By critically examining the work,we conducted a comprehensive bibliometric analysis on the role of nuclear factor erythroid 2-related factor 2(NRF2)in nervous system diseases.We also proposed suggestions for future bi...By critically examining the work,we conducted a comprehensive bibliometric analysis on the role of nuclear factor erythroid 2-related factor 2(NRF2)in nervous system diseases.We also proposed suggestions for future bibliometric studies,including the integration of multiple websites,analytical tools,and analytical approaches,The findings presented provide compelling evidence that ferroptosis is closely associated with the therapeutic challenges of nervous system diseases.Targeted modulation of NRF2 to regulate ferroptosis holds substantial potential for effectively treating these diseases.Future NRF2-related research should not only focus on discovering new drugs but also on designing rational drug delivery systems.In particular,nanocarriers offer substantial potential for facilitating the clinical translation of NRF2 research and addressing existing issues related to NRF2-related drugs.展开更多
BACKGROUND The Nuclear factor erythroid 2-related factor 2(NRF2)transcription factor has attracted much attention in the context of neurological diseases.However,none of the studies have systematically clarified this ...BACKGROUND The Nuclear factor erythroid 2-related factor 2(NRF2)transcription factor has attracted much attention in the context of neurological diseases.However,none of the studies have systematically clarified this field's research hotspots and evolution rules.AIM To investigate the research hotspots,evolution patterns,and future research trends in this field in recent years.METHODS We conducted a comprehensive literature search in the Web of Science Core Collection database using the following methods:(((((TS=(NFE2 L2))OR TS=(Nfe2 L2 protein,mouse))OR TS=(NF-E2-Related Factor 2))OR TS=(NRF2))OR TS=(NFE2L2))OR TS=(Nuclear factor erythroid2-related factor 2)AND(((((((TS=(neurological diseases))OR TS=(neurological disorder))OR TS=(brain disorder))OR TS=(brain injury))OR TS=(central nervous system disease))OR TS=(CNS disease))OR TS=(central nervous system disorder))OR TS=(CNS disorder)AND Language=English from 2010 to 2022.There are just two forms of literature available:Articles and reviews.Data were processed with the software Cite-Space(version 6.1.R6).RESULTS We analyzed 1884 articles from 200 schools in 72 countries/regions.Since 2015,the number of publications in this field has increased rapidly.China has the largest number of publications,but the articles published in the United States have better centrality and H-index.Among the top ten authors with the most published papers,five of them are from China,and the author with the most published papers is Wang Handong.The institution with the most articles was Nanjing University.To their credit,three of the top 10 most cited articles were written by Chinese scholars.The keyword co-occurrence map showed that"oxidative stress","NRF2","activation","expression"and"brain"were the five most frequently used keywords.CONCLUSION Research on the role of NRF2 in neurological diseases continues unabated.Researchers in developed countries published more influential papers,while Chinese scholars provided the largest number of articles.There have been numerous studies on the mechanism of NRF2 transcription factor in neurological diseases.NRF2 is also emerging as a potentially effective target for the treatment of neurological diseases.However,despite decades of research,our knowledge of NRF2 transcription factor in nervous system diseases is still limited.Further studies are needed in the future.展开更多
This study aims to analyze the clinical significance and mechanism of nuclear factor erythroid 2-related factor 2(NRF2)and glutathione peroxidase 4(GPX4)in primary hepatic carcinoma(PHC).Methods:The expression of NRF2...This study aims to analyze the clinical significance and mechanism of nuclear factor erythroid 2-related factor 2(NRF2)and glutathione peroxidase 4(GPX4)in primary hepatic carcinoma(PHC).Methods:The expression of NRF2 and GPX4 in peripheral blood of patients with PHC was determined to analyze the diagnostic value of the two combined for PHC.The prognostic significance of NRF2 and GPX4 was evaluated by 3-year followup.Human liver epithelial cells THLE-2 and human hepatocellular carcinoma cells HepG2 were purchased,and the expression of NRF2 and GPX4 in the cells was determined.NRF2 and GPX4 aberrant expression vectors were constructed and transfected into HepG2,and changes in cell proliferation and invasion capabilities were observed.Results:The expression of NRF2 and GPX4 in patients with PHC was higher than that in patients with LC or VH(p<0.05),and the two indicators combined was excellent in diagnosing PHC.Moreover,patients with high expression of NRF2 and GPX4 had a higher risk of death(p<0.05).In in vitro experiments,both NRF2 and GPX4 expression was elevated in HepG2(p<0.05).HepG2 activity was enhanced by increasing the expression of the two,vice versa(p<0.05).Conclusion:NRF2 and GPX4 combined is excellent in diagnosing PHC,and promotes the malignant development of PHC.展开更多
Salidroside,the main active ingredient extracted from Rhodiola crenulata,has been shown to be neuroprotective in ischemic cerebral injury,but the underlying mechanism for this neuroprotection is poorly understood.In t...Salidroside,the main active ingredient extracted from Rhodiola crenulata,has been shown to be neuroprotective in ischemic cerebral injury,but the underlying mechanism for this neuroprotection is poorly understood.In the current study,the neuroprotective effect of salidroside on cerebral ischemia-induced oxidative stress and the role of the nuclear factor erythroid 2-related factor 2（Nrf2）pathway was investigated in a rat model of middle cerebral artery occlusion.Salidroside（30 mg/kg）reduced infarct size,improved neurological function and histological changes,increased activity of superoxide dismutase and glutathione-S-transferase,and reduced malon-dialdehyde levels after cerebral ischemia and reperfusion.Furthermore,salidroside apparently increased Nrf2 and heme oxygenase-1 expression.These results suggest that salidroside exerts its neuroprotective effect against cerebral ischemia through anti-oxidant mechanisms and that activation of the Nrf2 pathway is involved.The Nrf2/antioxidant response element pathway may become a new therapeutic target for the treatment of ischemic stroke.展开更多
BACKGROUND Hepatocellular carcinoma(HCC) is one of the most common malignant tumors with high mortality-to-incidence ratios. Nuclear factor erythroid 2-like 3(NFE2 L3), also known as NRF3, is a member of the cap ‘n&#...BACKGROUND Hepatocellular carcinoma(HCC) is one of the most common malignant tumors with high mortality-to-incidence ratios. Nuclear factor erythroid 2-like 3(NFE2 L3), also known as NRF3, is a member of the cap ‘n' collar basic-region leucine zipper family of transcription factors. NFE2 L3 is involved in the regulation of various biological processes, whereas its role in HCC has not been elucidated.AIM To explore the expression and biological function of NFE2 L3 in HCC.METHODS We analyzed the expression of NFE2 L3 in HCC tissues and its correlation with clinicopathological parameters based on The Cancer Genome Atlas(TCGA) data portal. Short hairpin RNA(shRNA) interference technology was utilized to knock down NFE2 L3 in vitro. Cell apoptosis, clone formation, proliferation, migration,and invasion assays were used to identify the biological effects of NFE2 L3 in BEL-7404 and SMMC-7721 cells. The expression of epithelial-mesenchymal transition(EMT) markers was examined by Western blot analysis.RESULTS TCGA analysis showed that NFE2 L3 expression was significantly positively correlated with tumor grade, T stage, and pathologic stage. The qPCR and Western blot results showed that both the mRNA and protein levels of NFE2 L3 were significantly decreased after shRNA-mediated knockdown in BEL-7404 and SMMC-7721 cells. The shRNA-mediated knockdown of NFE2 L3 could induce apoptosis and inhibit the clone formation and cell proliferation of SMMC-7721 and BEL-7404 cells. NFE2 L3 knockdown also significantly suppressed the migration, invasion, and EMT of the two cell lines.CONCLUSION Our study showed that shRNA-mediated knockdown of NFE2 L3 exhibited tumor-suppressing effects in HCC cells.展开更多
Coronavirus disease 2019(COVID-19)caused by severe acute respiratory syndrome coronavirus 2 is a global pandemic and poses a major threat to human health worldwide.In addition to respiratory symptoms,COVID-19 is usual...Coronavirus disease 2019(COVID-19)caused by severe acute respiratory syndrome coronavirus 2 is a global pandemic and poses a major threat to human health worldwide.In addition to respiratory symptoms,COVID-19 is usually accompanied by systemic inflammation and liver damage in moderate and severe cases.Nuclear factor erythroid 2-related factor 2(NRF2)is a transcription factor that regulates the expression of antioxidant proteins,participating in COVID-19-mediated inflammation and liver injury.Here,we show the novel reciprocal regulation between NRF2 and inflammatory mediators associated with COVID-19-related liver injury.Additionally,we describe some mechanisms and treatment strategies.展开更多
Oxidative stress is a key driver in the development and progression of several diseases,including metabolic associated fatty liver disease(MAFLD).This condition includes a wide spectrum of pathological injuries,extend...Oxidative stress is a key driver in the development and progression of several diseases,including metabolic associated fatty liver disease(MAFLD).This condition includes a wide spectrum of pathological injuries,extending from simple steatosis to inflammation,fibrosis,cirrhosis,and hepatocellular carcinoma.Excessive buildup of lipids in the liver is strictly related to oxidative stress in MAFLD,progressing to liver fibrosis and cirrhosis.The nuclear factor erythroid 2-related factor 2(NRF2)is a master regulator of redox homeostasis.NRF2 plays an important role for cellular protection by inducing the expression of genes related to antioxidant,anti-inflammatory,and cytoprotective response.Consistent evidence demonstrates that NRF2 is involved in every step of MAFLD development,from simple steatosis to inflammation,advanced fibrosis,and initiation/progression of hepatocellular carcinoma.NRF2 activators regulate lipid metabolism and oxidative stress alleviating the fatty liver disease by inducing the expression of cytoprotective genes.Thus,modulating NRF2 activation is crucial not only in understanding specific mechanisms underlying MAFLD progression but also to characterize effective therapeutic strategies.This review outlined the current knowledge on the effects of NRF2 pathway,modulators,and mechanisms involved in the therapeutic implications of liver steatosis,inflammation,and fibrosis in MAFLD.展开更多
Redox balance is fundamentally important for physiological homeostasis. Pathological factors that disturb this dedicated balance may result in oxidative stress, leading to the development or aggravation of a variety o...Redox balance is fundamentally important for physiological homeostasis. Pathological factors that disturb this dedicated balance may result in oxidative stress, leading to the development or aggravation of a variety of diseases, including diabetes mellitus, cardiovascular diseases, metabolic syndrome as well as inflammation, aging and cancer. Thus, the capacity of endogenous free radical clearance can be of patho-physiological importance; in this regard, the major reactive oxygen species defense machinery, the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) system needs to be precisely modulated in response to pathological alterations. While oxidative stress is among the early events that lead to the development of insulin resistance, the activation of Nrf2 scavenging capacity leads to insulin sensitization. Furthermore, Nrf2 is evidently involved in regulating lipid metabolism. Here we summarize recent findings that link the Nrf2 system to metabolic homeostasis and insulin action and present our view that Nrf2 may serve as a novel drug target for diabetes and its complications.展开更多
Objective. To investigate the roles of mouse erythroid differentiation and denucleation factor (MKI)DF), a novel factor cloned in our laboratory recently, in erylhroid terminal differentiation.Method. Mouse erythroleu...Objective. To investigate the roles of mouse erythroid differentiation and denucleation factor (MKI)DF), a novel factor cloned in our laboratory recently, in erylhroid terminal differentiation.Method. Mouse erythroleukemia (MEL) cells were transfected with eukaryotie expression plasinid pcl)-NA-MEDDF. Then we investigated the changes on characteristics of cell growth by analyzing cells growth rate, mitotie index and colony-forming rate in semi-solid medium. The expressions of c-mye and p-globin genes were analysed by semi-quantitative RT-PCR.Results. MEL cells transfected with pcDNA-MEDDF showed significant lower growth rate, mitolic index,and colony-forming rate in semi-solid medium ( P<0. 01). The percentage of benzidine-positive cells was 32. 8%after transfection. The expression of β-globin in cells trarisfected with pcDNA-MEDDF was 3. 43 times higherthan that of control (MEL transfected with blank vector, pcDNA3. 1), and the expression of c-rnyc decreased by66. 3% .Conclusions. MEDDF can induce differentiation of MEL cell and suppress its malignancy.展开更多
目的探讨微生态制剂联合浙贝黄芩汤对急性淋巴细胞白血病(ALL)大剂量化疗后患者粒细胞集落刺激因子受体(G-CSFR)、粒单系集落形成单位(CFU-GM)、肠道菌群及红系爆式集落形成单位(BFU-E)的影响。方法选取延安大学附属医院2019年6月至2022...目的探讨微生态制剂联合浙贝黄芩汤对急性淋巴细胞白血病(ALL)大剂量化疗后患者粒细胞集落刺激因子受体(G-CSFR)、粒单系集落形成单位(CFU-GM)、肠道菌群及红系爆式集落形成单位(BFU-E)的影响。方法选取延安大学附属医院2019年6月至2022年12月收治的ALL患者130例作为研究对象,根据治疗方法将患者分为A组、B组、C组,3组患者均接受大剂量化疗,化疗结束48 h后A组患者实施常规治疗,B组患者单纯浙贝黄芩汤治疗,C组给予微生态制剂联合浙贝黄芩汤治疗,治疗12 d后,对3组患者G-CSFR、CFU-GM、BFU-E表达情况及血细胞数量进行检测。结果治疗后,C组血红蛋白、白细胞、血小板[(79±6)g/L、(3.8±0.4)×10^(9)/L、(66.4±3.6)×10^(9)/L]与A组[(59±7)g/L、(3.2±0.4)×10^(9)/L、(52.6±2.8)×10^(9)/L]、B组[(61±7)g/L、(3.1±0.3)×10^(9)/L、(52.8±2.6)×10^(9)/L]对比,差异有统计学意义(P<0.05)。C组G-CSFR(5.35±0.16)pg/ml和白细胞介素-11受体(IL-11R)(6.38±0.54)μg/kg水平均高于A组[(2.23±0.13)pg/ml和(1.49±0.24)μg/kg]和B组[(2.31±0.16)pg/ml和(2.31±0.49)μg/kg]差异有统计学意义(P<0.05)。治疗后,C组患者7 d CFU-GM(18.5±6.0)个和14 d BFU-E(83.5±7.5)个高于A组[7 d CFU-GM(9.5±2.0)个和14 d BFU-E(59.5±6.5)个]和B组[7 d CFU-GM(12.0±6.5)个和14 d BFU-E(63.5±5.0)个],差异有统计学意义(P<0.05)。7 d后,C组双歧杆菌(12.56±3.25)lgCFU/g、乳酸杆菌(13.56±2.58)lgCFU/g、肠杆菌(5.12±1.45)lgCFU/g、肠球菌(5.14±0.58)lgCFU/g高于A组[(9.26±1.03)lg CFU/g、(8.65±0.84)lg CFU/g、(8.08±0.64)lgCFU/g、(8.15±0.46)lgCFU/g]和B组[(11.35±1.36)lg CFU/g、(12.43±1.14)lgCFU/g、(6.49±0.55)lgCFU/g、(6.66±0.43)lgCFU/g],差异有统计学意义(P<0.05)。结论微生态制剂联合浙贝黄芩汤治疗可以有效提高ALL大剂量化疗后患者的G-CSFR、CFU-GM、BFU-E水平,可能更好地改善化疗引起的患者骨髓抑制情况,改善肠道菌群,具有临床研究价值。展开更多
基金Supported by The Guangdong Basic and Applied Basic Research Foundation,China,No.2024A1515011236.
文摘By critically examining the work,we conducted a comprehensive bibliometric analysis on the role of nuclear factor erythroid 2-related factor 2(NRF2)in nervous system diseases.We also proposed suggestions for future bibliometric studies,including the integration of multiple websites,analytical tools,and analytical approaches,The findings presented provide compelling evidence that ferroptosis is closely associated with the therapeutic challenges of nervous system diseases.Targeted modulation of NRF2 to regulate ferroptosis holds substantial potential for effectively treating these diseases.Future NRF2-related research should not only focus on discovering new drugs but also on designing rational drug delivery systems.In particular,nanocarriers offer substantial potential for facilitating the clinical translation of NRF2 research and addressing existing issues related to NRF2-related drugs.
文摘BACKGROUND The Nuclear factor erythroid 2-related factor 2(NRF2)transcription factor has attracted much attention in the context of neurological diseases.However,none of the studies have systematically clarified this field's research hotspots and evolution rules.AIM To investigate the research hotspots,evolution patterns,and future research trends in this field in recent years.METHODS We conducted a comprehensive literature search in the Web of Science Core Collection database using the following methods:(((((TS=(NFE2 L2))OR TS=(Nfe2 L2 protein,mouse))OR TS=(NF-E2-Related Factor 2))OR TS=(NRF2))OR TS=(NFE2L2))OR TS=(Nuclear factor erythroid2-related factor 2)AND(((((((TS=(neurological diseases))OR TS=(neurological disorder))OR TS=(brain disorder))OR TS=(brain injury))OR TS=(central nervous system disease))OR TS=(CNS disease))OR TS=(central nervous system disorder))OR TS=(CNS disorder)AND Language=English from 2010 to 2022.There are just two forms of literature available:Articles and reviews.Data were processed with the software Cite-Space(version 6.1.R6).RESULTS We analyzed 1884 articles from 200 schools in 72 countries/regions.Since 2015,the number of publications in this field has increased rapidly.China has the largest number of publications,but the articles published in the United States have better centrality and H-index.Among the top ten authors with the most published papers,five of them are from China,and the author with the most published papers is Wang Handong.The institution with the most articles was Nanjing University.To their credit,three of the top 10 most cited articles were written by Chinese scholars.The keyword co-occurrence map showed that"oxidative stress","NRF2","activation","expression"and"brain"were the five most frequently used keywords.CONCLUSION Research on the role of NRF2 in neurological diseases continues unabated.Researchers in developed countries published more influential papers,while Chinese scholars provided the largest number of articles.There have been numerous studies on the mechanism of NRF2 transcription factor in neurological diseases.NRF2 is also emerging as a potentially effective target for the treatment of neurological diseases.However,despite decades of research,our knowledge of NRF2 transcription factor in nervous system diseases is still limited.Further studies are needed in the future.
文摘This study aims to analyze the clinical significance and mechanism of nuclear factor erythroid 2-related factor 2(NRF2)and glutathione peroxidase 4(GPX4)in primary hepatic carcinoma(PHC).Methods:The expression of NRF2 and GPX4 in peripheral blood of patients with PHC was determined to analyze the diagnostic value of the two combined for PHC.The prognostic significance of NRF2 and GPX4 was evaluated by 3-year followup.Human liver epithelial cells THLE-2 and human hepatocellular carcinoma cells HepG2 were purchased,and the expression of NRF2 and GPX4 in the cells was determined.NRF2 and GPX4 aberrant expression vectors were constructed and transfected into HepG2,and changes in cell proliferation and invasion capabilities were observed.Results:The expression of NRF2 and GPX4 in patients with PHC was higher than that in patients with LC or VH(p<0.05),and the two indicators combined was excellent in diagnosing PHC.Moreover,patients with high expression of NRF2 and GPX4 had a higher risk of death(p<0.05).In in vitro experiments,both NRF2 and GPX4 expression was elevated in HepG2(p<0.05).HepG2 activity was enhanced by increasing the expression of the two,vice versa(p<0.05).Conclusion:NRF2 and GPX4 combined is excellent in diagnosing PHC,and promotes the malignant development of PHC.
基金supported by the Independent Research Project of Fujian Academy of Traditional Chinese Medicine in China,No.2012fjzyyk-4the Natural Science Foundation of Fujian Province in China,No.2014J01340+1 种基金the Research Project of Fujian Provincial Health and Family Planning Commission,No.2014-ZQN-JC-32a grant from the Platform for Preclinical Studies of Traditional Chinese Medicine and Quality Control Engineering Technology Research Center of Fujian Province in China,No.2009Y2003
文摘Salidroside,the main active ingredient extracted from Rhodiola crenulata,has been shown to be neuroprotective in ischemic cerebral injury,but the underlying mechanism for this neuroprotection is poorly understood.In the current study,the neuroprotective effect of salidroside on cerebral ischemia-induced oxidative stress and the role of the nuclear factor erythroid 2-related factor 2（Nrf2）pathway was investigated in a rat model of middle cerebral artery occlusion.Salidroside（30 mg/kg）reduced infarct size,improved neurological function and histological changes,increased activity of superoxide dismutase and glutathione-S-transferase,and reduced malon-dialdehyde levels after cerebral ischemia and reperfusion.Furthermore,salidroside apparently increased Nrf2 and heme oxygenase-1 expression.These results suggest that salidroside exerts its neuroprotective effect against cerebral ischemia through anti-oxidant mechanisms and that activation of the Nrf2 pathway is involved.The Nrf2/antioxidant response element pathway may become a new therapeutic target for the treatment of ischemic stroke.
基金the Changzhou High-Level Medical Talents Training Project,No.2016ZCLJ002
文摘BACKGROUND Hepatocellular carcinoma(HCC) is one of the most common malignant tumors with high mortality-to-incidence ratios. Nuclear factor erythroid 2-like 3(NFE2 L3), also known as NRF3, is a member of the cap ‘n' collar basic-region leucine zipper family of transcription factors. NFE2 L3 is involved in the regulation of various biological processes, whereas its role in HCC has not been elucidated.AIM To explore the expression and biological function of NFE2 L3 in HCC.METHODS We analyzed the expression of NFE2 L3 in HCC tissues and its correlation with clinicopathological parameters based on The Cancer Genome Atlas(TCGA) data portal. Short hairpin RNA(shRNA) interference technology was utilized to knock down NFE2 L3 in vitro. Cell apoptosis, clone formation, proliferation, migration,and invasion assays were used to identify the biological effects of NFE2 L3 in BEL-7404 and SMMC-7721 cells. The expression of epithelial-mesenchymal transition(EMT) markers was examined by Western blot analysis.RESULTS TCGA analysis showed that NFE2 L3 expression was significantly positively correlated with tumor grade, T stage, and pathologic stage. The qPCR and Western blot results showed that both the mRNA and protein levels of NFE2 L3 were significantly decreased after shRNA-mediated knockdown in BEL-7404 and SMMC-7721 cells. The shRNA-mediated knockdown of NFE2 L3 could induce apoptosis and inhibit the clone formation and cell proliferation of SMMC-7721 and BEL-7404 cells. NFE2 L3 knockdown also significantly suppressed the migration, invasion, and EMT of the two cell lines.CONCLUSION Our study showed that shRNA-mediated knockdown of NFE2 L3 exhibited tumor-suppressing effects in HCC cells.
基金Supported by National Natural Science Foundation of China,No.82070632.
文摘Coronavirus disease 2019(COVID-19)caused by severe acute respiratory syndrome coronavirus 2 is a global pandemic and poses a major threat to human health worldwide.In addition to respiratory symptoms,COVID-19 is usually accompanied by systemic inflammation and liver damage in moderate and severe cases.Nuclear factor erythroid 2-related factor 2(NRF2)is a transcription factor that regulates the expression of antioxidant proteins,participating in COVID-19-mediated inflammation and liver injury.Here,we show the novel reciprocal regulation between NRF2 and inflammatory mediators associated with COVID-19-related liver injury.Additionally,we describe some mechanisms and treatment strategies.
文摘Oxidative stress is a key driver in the development and progression of several diseases,including metabolic associated fatty liver disease(MAFLD).This condition includes a wide spectrum of pathological injuries,extending from simple steatosis to inflammation,fibrosis,cirrhosis,and hepatocellular carcinoma.Excessive buildup of lipids in the liver is strictly related to oxidative stress in MAFLD,progressing to liver fibrosis and cirrhosis.The nuclear factor erythroid 2-related factor 2(NRF2)is a master regulator of redox homeostasis.NRF2 plays an important role for cellular protection by inducing the expression of genes related to antioxidant,anti-inflammatory,and cytoprotective response.Consistent evidence demonstrates that NRF2 is involved in every step of MAFLD development,from simple steatosis to inflammation,advanced fibrosis,and initiation/progression of hepatocellular carcinoma.NRF2 activators regulate lipid metabolism and oxidative stress alleviating the fatty liver disease by inducing the expression of cytoprotective genes.Thus,modulating NRF2 activation is crucial not only in understanding specific mechanisms underlying MAFLD progression but also to characterize effective therapeutic strategies.This review outlined the current knowledge on the effects of NRF2 pathway,modulators,and mechanisms involved in the therapeutic implications of liver steatosis,inflammation,and fibrosis in MAFLD.
基金Supported by An operating grant from Canadian Institutes of Health Research,No.89887 to Jin TRa NSFC grant,No.81072300 to Jin TR and Yu ZWa NSFC grant,No.30730079 to Ling WH in part
文摘Redox balance is fundamentally important for physiological homeostasis. Pathological factors that disturb this dedicated balance may result in oxidative stress, leading to the development or aggravation of a variety of diseases, including diabetes mellitus, cardiovascular diseases, metabolic syndrome as well as inflammation, aging and cancer. Thus, the capacity of endogenous free radical clearance can be of patho-physiological importance; in this regard, the major reactive oxygen species defense machinery, the nuclear factor (erythroid-derived 2)-like 2 (Nrf2) system needs to be precisely modulated in response to pathological alterations. While oxidative stress is among the early events that lead to the development of insulin resistance, the activation of Nrf2 scavenging capacity leads to insulin sensitization. Furthermore, Nrf2 is evidently involved in regulating lipid metabolism. Here we summarize recent findings that link the Nrf2 system to metabolic homeostasis and insulin action and present our view that Nrf2 may serve as a novel drug target for diabetes and its complications.
基金This work supported by the National Natural Sciences Foundation of China(39670364)This work was originally published in Acta Academiae Medicinae Sinicae(200123: 32-35)in Chinese.
文摘Objective. To investigate the roles of mouse erythroid differentiation and denucleation factor (MKI)DF), a novel factor cloned in our laboratory recently, in erylhroid terminal differentiation.Method. Mouse erythroleukemia (MEL) cells were transfected with eukaryotie expression plasinid pcl)-NA-MEDDF. Then we investigated the changes on characteristics of cell growth by analyzing cells growth rate, mitotie index and colony-forming rate in semi-solid medium. The expressions of c-mye and p-globin genes were analysed by semi-quantitative RT-PCR.Results. MEL cells transfected with pcDNA-MEDDF showed significant lower growth rate, mitolic index,and colony-forming rate in semi-solid medium ( P<0. 01). The percentage of benzidine-positive cells was 32. 8%after transfection. The expression of β-globin in cells trarisfected with pcDNA-MEDDF was 3. 43 times higherthan that of control (MEL transfected with blank vector, pcDNA3. 1), and the expression of c-rnyc decreased by66. 3% .Conclusions. MEDDF can induce differentiation of MEL cell and suppress its malignancy.
文摘目的探讨微生态制剂联合浙贝黄芩汤对急性淋巴细胞白血病(ALL)大剂量化疗后患者粒细胞集落刺激因子受体(G-CSFR)、粒单系集落形成单位(CFU-GM)、肠道菌群及红系爆式集落形成单位(BFU-E)的影响。方法选取延安大学附属医院2019年6月至2022年12月收治的ALL患者130例作为研究对象,根据治疗方法将患者分为A组、B组、C组,3组患者均接受大剂量化疗,化疗结束48 h后A组患者实施常规治疗,B组患者单纯浙贝黄芩汤治疗,C组给予微生态制剂联合浙贝黄芩汤治疗,治疗12 d后,对3组患者G-CSFR、CFU-GM、BFU-E表达情况及血细胞数量进行检测。结果治疗后,C组血红蛋白、白细胞、血小板[(79±6)g/L、(3.8±0.4)×10^(9)/L、(66.4±3.6)×10^(9)/L]与A组[(59±7)g/L、(3.2±0.4)×10^(9)/L、(52.6±2.8)×10^(9)/L]、B组[(61±7)g/L、(3.1±0.3)×10^(9)/L、(52.8±2.6)×10^(9)/L]对比,差异有统计学意义(P<0.05)。C组G-CSFR(5.35±0.16)pg/ml和白细胞介素-11受体(IL-11R)(6.38±0.54)μg/kg水平均高于A组[(2.23±0.13)pg/ml和(1.49±0.24)μg/kg]和B组[(2.31±0.16)pg/ml和(2.31±0.49)μg/kg]差异有统计学意义(P<0.05)。治疗后,C组患者7 d CFU-GM(18.5±6.0)个和14 d BFU-E(83.5±7.5)个高于A组[7 d CFU-GM(9.5±2.0)个和14 d BFU-E(59.5±6.5)个]和B组[7 d CFU-GM(12.0±6.5)个和14 d BFU-E(63.5±5.0)个],差异有统计学意义(P<0.05)。7 d后,C组双歧杆菌(12.56±3.25)lgCFU/g、乳酸杆菌(13.56±2.58)lgCFU/g、肠杆菌(5.12±1.45)lgCFU/g、肠球菌(5.14±0.58)lgCFU/g高于A组[(9.26±1.03)lg CFU/g、(8.65±0.84)lg CFU/g、(8.08±0.64)lgCFU/g、(8.15±0.46)lgCFU/g]和B组[(11.35±1.36)lg CFU/g、(12.43±1.14)lgCFU/g、(6.49±0.55)lgCFU/g、(6.66±0.43)lgCFU/g],差异有统计学意义(P<0.05)。结论微生态制剂联合浙贝黄芩汤治疗可以有效提高ALL大剂量化疗后患者的G-CSFR、CFU-GM、BFU-E水平,可能更好地改善化疗引起的患者骨髓抑制情况,改善肠道菌群,具有临床研究价值。
