mg/L, 80 mg/L)作用绒癌JEG-3及JAR细胞后,基质金属蛋白酶2(MMP-2)mRNA和蛋白表达水平的影响。 结果 不同浓度二氢杨梅素作用绒癌JEG-3和JAR细胞24 h和48 h后,随着二氢杨梅素浓度增加,对JEG-3和JAR细胞增殖抑制作用增强(P<0.05)。二氢杨梅素作用绒癌JEG-3及JAR细胞后,显著抑制细胞迁移能力,且具有浓度依赖性(P<0.05)。不同浓度二氢杨梅素作用JEG-3和JAR细胞后,MMP-2 的mRNA和蛋白表达水平明显下降(P<0.05)。 结论 二氢杨梅素能够抑制JEG-3及JAR细胞的增殖能力且具有浓度依赖性,同时二氢杨梅素可能通过下调绒癌JEG-3及JAR细胞中MMP-2 mRNA和蛋白的表达,抑制绒癌细胞的侵袭迁移。 相似文献
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Jun Xie Jie Liu Tu-Ming Chen Qing Lan Qing-Yu Zhang Bin Liu Dong Dai Wei-Dong Zhang Li-Ping Hu Run-Zhi Zhu 《World journal of gastroenterology : WJG》2015,21(18):5473-5481
AIM: To assess the effects of dihydromyricetin(DHM) as a hepatoprotective candidate in reducing hepatic injury and accelerating hepatocyte proliferation after carbon tetrachloride(CCl4) treatment.METHODS: C57 BL/6 mice were used in this study. Mice were orally administered with DHM(150 mg/kg) for 4 d after CCl4 treatment. Serum and liver tissue samples were collected on days 1, 2, 3, 5 and 7 after CCl4 treatment. The anti-inflammatory effect of DHM was assessed directly by hepatic histology detection and indirectly by serum levels of aspartate aminotransferase(AST), alanine aminotransferase(ALT), albumin, and superoxide dismutase(SOD). Inflammatory cytokines, such as interleukin(IL)-1β, IL-6 and tumor necrosis factor-α(TNF-α), were detected using ELISA kits. Proliferating cell nuclear antigen(PCNA) staining was used to evaluate the role of DHM in promoting hepatocyte proliferation. Hepatocyte apoptosis wasmeasured by TUNEL assay.Furthermore,apoptosis proteins Caspases-3,6,8,and 9 were detected by Western blot.SP600125 were used to confirm whether DHM regulated liver regeneration through JNK/TNF-αpathways.RESULTS:DHM showed a strong anti-inflammatory effect on CCl4-induced liver injury in mice.DHM could significantly decrease serum ALT,AST,IL-1β,IL-6 and TNF-αand increase serum albumin,SOD and liver SOD compared to the control group after CCl4 treatment(P0.05).PCNA results indicated that DHM could significantly increase the number of PCNA positive cells compared to the control(348.9±56.0 vs 107.1±31.4,P0.01).TUNEL assay showed that DHM dramatically reduced the number of apoptotic cells after CCl4 treatment compared to the control(365.4±99.4 vs 90.5±13.8,P0.01).Caspase activity detection showed that DHM could reduce the activities of Caspases-8,3,6 and 9 compared to the control(P0.05).The results of Western blot showed that DHM increased the expression of JNK and decreased TNF-αexpression.However,DHM could not affect TNF-αexpression after SP600125 treatment.Furthermore,DHM could significantly improve the survival rate of acute liver failure(ALF)mice(73.3%vs 20.0%,P0.0001),and SP600125 could inhibit the effect of DHM.CONCLUSION:These findings demonstrate that DHM alleviates CCl4-induced liver injury,suggesting that DHM is a promising candidate for reversing liver injury and ALF. 相似文献
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