{"title":"对 \"芒果苷在砷中毒小鼠氧化应激介导的肝功能障碍中的减毒作用 \"的更正：\"芒果苷在砷中毒小鼠氧化应激介导的肝功能障碍中的减毒作用\"。","authors":"","doi":"10.1002/biof.2026","DOIUrl":null,"url":null,"abstract":"<p>Saha S, Rashid K, Sadhukhan P, Agarwal N, Sil PC. Attenuative role of mangiferin in oxidative stress-mediated liver dysfunction in arsenic-intoxicated murines. Biofactors. 2016;42(5):515–532. https://doi.org/10.1002/biof.1276</p><p>The authors detected an editing error in Figure 5A. During the proofing stage of Figure 5A, the “Normal” liver subpanel was erroneously pasted twice, slightly overlapping. The correct Figure 5A is shown below. The authors confirm that all the experimental results and corresponding conclusions mentioned in the paper remain unaffected.</p><p>Phase contrast micrographs of rat liver (H & E) (200×) showing normal hepatic architecture, MAG-exposed group exhibiting normal architecture, arsenic-exposed disrupted hepatic architecture, indicating loss of hepatic integrity with altered membrane morphologies like vacuolated cytoplasm. Mangiferin post-treatment decreases this loss of hepatic architecture dose dependently comparable to the arsenic group. Mangiferin simultaneous treatment with the optimum dose showing marked improvement in the hepatic architecture altering morphological changes associated with arsenic intoxication.</p><p>We apologize for this error.</p>","PeriodicalId":8923,"journal":{"name":"BioFactors","volume":null,"pages":null},"PeriodicalIF":5.0000,"publicationDate":"2023-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1002/biof.2026","citationCount":"0","resultStr":"{\"title\":\"Correction to “Attenuative role of mangiferin in oxidative stress mediated liver dysfunction in arsenic intoxicated murines”\",\"authors\":\"\",\"doi\":\"10.1002/biof.2026\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p>Saha S, Rashid K, Sadhukhan P, Agarwal N, Sil PC. Attenuative role of mangiferin in oxidative stress-mediated liver dysfunction in arsenic-intoxicated murines. Biofactors. 2016;42(5):515–532. https://doi.org/10.1002/biof.1276</p><p>The authors detected an editing error in Figure 5A. During the proofing stage of Figure 5A, the “Normal” liver subpanel was erroneously pasted twice, slightly overlapping. The correct Figure 5A is shown below. The authors confirm that all the experimental results and corresponding conclusions mentioned in the paper remain unaffected.</p><p>Phase contrast micrographs of rat liver (H & E) (200×) showing normal hepatic architecture, MAG-exposed group exhibiting normal architecture, arsenic-exposed disrupted hepatic architecture, indicating loss of hepatic integrity with altered membrane morphologies like vacuolated cytoplasm. Mangiferin post-treatment decreases this loss of hepatic architecture dose dependently comparable to the arsenic group. Mangiferin simultaneous treatment with the optimum dose showing marked improvement in the hepatic architecture altering morphological changes associated with arsenic intoxication.</p><p>We apologize for this error.</p>\",\"PeriodicalId\":8923,\"journal\":{\"name\":\"BioFactors\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":5.0000,\"publicationDate\":\"2023-12-22\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"https://onlinelibrary.wiley.com/doi/epdf/10.1002/biof.2026\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"BioFactors\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://onlinelibrary.wiley.com/doi/10.1002/biof.2026\",\"RegionNum\":3,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q1\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"BioFactors","FirstCategoryId":"99","ListUrlMain":"https://onlinelibrary.wiley.com/doi/10.1002/biof.2026","RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
Saha S, Rashid K, Sadhukhan P, Agarwal N, Sil PC.芒果苷对砷中毒小鼠氧化应激介导的肝功能障碍的抑制作用。Biofactors.2016;42(5):515-532. https://doi.org/10.1002/biof.1276The 作者发现图 5A 中有一处编辑错误。在图 5A 的校对阶段，"正常 "肝脏子面板被错误地粘贴了两次，略有重叠。正确的图 5A 如下所示。大鼠肝脏相衬显微照片（H & E）（200×）显示正常肝脏结构，MAG 暴露组显示正常结构，砷暴露组显示肝脏结构破坏，表明肝脏完整性丧失，膜形态改变，如空泡化细胞质。芒果苷后处理可减少肝脏结构的损失，其剂量依赖性与砷组相当。与最佳剂量的芒果苷同时治疗可明显改善与砷中毒相关的肝脏结构形态变化。
Correction to “Attenuative role of mangiferin in oxidative stress mediated liver dysfunction in arsenic intoxicated murines”
Saha S, Rashid K, Sadhukhan P, Agarwal N, Sil PC. Attenuative role of mangiferin in oxidative stress-mediated liver dysfunction in arsenic-intoxicated murines. Biofactors. 2016;42(5):515–532. https://doi.org/10.1002/biof.1276
The authors detected an editing error in Figure 5A. During the proofing stage of Figure 5A, the “Normal” liver subpanel was erroneously pasted twice, slightly overlapping. The correct Figure 5A is shown below. The authors confirm that all the experimental results and corresponding conclusions mentioned in the paper remain unaffected.
Phase contrast micrographs of rat liver (H & E) (200×) showing normal hepatic architecture, MAG-exposed group exhibiting normal architecture, arsenic-exposed disrupted hepatic architecture, indicating loss of hepatic integrity with altered membrane morphologies like vacuolated cytoplasm. Mangiferin post-treatment decreases this loss of hepatic architecture dose dependently comparable to the arsenic group. Mangiferin simultaneous treatment with the optimum dose showing marked improvement in the hepatic architecture altering morphological changes associated with arsenic intoxication.
期刊介绍：
BioFactors, a journal of the International Union of Biochemistry and Molecular Biology, is devoted to the rapid publication of highly significant original research articles and reviews in experimental biology in health and disease.
The word “biofactors” refers to the many compounds that regulate biological functions. Biological factors comprise many molecules produced or modified by living organisms, and present in many essential systems like the blood, the nervous or immunological systems. A non-exhaustive list of biological factors includes neurotransmitters, cytokines, chemokines, hormones, coagulation factors, transcription factors, signaling molecules, receptor ligands and many more. In the group of biofactors we can accommodate several classical molecules not synthetized in the body such as vitamins, micronutrients or essential trace elements.
In keeping with this unified view of biochemistry, BioFactors publishes research dealing with the identification of new substances and the elucidation of their functions at the biophysical, biochemical, cellular and human level as well as studies revealing novel functions of already known biofactors. The journal encourages the submission of studies that use biochemistry, biophysics, cell and molecular biology and/or cell signaling approaches.
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