Background:Mild traumatic brain injury(mTBI)is a common neurological trauma that can lead to cognitive impairment.The sirtuin-1(SIRT-1)/peroxisome proliferator-activated receptor gamma coactivator-1α(PGC-1α)pathway ...Background:Mild traumatic brain injury(mTBI)is a common neurological trauma that can lead to cognitive impairment.The sirtuin-1(SIRT-1)/peroxisome proliferator-activated receptor gamma coactivator-1α(PGC-1α)pathway has been reported to have neuroprotective effects in rats with craniocerebral injury.We evaluated potential mechanisms underlying electroacupuncture-mediated recovery of cognitive function after mTBI,focusing on the SIRT-1/PGC-1α/mitochondrial pathway.Methods:We included forty 6-week-old male Sprague-Dawley rats in this study.Rats were randomly divided into four groups:controlled cortical impactor(CCI,n=10),sham operation(sham,n=10),electroacupuncture-treated CCI(CCI+EA,n=10),and electroacupuncture-treated sham(sham+EA,n=10)group.Randomization was performed by assigning a random number to each rat and using a random number table.The mTBI rat model was established using a controllable cortical impactor.Electroacupuncture therapy was performed on the back of rats,by inserting acupuncture needles to the specific acupoints and setting appropriate parameters for treatment.We evaluated spatial learning and memory functions with the Morris water maze test.We performed quantitative real-time polymerase chain reaction(qRT-PCR),western blotting,adenosine triphosphate(ATP)determination,and mitochondrial respiratory chain complex I(MRCC I)determination on rat hippocampal tissue.We analyzed SIRT-1/PGC-1α expression levels and the results of mitochondrial function assays,and compared differences between groups using bilateral Student’s t-tests.Results:Compared with the sham group,SIRT-1/PGC-1α expression was downregulated in the hippocampus of CCI group(P<0.01).Although this expression was upregulated following electroacupuncture,it did not reach the levels observed in the sham group(P<0.05).Compared with the sham group,MRCC I and ATP levels in the CCI group were significantly reduced,and increased after electroacupuncture(P<0.01).In the Morris water maze,electroacupuncture reduced the incubation period of rats and increased average speed and number of crossing platforms(P<0.05).Conclusion:Electroacupuncture may improve cognitive function in the mTBI rat model by regulating the SIRT-1/PGC-1α/mitochondrial pathway.展开更多
Background and aims:Free fatty acids(FFAs)are one of the important regulators of the progression of nonalcoholic fatty liver disease.The FFAs are shown to modulate the metabolic status of the liver by modulating sever...Background and aims:Free fatty acids(FFAs)are one of the important regulators of the progression of nonalcoholic fatty liver disease.The FFAs are shown to modulate the metabolic status of the liver by modulating several cellular pathways in hepatocytes.Here,we elucidated the role of miR-22 in modulating FFAs-mediated gluconeogenesis.Methods:Huh7 and WRL68 cells were transfected with nonspecific miRNA,miR-22 premiRs or anti-miR-22 oligos followed by incubation with palmitic acid,oleic acid,and linoleic acid(300μM each)for 48 and 72 h after transfection.The expression of miR-22 was performed using real-time polymerase chain reaction and Western blots were performed for SIRT-1,PGC-1α,PEPCK,and glucose-6-phosphatase.Three groups of C57BL/6 mice(6 mice per group)were fed with standard diet,choline sufficient L-amino acid defined diet or choline-deficient L-amino acid defined(CDAA)diet for 6,18,32,or 54 weeks.Triglycerides content was measured in the serum.Expression of miR-22 and the protein expression of gluconeogenic enzymes were analyzed in the tissue samples.Results:Incubation of miR-22-transfected cells with FFAs inhibited the expression of SIRT-1,PGC-1α,PEPCK,and glucose-6-phosphatase,while miR-22 expression was increased.These changes were reversed when the cells were transfected with anti-miR-22 oligos.CDAA-fed mice showed the significant increase in triglycerides content and miR-22 expression,while there was an inhibition of SIRT-1,PGC-1α,PEPCK,and glucose-6-phosphatase expression in CDAA-fed mice.展开更多
目的:探讨沉默信息调节因子-1(silence signal regulating factor-1,SIRT-1)和上皮性钙黏附素(epithelial cadherin,E-cadherin)在胃癌组织中的表达及其相关性。方法:采用HE染色观察正常胃黏膜组织及癌组织的病理结构;采用免疫组织化学...目的:探讨沉默信息调节因子-1(silence signal regulating factor-1,SIRT-1)和上皮性钙黏附素(epithelial cadherin,E-cadherin)在胃癌组织中的表达及其相关性。方法:采用HE染色观察正常胃黏膜组织及癌组织的病理结构;采用免疫组织化学方法检测SIRT-1和E-cadherin在正常胃黏膜组织及癌组织中的表达水平;Spearman相关检验检测SIRT-1与E-cadherin表达的相关性。结果:HE染色结果:胃癌组织中癌细胞分化差,多形性,大小不一,可呈假复层,核大,胞浆少,容易找到核分裂。免疫组织化学检测结果:SIRT-1在正常胃黏膜组织和胃癌组织的阳性表达率分别为40.5%和64.3%;E-cadherin的阳性表达率分别为73.8%和40.5%。两组SIRT-1和E-cadherin的阳性表达率差异有统计学意义(P<0.05)。Spearman相关分析显示SIRT-1与E-cadherin的表达水平呈负相关(P<0.05)。胃癌组织中SIRT-1蛋白阳性表达与肿瘤大小及病理类型有关(P<0.05);而与患者的年龄、性别、TNM分期及淋巴结转移无关(P>0.05)。结论:胃癌组织中SIRT-1高表达可能通过抑制E-cadherin促使肿瘤组织细胞发生侵袭、转移。展开更多
基金funded by a scientic research fund from Beijing Jishuitan Hospital(No.ZR-202107).
文摘Background:Mild traumatic brain injury(mTBI)is a common neurological trauma that can lead to cognitive impairment.The sirtuin-1(SIRT-1)/peroxisome proliferator-activated receptor gamma coactivator-1α(PGC-1α)pathway has been reported to have neuroprotective effects in rats with craniocerebral injury.We evaluated potential mechanisms underlying electroacupuncture-mediated recovery of cognitive function after mTBI,focusing on the SIRT-1/PGC-1α/mitochondrial pathway.Methods:We included forty 6-week-old male Sprague-Dawley rats in this study.Rats were randomly divided into four groups:controlled cortical impactor(CCI,n=10),sham operation(sham,n=10),electroacupuncture-treated CCI(CCI+EA,n=10),and electroacupuncture-treated sham(sham+EA,n=10)group.Randomization was performed by assigning a random number to each rat and using a random number table.The mTBI rat model was established using a controllable cortical impactor.Electroacupuncture therapy was performed on the back of rats,by inserting acupuncture needles to the specific acupoints and setting appropriate parameters for treatment.We evaluated spatial learning and memory functions with the Morris water maze test.We performed quantitative real-time polymerase chain reaction(qRT-PCR),western blotting,adenosine triphosphate(ATP)determination,and mitochondrial respiratory chain complex I(MRCC I)determination on rat hippocampal tissue.We analyzed SIRT-1/PGC-1α expression levels and the results of mitochondrial function assays,and compared differences between groups using bilateral Student’s t-tests.Results:Compared with the sham group,SIRT-1/PGC-1α expression was downregulated in the hippocampus of CCI group(P<0.01).Although this expression was upregulated following electroacupuncture,it did not reach the levels observed in the sham group(P<0.05).Compared with the sham group,MRCC I and ATP levels in the CCI group were significantly reduced,and increased after electroacupuncture(P<0.01).In the Morris water maze,electroacupuncture reduced the incubation period of rats and increased average speed and number of crossing platforms(P<0.05).Conclusion:Electroacupuncture may improve cognitive function in the mTBI rat model by regulating the SIRT-1/PGC-1α/mitochondrial pathway.
基金funded by the Department of Science and Technology of Govt.of India and South Asian University,New Delhi.
文摘Background and aims:Free fatty acids(FFAs)are one of the important regulators of the progression of nonalcoholic fatty liver disease.The FFAs are shown to modulate the metabolic status of the liver by modulating several cellular pathways in hepatocytes.Here,we elucidated the role of miR-22 in modulating FFAs-mediated gluconeogenesis.Methods:Huh7 and WRL68 cells were transfected with nonspecific miRNA,miR-22 premiRs or anti-miR-22 oligos followed by incubation with palmitic acid,oleic acid,and linoleic acid(300μM each)for 48 and 72 h after transfection.The expression of miR-22 was performed using real-time polymerase chain reaction and Western blots were performed for SIRT-1,PGC-1α,PEPCK,and glucose-6-phosphatase.Three groups of C57BL/6 mice(6 mice per group)were fed with standard diet,choline sufficient L-amino acid defined diet or choline-deficient L-amino acid defined(CDAA)diet for 6,18,32,or 54 weeks.Triglycerides content was measured in the serum.Expression of miR-22 and the protein expression of gluconeogenic enzymes were analyzed in the tissue samples.Results:Incubation of miR-22-transfected cells with FFAs inhibited the expression of SIRT-1,PGC-1α,PEPCK,and glucose-6-phosphatase,while miR-22 expression was increased.These changes were reversed when the cells were transfected with anti-miR-22 oligos.CDAA-fed mice showed the significant increase in triglycerides content and miR-22 expression,while there was an inhibition of SIRT-1,PGC-1α,PEPCK,and glucose-6-phosphatase expression in CDAA-fed mice.
文摘目的:探讨沉默信息调节因子-1(silence signal regulating factor-1,SIRT-1)和上皮性钙黏附素(epithelial cadherin,E-cadherin)在胃癌组织中的表达及其相关性。方法:采用HE染色观察正常胃黏膜组织及癌组织的病理结构;采用免疫组织化学方法检测SIRT-1和E-cadherin在正常胃黏膜组织及癌组织中的表达水平;Spearman相关检验检测SIRT-1与E-cadherin表达的相关性。结果:HE染色结果:胃癌组织中癌细胞分化差,多形性,大小不一,可呈假复层,核大,胞浆少,容易找到核分裂。免疫组织化学检测结果:SIRT-1在正常胃黏膜组织和胃癌组织的阳性表达率分别为40.5%和64.3%;E-cadherin的阳性表达率分别为73.8%和40.5%。两组SIRT-1和E-cadherin的阳性表达率差异有统计学意义(P<0.05)。Spearman相关分析显示SIRT-1与E-cadherin的表达水平呈负相关(P<0.05)。胃癌组织中SIRT-1蛋白阳性表达与肿瘤大小及病理类型有关(P<0.05);而与患者的年龄、性别、TNM分期及淋巴结转移无关(P>0.05)。结论:胃癌组织中SIRT-1高表达可能通过抑制E-cadherin促使肿瘤组织细胞发生侵袭、转移。
